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Cytomegalovirus (CMV) infects approximately 40-90% of the world population. The infection is usually asymptomatic in immunocompetent persons. However, it may have negative impact on physiological status or accompanying diseases especially in the elderly. In particular, increasing number of data suggests that persistent infection with CMV is associated with accelerated aging of the immune system accompanying by the decrease in the number of naïve T cells, the increase in in the number of late-differentiated T cells, and reduced TCD4/ TCD8 ratio. This constellation reduces immunity against a variety of diseases, including infectious diseases, cancer, autoimmune diseases, and alters the response to vaccinations. CMV infection could also influence the pathophysiology of age-related diseases, including cardiovascular diseases, however, the mechanism of such influence is still not clear. It is not clear as well, whether CMV infection influences the all-cause and cardiovascular diseases-related mortality. In conclusion, CMV infection could intensify immunosenescence and contribute to age-related diseases, but inconsistent results of many experiments do not allow currently to define clear guidelines for the treatment of CMV infection in elderly.

The purpose of the immune system is not only to fight off pathogens but also to keep a tolerance to self-antigens. In central tolerance, major mechanisms include apoptosis (for T cells) and receptor editing (for B cells). Regulatory T cells appear to be the most important in peripheral tolerance. Innate immune cells also influence the maintenance of immune tolerance. We have provided an overall review of all these mechanisms. Successful restoration of the immune tolerance is the target of new strategies in autoimmune diseases therapy.

Until recently, the basic test to identify latent tuberculosis infection (LTBI) was the tuberculin skin test, despite its limitations in the form of low sensitivity and specificity. Currently, Interferon Gamma Release Assays from peripheral blood are used for a rapid diagnosis of LTBI and measurement of the interferon gamma (IFN-g) levels secreted by specific T cells stimulated with Mycobacterium tuberculosis antigens. Detection of LTBI is important in the control of people potentially at risk of TB disease, such as people remaining in close contact with BK (+) tb patient and for patients evaluated for biological treatment. The paper presents the value of IGRA in three selected clinical situations: in two cases of latent tuberculosis infection and in one case of active tuberculosis.

Apoptosis is a form of programmed cell death essential for maintaining homeostasis, including onset, progress and resolution of immune reactions. Two major apoptosis pathways: extrinsic (mediated by death receptors) and intrinsic (mitochondrial), were distinguished. Lymphocytes with cytotoxic activity may also initiate apoptosis of target cells by granzyme/perforin (pseudoreceptor) pathway. The specific apoptotic processes, i.e. activation induced cell death (AICD) and neglect induced death (NID), are types of extrinsic and intrinsic pathways, respectively. They both seem to be crucial in apoptosis of antigen-primed T cells during the contraction phase of inflammation. Alveolar lymphocytes (AL) are almost exclusively T effector cells, engaged in interstitial lung disease (ILD) pathophysiologies. The AL numbers in lower airways depends on recruitment to the lung, proliferation and local apoptosis. According to the references, it should be noted that AL usually do not proliferate in alveoli; their apoptosis rate accounts, on average, for 1% of cells in healthy subjects, and this is significantly decreased in disorders with lymphocytic alveolitis such as sarcoidosis and extrinsic allergic alveolitis (EAA). The mechanisms of AL apoptosis have not been completely explained. However, it is the NID process that is probably critical for the culling of T-cell response, as in EAA or sarcoidosis remission, with AICD as an auxiliary and/or modulating mechanism only. It should be emphasised that many ILDs are chronic disorders with no remission or improvement, and it is difficult to describe the AL response in terms of immune expansion/contraction.

Prolactin (PRL) is a hormone synthesized and secreted by lactotroph cells in the anterior pituitary gland. There is also extrapituitary hormone secretion by many cells, including cells of the immune system. In physiological conditions PRL is responsible for lactogenesis and other processes associated with it. PRL plays a significant role during the immune response as a cytokine, affecting proliferation and differentiation of many immune system cells. The biological effect of the hormone depends on binding with the specific prolactin receptor PRL-R, and activation of the transcription factors of targeted genes. For T lymphocyte stimulated PRL, that factor is mainly the interferon regulatory factor (IRF-1), which gives the possibility of adjusting the prolactin immune response. Literature data indicate that hyperprolactinemia (HPRL) is one of the important factors in the pathogenesis and course of autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, systemic sclerosis and Sjogren's syndrome. HPRL is diagnosed in nearly one-third of these patients. However, only a few data indicate the role of prolactin in psoriatic arthritis (PsA), whose etiology and disease progression are not fully elucidated, and the diagnosis is very difficult. Currently there is indicated a pronounced connection between the course of HPRL and activity of PsA. It seems also to be interesting that, regardless of the PRL levels in serum of patients with PsA, administration of bromocriptine--drug-lowering hormone--improves joint and skin symptoms, which indicates a decrease in disease activity, and is a promising way of alternative therapy for psoriatic arthritis. However, the effect of PRL on the pathogenesis and the severity of psoriatic arthritis has not yet been fully understood and further research will provide a possibility to assess the prognostic and diagnostic significance of prolactin in patients with PsA.

Unlabelled: The causes of osteosarcoma (OS) and effector mechanisms of the immune response against OS and other neoplastic diseases remain unknown. According to current knowledge, the major role is attributed to cytotoxic T lymphocytes, NK, NKT and Tăä lymphocytes, which are engaged directly in the destruction of the tumour cells. Helper T lymphocytes (CD4+) and indirectly B lymphocytes are of special importance. There is sparse data on the state and efficiency of the immune system in children with neoplastic disease, with bone tumours in particular. THE AIM OF THE STUDY was the evaluation of selected elements of cellular immunity in children with osteosarcoma at the time of diagnosis., Materials and Methods: The study was performed on a group of 44 children with osteosarcoma, aged from 6 to 20 years (median 15.0 years). The control group consisted of 22 children of the same age (median 14.5 years) without the diagnosis of neoplastic disease and active inflammatory state. T lymphocytes with their subpopulations, activated T lymphocytes (CD3+/HLA-DR+), B lymphocytes, NK and NKT cells were analyzed in peripheral blood using the flow cytometry method. Examinations were performed before the therapy - in the diagnostic period., Results: A lower number of peripheral blood lymphocyte population in children with osteosarcoma at diagnosis, compared to the control group was observed. The differences concerned T lymphocytes CD3+(1609.0 vs 3038.0 kom/μl, p<0.001) CD4+(598.0 vs 1071.0 kom/l; p<0.001) and their cytotoxic subpopulation CD8+ (386.0 vs. 866.0 cells/μL; p<0.001), activated T lymphocytes CD3+/HLA-DR+(39.0 vs. 81.0 cells/μL; p<0.025), B lymphocytes CD19+(205.0 vs. 381.0 cells/μL; p<0.025) and NK cells (161.0 vs. 339.0 cells/μL; p<0.005). The number and percentage of peripheral blood lymphocytes in children and youth with osteosarcoma at diagnosis is over 50% lower compared to the patients without neoplastic disease., Conclusions: 1. The general analysis of peripheral blood without differentiating lymphocyte subpopulations is insufficient to determine disturbances which are forming in the immune system of patients developing the neoplastic disease. 2. The course of the neoplastic disease (osteosarcoma) in patients of developmental age is very diverse, and associated with individual biological variation. 3. The evaluation of the immunologic status in patients with osteosarcoma may have prognostic meaning for the further course of the disease, may prevent the formation of unfavourable clinical changes, and be the basis for correcting the administration of cytostatic agents.

Diisocyanates are currently the most common cause of occupational asthma in industrialized countries, where its prevalence ranges from less than 5% to 15%. They are mainly used in the production of polyurethane foam, plastic packagings, laminates and polyurethane paints. The diagnosis of diisocyanate asthma is often problematic due to the lack of simple diagnostic or screening tests, uncertainty of underlying mechanisms, and a multitude of other potential occupational and environmental causes of asthma. At present, only a specific standardized challenge test with diisocyanates in concentrations not exceeding the adopted hygiene standards has been found to show a real diagnostic value. The diisocyanate-inducedsensitization, is associated with the recruitment of CD4 T lymphocytes to the lungs and the production of Th2-type cytokines, including IL-4, IL-5 and IL-13. However, clinical studies have suggested that an immunological response to diisocyanates may involve both Th1 and Th2 cells. The development of animal models has been instrumental in furthering the understanding of the pathogenesis of many diseases, including bronchial asthma. Murine models of diisocyanate-induced asthma have proved to be the most useful. Mouse models offer distinct advantages of a better-defined genome than that of guinea pigs or rats and the availability of antibody reagents and transgenic strains to investigate detailed mechanistic pathways. A better understanding of the immunopathogenesis of diisocyanate asthma will hopefully lead to early markers of sensitization and asthma, as well as to a profound comprehension of exposure and host risk factors, both of them should greatly facilitate the development of much-needed diagnostic and preventive strategies for diisocyanate asthma.

The HLA-E protein is one of the most extensively studied MHC class Ib antigens and the least polymorphic one compared to other MHC class I molecules. In the human population there have been reported just ten alleles encoding three different peptides. Only two of these alleles, namely HLA-E*0101 and HLA-E*0103, are widely distributed (around 50% each). The proteins encoded by these alleles differ from each other in one amino acid at position 107. In HLA-E*0101 it is arginine and in HLA-E*0103 it is glycine. The difference between these proteins manifests itself in surface expression levels, affinities to leader peptides and thermal stabilities of their complexes. The HLA-E molecule is a ligand for CD94/NKG2 receptors on NK cells and TCR receptors on NK-CTL (NK-cytotoxic T lymphocyte) cells, so it plays a double role in both innate and adaptive immunity. This paper reviews the knowledge on the role of the HLA-E molecule in the immunological response. Aspects related to polymorphism of the HLA-E gene and the course of several diseases including type I diabetes, ankylosing spondylitis, HCV and HIV infections, nasopharyngeal cancer and recurrent spontaneous abortions, as well as the outcome of hematopoietic stem cell transplantation, are presented and discussed in more detail.

Introduction: The diagnosis of latent tuberculosis infection (LTBI) is currently based on the century-old tuberculin skin test (TST). However a positive reaction can result from infection by Mycobacterium tuberculosis, BCG vaccination or cross-reaction with nontuberculous mycobacteria. T-SPOT.TB assay is a new test to diagnose tuberculosis infection by measuring in vitro T-cell interferon gamma release in response to two Mycobacterium tuberculosis-specific antigens: ESAT-6 and CFP 10., Material and Methods: T-SPOT.TB assay has been performed on whole blood samples (n = 137) from March to September 2010. A tuberculin skin test result was available for 96 of participants. A positive TST result was considered if the induration was 10 mm or more., Results: Of the 137 patients tested, T-SPOT.TB assay results were positive in 37 (27%), negative in 98 (71.5%) and indeterminate in only 2 (1.5%) persons. We analyzed T-SPOT.TB and TST results in the 96 patients for whom both test were available. Concordance between T-SPOT.TB and TST results (10 mm skin reaction interpreted as positive) was 79%. Fifteen (15.6%) patients had a positive TST result and a negative T-SPOT.TB and 5 (5.2%) patients had a negative TST result and a positive T-SPOT.TB. We observed good correlation between positive T-SPOT.TB results and the size of induration ≥ 15 mm in TST results., Conclusions: T-SPOT.TB offers a more accurate approach than TST for identification tuberculosis infection. The study shows that the test T-SPOT.TB is a good diagnostic tool in identifying persons with tuberculosis infection. For full confirmation of this assessment, it is necessary to examine more cases.

Previous neuroimmunological studies focused mostly on depression, regardless of its diagnostic category. In this paper, the studies on the immunological system in patients with bipolar affective illness, including manic episode, have been presented. Research possibilities of neuroimmunology of affective disorders using molecular-genetic methods have also been shown. The studies on the neuroimmunology of depression have always been connected with studies on changes in the immunological system related to stress situations. Disturbances of the immunological system regulation have features of either decrease or pathological increase of the immunological system, with increased activity of pro-inflammatory cytokines (interleukin 1 and 6, interferon). Some pathogenic role for the disturbances of immunological system in depression is also played by viral infections (herpes, Borna viruses). The changes of the immunological system in mania are mostly similar to those observed during depression. An increase of activity of pro-inflammatory cytokines, connected with the lymphocyte Th1 system is especially evident. Like in depression, the role of viral infections has been pointed out (herpes, Borna, parvovirus B19). The oldest mood-stabilizing drug, lithium, has been shown to have strong action against herpes viruses. Molecular-genetic studies point to an association of some genes of the immunological system with both bipolar disorder and schizophrenia. An association of some genes with a predisposition to depression and efficacy of antidepressant drugs has also been shown.

In mycoses congenital--nonspecific innate as well as acquired immunity (involving neutrophiles, monocytes, macrophages, dendritic cells and lymphocytes) both play important roles in host defence. Th1 lymphocytes release cytokines (IL-2, IL-12, IFN gamma) and stimulate cytotoxic cells and neutrophiles to destroy fungal cells. Th2 lymphocytes, on the other hand, suppress cellular immunity by releasing the cytokines IL-4, IL-6 and IL-10 which counter regulate the secretion of IL-2, IL-12, IFN gamma and depress the activity of macrophages. Cellular mechanisms play essential roles in host responses to fungal infections. Dysfunction of T lymphocytes and a reduction in their number are typically observed in patients with mycotic diseases. There occurs a reduction of both T lymphocyte populations and the T-helper to T-suppressor cell number ratio, and these are of critical importance in explaining the diminished IgA production and enhanced adhesion of fungal cells to the surface of host cells as well as in facilitating the intrusion of fungi throughout the skin and mucous membranes. The specific immunological reaction, associated with the synthesis of antibodies against fungal cell wall or cytoplasmic antigens, is of little significance in protective immunity, but nevertheless has a rather important role to play in diagnosis as well as in supporting phagocytosis by inhibition of fungal cell adherence. In patients with mycoses, typically low blood serum level of the immunoglobulin class G and A and low sIgA in saliva are observed. A detailed understanding the nature and function of the immune system in mycoses is necessary to enable improvements in pharmacotherapy with antifungal antibiotics and chemotherapeutics, as well as to treatments based on immunotherapy and vaccination.

Many individuals infected with HBV become chronic carriers and they liver disease may progress to cirrhosis and HCC. The newest data suggests that the interaction between positive and negative costimulatory molecules expressed on T cells are performing the role in the regulation ofT cells immune response. In the last years they were described programmed death-1 (PD-1) [CD279] and programmed death-ligand 1 (PD-L1) [CD274] in immunopathology of HBV infections. In acute exacerbation of hepatitis B, high level of PD-1 expression significantly mediated CD8+T cells apoptosis and protecting before damaging the liver. In the period of recovering, activation of the PD-1/PD-L 1 pathway should dynamically decrease, and if it isn't taking place, increased expression of the PD-1 plays a crucial role in inhibiting the function of virus-specific CD4+ and CD8+ T cells in chronic viral infections. The aim of this article was to explore the potential role of (PD-1/PD-L) pathway in antiviral immunity during HBV infection. Blockade of PD-1/PD-L1 pathway may open a novel therapeutic strategy for restoring the function of the exhausted CD8+ T cells, and enhancing viral control during chronic viral infections.

Aim of Study: To define a relationship between emergency and elective indications for cesarean section and quantitative changes of percentage and quantity of T and B lymphocytes and their subpopulations in healthy full-term neonates., Material and Methods: The study included 43 healthy neonates born in the years 1998 - 2003 in the Department of Perinatology and Gynecology of Silesian Medical University in Zabrze, Taking into account operative delivery, a group of 43 full-term neonates born by cesarean section were examined, including 25 neonates with elective indications [Ibe] and 18 with emergency indications (Ibn). Immunological studies included evaluation of the percentage of T and B lymphocytes and of their subpopulations in umbilical blood. Our study applied a method of umbilical blood sampling with the following red blood cells lysis., Results: The study showed that mean number of CD3+, CD23+, CD25+ lymphocytes and mean percentage and number of CD8+ lymphocytes in full-term neonates born by elective Cesarean was statistically significantly lower than in neonates born by emergency Cesarean section. No statistically significant differences were found in mean values of other parameters among the study groups., Conclusions: Cesarean section performed in a mother with emergency indications can favor an increase of mean quantity of T lymphocytes, cytotoxic - suppressor T lymphocytes, activated T lymphocytes, B CD23 lymphocytes in full-term neonates.

Introduction: Adenoid has particular meaning to develop of immunological response to inflammations in upper respiratory inclusive middle ear. The mining of antigen CD27 on lymphocytes T and B in creation of memory cells is still unclear., Aim: CD27 on lymphocytes T and B has a crucial role in development of immune response against inflammatory state. Aim of this study was evaluation functions of lymhocytes with expression CD27 in hypertrophied adenoid in children with otitis media with effusion., Material and Methods: [corrected] We tested 24 children in examine group with hypertrophied adenoid and otitis media with effusion (OME), and 29 children in comparative group only with hypertrophied adenoid (HA). We also divided both groups into two groups, above 5 and over 5 years old. We made the research by flow cytometry method. We used anty-CD19, anty-CD3, anty-CD5 and anty-CD27 monoclonal antibodies to examinations., Results: We showed the lowest percentage lymphocytes B CD5+ with expression of CD27 in subgroup older children with otitis media with effusion (O.M.E. 22.43 +/- 2.66%) in compartative to younger children in the same group (15.96 +/- 5.31%; p < 0.005) and to older comparative subgroup (H.A. 15.50 +/- 8.03; p < 0.001). Percentages of B CD5 cells with expression of CD27 was statistical lower in examinated group (7.25 +/- 3.81) than in comparative group (H.A. 16.26 +/- 5.82; p < 0.04). In group with hypertrophied adenoid showed higher percentages of CD5-CD27+CD19+ cells both in younger and older supgroup than in equivalent supgroups with O.M.E., Conclusions: Iteraction of CD27-CD70 regulates many functions of T and B lymphocytes. It seems that disorders humoral immunologucal answer in hypertrophied adenoids are supported to develop of otitis media with effusion.

Grave's disease and autoimmune hypothyroidism represent the two main autoimmune thyroid diseases, where an immune response is directed against the thyroid gland. The essence of these diseases is loss of tolerance of own tissues caused by malfunction of the T lymphocytes, which effect the production of antibodies reacting with particular cell structures and tissues. Cytokines participate in the induction and effector phase of the immune and inflammatory response and therefore play a critical role in the development of autoimmune thyroid diseases. Regulatory T cells take part in regulation of immune response and play a leading role in developing immune tolerance through active suppression.

The main immunological elements that control infection with herpes simplex virus type 1 include interferon, NK cells, and specific T and B cells. The aim of this study was to determine the influence of Namalwa cells (B cell immortalized by EBV) which produce IFN alpha in large amount on inhibition of HSV-1 replication in CV-1 and MDBK cells. Inhibition of HSV-1 replication was measured by MTT assay. Addition Namalwa cells to CV-1 or MDBK cells infected HSV-1 inhibited virus replication. Degree of inhibition was connected with amount of added cells and with time of addition (before infection or after infection). The highest inhibition of HSV-1 replication showed Namalwa cells added one hour before infection (72% for CV-1 infected HSV-1 and 68% for MDBK infected HSV-1).

In this paper we summarized the current knowledge about the new mechanism of immunosuppression in cancer i.e. the lately discovered myeloid-derived suppresor cells (MDSC). MDSC are produced in bone marrow under the influence of tumor cell derived substances. MDSC show negative effect on T lymphocytes function through arginine depletion and nitric oxide production. In mice MDSC are characterized by Gr-1 and CD11b expression, however in human there are no definitive markers of this subpopulation. Some laboratory experiments in turning back the negative influence of MDSC on immunological system are provided, mainly through the administration of monoclonal antibodies against MDSC or drugs which block their function. The elucidation of MDSC characteristics can allow us to build new immunotherapeutic protocols in the future.

Neopterin (NPT) concentration reflects the activation of the cellular immune system. Neopterin is released by macrophages stimulated by interferon gamma which is produced by activated T lymphocytes. Raised NPT concentrations in body fluids are found in various disorders, e.g., viral infections, infections caused by intracellular bacteria, autoimmune disorders and malignancy. Neopterin concentration is low or not significantly high in bacterial infections (except for induced by intracellular bacteria).

Kidney transplantation causes an immune response to non-self antigens called allograft rejection. The response to a kidney allograft can be divided into three phases: recognition of the alloantigen, activation of antigen-specific lymphocytes, and the effector phase of graft rejection. Full T-cell activation requires two distinct signals: one through the TCR and a second costimulatory signal through accessory molecules. These accessory molecules play two important roles. The first is to maintain contact between the T cells and APCs, thus providing time for the TCR to sample the antigen on the APC (ICAM-1/LFA-1). The second role is to cooperate with TCR-initiated signals in T-cell activation. The most important second costimulatory signals influencing T-cell clonal expansion and differentiation are provided by the B7/CD28 family of molecules. In the effector phase of graft rejection, foreign cells are damaged by means of three possible mechanisms: 1) T-cell cytotoxicity, 2) delayed-type hypersensitivity, and 3) antibody-dependent cell-mediated cytotoxicity.

Psoriasis is a chronic, inflammatory skin disorder, which occurs in about 1-3% of general population. Skin lesions are a result of hyperproliferation of epidermis and of time shortening of the transposition of keratinocytes from basal to corneal layer of epidermis. In healthy subjects this time is estimated on about 26-28 days, whereas in psoriatic individuals lasts only 3-4 days. Despite many investigations, the etiopathogenesis of psoriasis still remains unclear. Observations that psoriasis could occur in the same family members, indicated the importance of genetic factors. Moreover, high effectiveness of immunosuppressive drugs in the treatment of psoriasis suggested also a significant role of immune system in the development of this disease. Here, we present the current knowledge on the role of genetic and immunological factors in the development of psoriasis.

The CD28 molecule is a glycoprotein presented mainly on T lymphocytes. It performs several functions in the organism, an important one being its role of costimulator for the activation of T lymphocytes. Binding with B7-1 (CD80) and B7-2 (CD86) ligands on antigen-presenting cells (APCs) induces the second signal essential for the activation of T lymphocytes and facilitates close apposition of the cell membranes of the APC and T cell. Costimulation through CD28 enhances the transcription and stability of IL-2 mRNA, the expression of Bcl-XL antiapoptotic molecules (thus supporting the proliferation of activated T lymphocytes), and also changes the polarization of Th lymphocytes towards the Th2 type. CD28 is mainly a positive regulator of T-cell activation, but it was also found to influence the negative selection of peripheral T lymphocytes. CD28 signals contributing to clonal expansion and effectory functions make T cells more sensitive to activation-induced cell death (AICD). When T lymphocytes are involved as a result of a strong TCR signal, the CD28 signal reduces the expansion of T cells, enhances apoptosis, and facilitates tolerance. CD8+ T lymphocytes, which lack the CD28 marker, play the role of regulatory cells. Blockade of the CD28-B7 interaction could be useful in preventing undesirable activation of the immune system in allergies, after transplantation, and in autoimmune diseases. Recently, more and more attention is being paid to anti-CD28 monoclonal antibodies and the possibilities of treating patients with autoimmune diseases and patients after transplantation.

Kidney transplantation causes an immune response to non-self antigens called allograft rejection. The response to a kidney allograft can be divided into three phases: recognition of the alloantigen, activation of antigen-specific lymphocytes, and the effector phase of graft rejection. Allogeneic major histocompatibility complex (MHC) class I and class II molecules elicit a vigorous T-cell response. The alloresponse comprises CD4+ T cells that recognize allogeneic MHC indirectly after processing the molecules into peptide fragments. The majority of alloreactive T cells directly recognize intact allogeneic MHC molecules expressed on foreign cells. The interaction between the TCR of a T cell and the MHC/peptide complex on an antigen-presenting cell (APC) determines the specificity of the immune response. Two distinct signals are required for T-cell activation: one signal through the TCR and a second costimulatory signal through accessory molecules.

Background: Food allergy is an abnormal response of the immunological system, especially of mucosal immunological system on antigens supplied per os. There are very complicated and still unexplained immunological mechanisms, which lead to hypersensitivity reaction. Most often food hypersensitivity is identified as the effect of atopy, which is connected with humoral response (specific IgE antibody). On the other hand cell immunological response are less investigated, however they can be very important, especially as a significant factor to initiate pathological allergic processes., Aim: To investigate, the usefulness of flow cytometry for estimation of specific sensitization of subpopulation of lymphocytes on food allergens in the allergy diagnosis., Patients and Methods: The investigations were performed on 60 children from 6 months to 5 years old: 20 children with CM A IgE dependent, 20 with CM A IgE independent and 20 healthy children. IgE total, sIgE, IgG, IgA, IgM, basic immunological panel, CD 23, CD25, CD26, CD30, CD69, PCNA were measured., Results: We noticed decrease of expression of CD4+CD30+ between I and II examination (p=0.029), between I and III (p=0.009); decrease of expression of CD8+CD26+ between I and III test (p=0.038); decrease of expression of CD19+CD23+ between I and II examination (p=0.012) in I type of hypersensitivity. We observed a decrease of expression of CD4+CD25+ between I and III examine (p=0.026) and decrease of expression of CD4+ CD26+ between I and III examination (p=0.036) in IV type of hypersensitivity. Expression of CD69 was decreased after diet in IgE dependent allergy. Values of expression of PCNA are similar in I and IV type of hypersensitivity in children with CM A. Decrease of expression of PCNA in II examination was observed in both cases. Reintroduced allergen caused increase of expression of PCNA in both types of allergy (p=0.048 and p=0.041)., Conclusions: Our recent research confirms changes of the expression of T lymphocytes activation markers. It is connected with in vivo stimulation to allergen or with allergen elimination. The study of expression of activation markers using flow cytometry in food allergy in children can be helpful in observation of the dynamic progress process, but it cannot be used as a single diagnosis test.

Inflammation is key element in effector phase of all immune processes and create a cascade system of specific enzyme functions regulated in autocrine way. Humoral antigen-antibody reaction activate the complement system which is responsible for secondary mediatots generation and tissues destruction. Liberated mediators like kinins, leukotriens inflammatory cytokines and activated cell bound metalloproteases in tissues and blood vessels are responsible for oedema of tissues, pain, cell destruction and organ dysfunction. Induction of T cell dependent inflammatory reaction involve antigen dependent activation of T cells which usually is delayed and long lasting. The immune reactions responsible for specific activation induce inflammation.

In recent years new potential therapies of systemic lupus erythematosus, called biological therapies, have been developed. These agents influence some immunological reactions, essential for genesis of systemic lupus erythematosus, ie. T cells and B cells activation, antibodies production, cytokines and complement components activation. Pathogenic basis of using these therapies, their safety and efficacy assessment have been presented.

Unlabelled: The aim of the study was to assess the role of costimulatory molecules in pathogenesis of nonallergic bronchial asthma., Material: The studied group consisted of 30 patients with nonallergic asthma, 24 with nonallergic asthma and recurrent respiratory tract infections and 20 healthy controls., Results: In nonstimulated and lipopolysaccharide (LPS) stimulated cultures of control group the mean value of CD16+ + 56+ CD28+ subpopulation were significantly decreased compared to values in both types of asthma. Similar dependence was observed in cultures of asthmatic patients with infection and healthy person, stimulated with IL-15 and in CD4+CD28+, CD8 +CD28+ and NKCD28+ cultures from all studied groups, stimulated with LPS plus IL-15. In nonallergic asthma and infection asthma mean values of CD4 +CD152+ and CD16+ +CD56 +CD152+ from nonstimulated and IL-15 stimulated cultures were significantly increased compared to analogical values in control group., Conclusion: The results of our studies suggest that in nonallergic asthma the disturbed expression of costimulatory molecules may play an important role in pathomechanism of disease.

Aim: In the present study, we conducted the quantitative analysis of peripheral blood lymphocytes population and subpopulation in patients with stomach cancer, based on flow cytometry immunophenotyping., Material and Method: The results were compared with the advancement of the disease (UICC/TNM), histological type (Lauren classification), and grade of differentiation of stomach cancer. Lymphocyte CD: (CD3/CD19, CD3/CD4, CD3/CD8, CD3/CD16, 56) were determined in 50 cancer patients and 30 healthy humans., Results: The significant deficiency of total lymphocyte number, T and B lymphocytes, as well as CD4+ and CD8+ was found in stomach cancer patients. There was no depletion in NK cells number. In advanced stomach cancer, the number of NK cells decreased, along with further deterioration of lymphocytes T and B populations. In patients with diffuse-type of stomach cancer and III or IV stage, the more pronounced deficiency in T, CD4+ and CD8+ population was noted. The decrease grade of differentiation was correlated with the increase of NK cell population. There was no correlation between the number of B lymphocytes and the histologic type or grade of differentiation of stomach cancer., Conclusion: The obtained data demonstrated significant quantitative defect in defence of stomach cancer patients.

This article is focusing on the etiology of the multiple sclerosis (MS). MS is the disease of autoimmune origin, concerning mainly young people with its complicated nature. The course of the degenerative and inflammatory process is variable and unexpected, from featureless to the vast and rapidly progressing nature, leading to the considerable disability. The etiological factors are not still well known. We can distinguish different agents: genetic, immunological and environmental, among them tobacco smoking also. Authors survey the etiopathological basis of the disease.

Multiple Sclerosis (MS) is a chronic inflammatory autoimmune disease of the central nervous system (CNS) characterized by the presence of cellular infiltrates consisting primarily of lymphocytes and macrophages and localized areas of demyelination in the CNS. MS is thought to be initiated by self-reactive CD4(+) Th1 T cells. Thus far, treatment modalities for MS are limited, with the most common acting nonspecifically on the immune system, resulting in a general immunosuppression accompanied by severe side effects. There is a large demand for developing MS therapy that particularly targets pathogenic myelin-specific T cells. Experimental allergic encephalomyelitis (EAE) is a well-characterized animal model that mimics many of the disease symptoms of MS, including the presence of cellular infiltrates and demyelination. EAE can be actively induced in genetically susceptible strains of mice, rats, and monkeys and is mediated by activated autoreactive CD4(+) T cells that are specific to MBP (myelin basic protein). The knowledge acquired using EAE allows us to better understand the pathogenesis of MS and thus manipulate particular components of the immune response in order to develop an efficient therapy.

Introduction: Otitis media with effusion (WZU) is highly prevalent among young children. The hypertrophied adenoid favorables to development (WZU). The pharyngeal tonsil delivers the essential lymphocytes for developed immunological answer. The migrations of lymphocytes to pharyngeal tonsil and to places inflammatory proceed with part of adhesive molecules (CD11a, CD54) presented on lymphocytes. The aim of this study was examination the percentage of the lymphocytes CD4+, CD8+ and lymphocytes B with expression of adhesion molecules ICAM-1 (CD54) and LFA-1 (CD11a). We examined their expression in hypertrophied adenoid by children with otitis media with effusion., Results: In investigations was showed statistically significant decrease of percentage of lymphocytes CD4+CD11a+ and CD8+CD11a+ and increase of percentage of lymphocytes CD19+CD54+ in otitis media with effusion in comparison to group with hypertrophied adenoid., Conclusions: Molecule adhesive ICAM-1 and LFA-1 fulfills important part in many immunological processes proceed to pharyngeal tonsil. The considerably lower percentage of lymphocytes T CD4+ and CD8+ with expression LFA-1 in hypertrophied adenoids is possibly of causes of incorrect their immunological answer, and the same factor favourables to prolonging the otitis media with effusion at children.

Introduction: The expansion of an optimal immune response requires fully activated T lymphocytes. For complete activation several signals are needed. The first signal is an antigen dependent via the TCR receptor, and the second signal is a costimulatory that can be delivered by the CD28 molecule after binding to their ligands. Fully activated T lymphocytes are competent to deliver activation to B cells. We suppose that this way can be important for development of immune response in hypertrophied adenoid (AH) in children with otitis media with effusion (OME). The aim of this study was evaluation of the percentage and MFI (mean fluorescence intensity) of lymphocytes CD4+, CD8+, CD19+ with expression of superficial adhesive molecule CD28 in hypertrophied adenoids in children with otitis media with effusion., Material and Methods: 37 children with otitis media with effusion and 35 children with hypertrophied adenoids were tested. Children were also divided into two subgroups: young (below 5 years) and older children (above 5 years old). Expression of adhesion molecule CD28 on lymphocytes of adenoids tissue was estimated by flow cytometry method., Results: This study showed significantly higher percentage of lymphocytes CD4+CD28+ in children with otitis media with effusion (OME 93,87%) than in comparative group with hypertrophied adenoids (AH 91,01%). Mean fluorescence intensity CD28 was higher on subpopulation lymphocytes CD4+ to children with OME (3,94) than AH (3,32). We did not find difference between OME and AH in percentages and MFI of subpopulations CD8+CD28+ and CD19+CD28+ lymphocytes., Conclusions: Adhesion molecule CD28 is very important for adenoidal lymphocytes activation and protection against apoptosa. Higher percentage of lymphocytes CD4 with expression CD28 confirms their participation in developing and forming of immunological response in otitis media with effusion.

The Notch family of cell surface receptors and their ligands constitute an evolutionarily conserved signaling pathway that is used by invertebrates and vertebrates to regulate a broad spectrum of cell specification events through local cell interactions. After ligand binding Notch receptor undergoes proteolytic processing ultimately liberating the cytoplasmic domain of the Notch receptor which translocates to the nucleus and activates target genes. In all animal models tested, mutations in Notch genes invariably resulted in developmental abnormalities. In mammals, Notch signaling controls key stages of lymphocyte differentiation as well as activation and several abnormalities in Notch pathway have been suggested to cause human leukemias. Cre-loxP mediated conditional gene targeting significantly contributed to our current understanding of the physiological roles of different Notch family members in hematopoietic compartment. This technique helped to overcome embryonic lethality of Notch mutants providing the opportunity to inactivate specific Notch gene in adulthood.

Introduction: Otitis media with effusion (OME) and hypertrophy adenoid (AH) are still common diseases during childhood. Adenoid has particular meaning in develop of immunological answer to inflammation in upper respiratory inclusive middle ear. The CD62L lymphocyte adhesion molecule plays an important role in controlling lymphocyte extravasations into adenoid and at sites of tissue infection. The aim of this study was evaluation of the percentage lymphocytes CD4+, CD8+, CD19+ with expression of superficial adhesive molecule CD62L and its expression in hypertrophied adenoids at sick's children with otitis media with effusion., Material and Methods: In investigations has tested 37 children with otitis with effusion and 35 children from hypertrophied adenoids. Expression of adhesion molecule CD62L on lymphocytes of tissue adenoids estimated by flow cytometry method., Results: In this study showed higher significant percentage of lymphocytes CD19+CD62L+ in children in otitis media with effusion (OME. 59.33 +/- 9.65%) with reference to comparative group with hypertrophied adenoids (AH 53.47 +/- 9.67%). Mean fluorescence intensity CD62L was higher on subpopulation lymphocytes CD8+ and CD19+ at children with OME than AH., Conclusions: The increase of percentage's lymphocytes CD62L+ in tissue of adenoids can to testify to enlarged migration lymphocytes from whole blood to adenoid. The increase of density of CD62L receptor on lymphocytes can be effect local inflammatory process.

Hemophagocytic syndrome (HS) is a rare but life-threatening disease caused by inappropriate activation of T-lymphocytes and histiocytes, hipercytokinemia and hemophagocytosis. The most common symptoms are fever, hepatosplenomegaly, unspecific neurological abnormalities, pancytopenia, coagulopathy, hiperferritinemia and lipid abnormalities. HS is classified into two forms: primary, inherited (Familial Hamophagocytic Lymphohistiocytosis--FHL) and secondary (associated with infection, malignancy, autoimmune disease). In spite of the fact that diagnostic guidelines are available it often remains unrecognised. Prognosis of HS depends on the form of disease and in case of secondary HS on the underlying disease. Development of the treatment protocols (HLH-94, HLH-2004) which combine immunochemiotherapy with hematopoietic stem cell transplantation has strongly improved prognosis in HS especially in the primary form. Three-year overall survival for children with HS is now over 50%. Early diagnosis and appropriate therapy is crucial for effectiveness of the treatment. Popularisation of the knowledge about the syndrome, diagnostic guidelines and treatment protocols can contribute to more frequent appropriate recognition of HS and to improvement of the treatment results.

Cigarette smoking is the main trigger for the development of chronic obstructive pulmonary disease (COPD). For years the inflammatory reaction in COPD was focused on neutrophils, macrophages and protease-antiprotease balance. The concept of inflammation has been changed since the findings in the bronchoalveolar lavage (BAL) of smokers and COPD patients. It is now evident that the inflammatory reaction composed of neutrophils and macrophages represents the innate immunity reaction. This reaction will proceed over time to damage the lung, producing peptides and modified proteins from matrix destruction, cell necrosis and cell apoptosis. These products have the potential to act as antigen determinants. Dendritic cells which are abundantly present in smokers' lungs are important link between innate and adaptive immunity involving T-cells. These cells mature and migrate to draining lymphatic organs, where they could present antigens to CD-4+ and CD-8+. T-cells that induce their activation and differentiation. As a result T-cells are important component of the chronic inflammation in smokers and in COPD patients. So one of the possible conclusions could be that COPD is a disease produced, at least in part, by self-antigens from the lung secondary to smoking.

Introduction: The quantity of lymphocytes in adenoid and their cooperation in immunological processes is dependent on proliferation process and their migration to the effectory places. The most important process provide for equilibrium between lymphocytes of tonsils is apopotosis. Special meaning in induction this process has Bcl-2 family proteins with can be divided into pro-apoptotic and anti-apoptotic. An investigation was executed in hypertrophied adenoids with or without otitis media with effusion., Material and Methods: By flow cytometry percentage of lymphocytes CD4+, CD8+, CD19+ and percentage of these lymphocytes with expression Bcl-2 proteins in hypertrophied adenoid and hypertrophied adenoid and otitis media with effusion was analyzed., Results: The percentage of lymphocytes CD4+Bcl-2+, CD8+Bcl-2+, CD19+Bcl-2+ was lower in hypertrophied adenoid and otitis media with effusion compared to the control group., Conclusions: Tendency to lowered percentage of lymphocytes T and B with expression Bcl -2 protein in adenoids reflects likely the local immunity alterations.

Introduction: The cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) is a transmembrane molecule present on T cells that plays a critical role in the down regulation of antigen-activated immune response. Its gene polymorphism is a strong candidate gene for conferring susceptibility to thyroid autoimmunity. THE AIM of the study was to analyse the surface CTLA-4 (CD 152) expression on peripheral blood lymphocytes., Material and Methods: Blood samples from 66 children were analysed: 36 with Hashimoto's thyroiditis and 30 healthy, age-matched controls, mean age: 13.4 years. The percentages of peripheral blood lymphocyte subsets were analysed by evaluation of CD antigens surface expression with three colour flow cytometry using Coulter EPICS XL cytometer. CD28, CD152, CD4, CD8 antigens were evaluated. Statistical analysis was performed using t- test and other tests of the Statistica programme. P-value <0.05 was considered as statistically significant., Results: In children with Hashimoto's thyroiditis the surface expression of CD8(+) CD152(+) T cells was statistically significant lower than in healthy controls. P-value was 0,02. Percentage of other CD examined in the study did not differ significantly in patients and in the control group., Conclusion: In children with Hashimoto's thyroiditis the surface expression of CTLA-4 (CD152) on peripheral blood lymphocytes CD8(+) was statistically significantly lower than in healthy controls.

Sarcoidosis (SA) is a systemic granulomatous disorder of unknown etiology. The diagnosis is firmly established when clinicoradiological findings are supported by histological evidence of noncaseating epithelioid cell granulomas found on tissue biopsy Diagnosis of SA requires exclusion of other causes of granuloma formation, first of all Mycobacterium tuberculosis. Sarcoidosis is a disease known to be associated with various immunological alterations, including depression of cutaneous delayed-type hypersensitivity and an activation of monocytes/macrophages and a heightened helper T cell type 1 immune response at sites of disease but the mechanism leading to the persistent accumulation of inflammatory cells is not understood. In some studies, apoptosis is considered as factor in pathogenesis of sarcoid and tuberculous granuloma. Apoptosis--programmed cell death is a genetically encoded cell elimination program which ensures equilibrium between cell proliferation and cell death and by which crippled, useless or infected cells are eliminated as part of normal physiology. Aberrations in signalling, in receptors or alterations in mechanism of apoptosis are involved in the occurrence of tuberculosis. To date, there are a few of papers concerning alternations of apoptosis of peripheral and alveolar mononuclear cells in sarcoidosis have been published but the results have been controversial.

The immonomodulatory mechanisms responsible for allergens tolerance in healthy subjects were described on the basis of the newest medical literature, including own papers and experience. It was detected that the same immunological mechanisms are built by specific immunotherapy. IL-10 and TGF-beta cooperate in the regulatory T-cell response to aeroallergens, food allergens and allergens of bee and yellow jacket venoms in healthy subjects as well as during specific immunotherapy making the tolerance to these allergens. The actual progress in improvement of specific immunotherapy methods is described.

Celiac disease results from genetic abnormal immune response to gluten. This leads to local activation of immune system. There are several clinical manifestations of the disease (e.g. active, silent and latent). Fundamental processes of celiac disease occur in small intestine mucosa. As a result of immunological reactions the development of inflammatory process with typical histopathological lesions is observed. In pathogenesis of celiac disease immunological cellular response with significant role of T lymphocytes is of great importance. According to one hypothesis in the disease non proliferative activation of lamina propria CD4+ lymphocytes and proliferative activation of intra-epithelial TcR alpha/beta CD8+ and TcR gamma/delta lymphocytes is postulated. Probably in immunological reaction to gluten besides T lymphocytes other cells are involved (lymphocytes B, NK cells, neutrophils, eosinophils, macrophages, mastocytes) but their role was not clearly established. Recently in pathogenesis of celiac disease participation of cytokines produced locally in small intestine is often emphasized.

The mechanisms of immunosuppression and immunotherapy in vitro in leukemia are reviewed. A predominance of Th2 lymphocytes, diminished percentages of T lymphocyte with costimulatory molecule expression and impaired monocyte function play major roles in impaired immunity in this group of diseases. Neoplastic cells can produce immunosuppressive cytokines and have low expressions of costimulatory molecules. In immunotherapy in vitro, blasts are converted to antigen-presenting cells by cytokines (acute myeloid leukemia blasts) or CD40L stimulation (acute lymphoblastic leukemia blasts). Manipulation of the immune system to stimulate anticancer response can be a promising tool in hematology and oncology.

The influence of trauma, especially surgical operation on immunological response has not been clarified sufficiently. The authors discuss the influence of surgical trauma on humoral and cell mediated immune response and on phagocytosis as well. The role of Tgammadelta+ lymphocytes in immunological processes that occur after trauma have been also discussed.

Regulatory cells comprise a highly heterogeneous T-cell population. It is assumed they are generated both in the thymus and periphery. According to some immunologists, any T-cell population has the potential to differentiate into cells with regulatory properties in the periphery. Following the discovery of their role in maintaining T-cell homeostasis and their ability to prevent autoimmune disease, allergy, and other types of hypersensitivity, regulatory cells have been the focus of intense studies over the last decade. During pregnancy, regulatory cells are believed to mediate tolerance to the fetus. In the unnatural event of transplantation, regulatory cells induce and maintain tolerance to the transplanted tissues or cells and prevent graft-versus-host disease. At the same time, however, regulatory cells are responsible for decreased immunity against tumors and infections. The data which have emerged to date concerning regulatory cells have not allow them to be definitively identified nor their characteristics to be clearly defined. This may be due to the existence of various regulatory cell populations as well as different modes of action depending on the experimental model. Contradictory in vitro and in vivo results and lack of certainty as to how the results of animal trials correspond with the human model are why the notion of harnessing regulatory cells as therapeutic agents is still a distant one, although raising great hopes. The aim of the following article is to make sense of the patchwork of available data concerning regulatory cells and review the potential use of these cells in the field of transplantation.

The development of molecular biological techniques during the last decade has led to the recognition of a series of polymorphic sites in the regulatory regions of cytokine-encoding genes. Different alleles are associated with the binding of transcriptional factors and various degrees of cytokine production. Therefore each person has an individual profile of high and low cytokine responses. Some individuals are more susceptible to inflammatory conditions and the development of an immune response after transplantation. It has been documented that in heart transplantation high TNF-alpha/low IL-10 producers had high levels of graft rejection, while in renal transplants high TNF- alpha /high IL-10 producers were characterized with worse prognosis. The polymorphic features of genes encoding cytokines also associate with the outcome of bone marrow transplantation. It was shown that recipient TNFd, IFN- gamma (CA) and IL-10(-1064) microsatellite polymorphisms and IL-10 (-1082) and IL-6 (-174) SNP polymorphisms are associated with acute GvHD manifestation. No relation was found between TNFA (-308) and aGvHD. Recently, the influence of donor polymorphism within the IL-10 and IL-6 genes was documented. Polymorphism of the TNFd, TNFA (-308), TNFA (-238), TNFB (-252), and IFN- gamma (+874) genes in donors were not related to this complication. In addition, donor and recipient IL-6 gene polymorphism and recipient IFN- gamma and IL-10 alleles were described as risk factors of cGvHD.

Unlabelled: In the last years one rises importance of costimulatory molecules in immune response in leukemias. Aim of the study was to assess lymphocytes T function in children with acute lymphoblastic leukemia during remission induction on the grounds of chosen costimulatory and activatory molecules expression. To assess percentages of lymphocytes subpopulations we used tricolor flow cytometry., Results: 1. In the moment of diagnosis and remission induction we noted higher percentages of lymphocytes T with adhesion molecule ICAM-1; 2. During remission induction we observed lower percentage values of lymphocytes T with CD38 coexpression; 3. In the end of remission induction rised the percentage values of lymphocytes T helper with IL-2 receptor expression; 4. In the group of patients with fever/infection we observed higher percentage of activated lymphocytes T (CD3-HLA-DR) comparing to non-infected patients. Summarizing, we suggest lymphocytes T activation during appearance and remission induction of acute lymphoblastic leukemia in children. This confirms participation of cellular immunity in leukemic process.

One of possible immunosuppression mechanisms during cancer disease is apoptotic death of immunology system cells. Factor FAS and xi chain of TCR-CD3 complex take part in induction of apoptosis of lymphocyte which infiltrate neoplasm as well as lymphocytes of peripheral blood (PBL). Expression of the two factors was estimated in PBL of patients with cancer of bottom of oral cavity and granuloma fissuratum (control group). During cancer disease higher level of FAS factor in PBL was observed in comparison to control group. Lymphocytes of peripheral blood in cases of cancer disease shown lower expression of TCR-xi.

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). It is thought that autoimmunity plays a major role in the development of the disease. Despite understanding MS as the cell-mediated autoimmune disease, recent studies suggest a role of humoral response in MS pathogenesis. The contribution of antibodies with anti-MOG specificity in the pathology of EAE (experimental allergic encephalomyelitis), an animal model of MS, in rodents and recently in primates has been demonstrated. B lymphocytes, plasma cells, and autoantibodies reacting with myelin proteins are present in the chronic and active plaques of MS patients. These antibodies, which recognize myelin basic protein (MBP), proteolipid protein (PLP), myelin-associated glycoprotein (MAG), myelin-oligodendrocyte glycoprotein (MOG), oligodendrocyte-specific protein (OSP), 2',3' cyclic nucleotide 3'-phosphodiesterase (CNP), and transaldolase (TAL), have been identified mostly in cerebrospinal fluid and in serum. So far, the antibodies directed against MBP, MOG, and OSP have been characterized in detail. However, the role of autoantibodies in MS pathogenesis is still controversial. A direct role in the demyelination process, by the activation of complement and cytotoxic cells, has been shown only for the anti-MOG antibodies. Identification of the antigens and epitopes targeting the autoimmune response in MS is of great importance, not only for understanding of MS pathology, but also for potential therapeutic use. Recently, antigen therapy trials have been conducted in MS patients. It seems, however, that only the recognition of the individual immunological response in each MS patient, including autoantigens and the subspecificity of autoreactive T and B lymphocytes, can allow for an effective fight against this destructive disease.

The highly toxic organophosphorus compound (isopropylmethylphosphonofluoridate--IMPF) belonging to the group of the so called toxic of warfare agents can impair immune effector mechanisms determining the development of parasitic infection. Preliminary studies have demonstrated that IMPF delays elimination of adults Trichinella spiralis forms from the intestine of C57B1/6 mice and B6C3F1 hybrids. Besides, the studied compound modifies the proliferative activity of T-cells in the above mentioned mice and reduces the production of anti-SRBC antibodies in C57B1/6 strain. The mechanisms are discussed of the organophosphorus compound effect on neuroimmunological processes connected with antiparasitic immunity, paying attention also to the function of these processes by the parasitic infection itself, in host-parasite relationship. The probability is also considered of increased sensitivity to Leishmania infection in humans poisoned with IMPF and/or other organophosphorus compounds.

Background: Type 1 diabetes is mediated by autoreactive - T lymphocytes recognizing pancreatic islet cell antigens. CD28/CTLA-4 costimulatory molecules participate in the transduction of the necessary signal in T lymphocytes proliferation and play an important role in the development of autoimmunological process., Objectives: The purpose of this study was: to evaluate whether the expression of CD28, CTLA-4 molecules on peripheral blood T lymphocytes alters in the course of disease -- diabetes lasting less than 5 years and over 5 years; to assess a relationship between the percentage of CD28, CTLA-4 on T cells and the evolution of vascular complications (microalbuminuria, arterial hypertension, diabetic retinopathy)., Material and Methods: The study was carried out in three groups of subjects - 60 children (aged 9-20) with diagnosed type 1 diabetes: (a) (20 n) with the disease lasting >5 years, (b) (20 n) with type 1 diabetes lasting >5 years without vascular complications, (c) (20 n) with type 1 diabetes and vascular complications (microalbuminuria, arterial hypertension, diabetic retinopathy). The control group consisted of 20 healthy volunteers (aged 6-17). The expression of adhesion molecules has been evaluated by using three-color flow cytometry (Coulter EPICS XL). HbA1c concentration has been analysed by liquid chromatography technique HPLC-Variant (Bio-Rad)., Results: In the study, the superficial expression of CTLA-4 receptor on T lymphocytes was enhanced in children with diabetes lasting <5 years (p<0.005) and over 5 years without vascular complications (p<0.01) versus healthy patients and tend to normalize in the presence of developing vascular complications In contrast, the expression of costimulatory molecule CD28 was decreased in children with type 1 diabetes lasting <5 years (p<0.05) as well as in children with developing vascular complications (p<0.01) versus the control group.