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Objective: The present study aims to examine the effects of nisin on the survival and apoptosis of the hepatoma cell line HepG2 and to investigate possible apoptosis pathways activated by nisin. Materials and methods: For this purpose, viability and apoptosis of the cells were accomplished by the nisin treatment using the MTT assay and Annexin-V-fluorescein/propidium iodide (PI) double staining, respectively. Additionally, the human apoptosis PCR array was performed to determine pathways or genes activated by nisin during possible apoptosis. Results: The results of the present study showed that nisin was able to decrease cell viability (IC50 ~ 40 µg/ml) in a dose-dependent manner and could induce apoptosis in HepG2 cells. PCR data indicated a considerable increase in the expression of genes, such as caspase and BCL2 families, involved in the induction of apoptosis. Conclusions: The data from this study showed that overexpression of genes involved in the intrinsic pathway of apoptosis, especially caspase-9 and BID, increased apoptosis in HepG2 cells treated by nisin, compared to the control group.

Th9- and regulatory T (Treg) cells exert pro- and anti-allergic activity, respectively. Mesenchymal stem cell (MSC)-related immunomodulatory impacts can be enhanced by inflammatory cytokines. Here, the modulatory effects of IFN-γ/TNF-α-induced MSCs on Th9- and Treg cell-related parameters were investigated using an asthma model.Allergic asthma was induced in BALB/c mice using sensitized and challenging with ovalbumin (OVA). The asthmatic groups were treated intraperitoneally with PBS, MSCs, IFN-γ-induced MSCs, TNF-α-induced MSCs and 'IFN-γ + TNF-α'-induced MSCs before the challenge phase. The mice were sacrificed 24 h after challenge. The serum IL-9 and IL-35 levels, as well as gene expression of IL-9, PU.1, IL-35-EBI3, and FOXP3 in the lung tissues were assessed using ELISA and real time-PCR, respectively.The differences of Th9 and Treg-related parameters were not significant between untreated asthmatic mice and those treated with non-induced MSCs. In comparison with untreated asthmatic group, treatment with IFN-γ-induced MSCs significantly reduced serum IL-9 levels, reduced lung expression of IL-9 and PU.1, while increasing serum IL-35 levels as well as lung expression of FOXP3; treatment with TNF-α-induced MSCs significantly reduced serum IL-9 levels as well as lung expression of IL-9, and treatment with 'IFN-γ + TNF-α'-induced MSCs, significantly modulated all investigated Th9 and Treg-related parameters. In comparison to mice treated with non-induced MSCs, serum IL-9 levels were remarkably decreased in mice treated with IFN-γ-induced and 'IFN-γ + TNF-α'-induced MSCs.IFN-γ-and 'IFN-γ + TNF-α' treated MSCs exerted almost comparable impacts, but were more efficient than TNF-α-exposed MSCs. Thus, IFN-γ alone can be sufficient to promote immunomodulatory effects of MSCs.

The aims of this study were to compare mRNA levels of melanoma differentiation-associated protein 5 (MDA5) and retinoic acid-inducible gene 1 (RIG-1) in multiple sclerosis (MS) patients in comparison to the healthy controls as well as investigating the effects of IFN-β 1a on the expression of these molecules. In this study, mRNA levels of MDA5 and RIG-1 in peripheral leukocytes of 30 new cases of MS patients and 35 healthy controls were evaluated using the real-time-PCR method. mRNA levels of MDA5 and RIG-1 were determined in the MS patients 6 months after treatment with standard doses of IFN-β 1a. mRNA levels of MDA5 and RIG-1 were significantly decreased in the MS patients in comparison to the healthy controls. The analysis also revealed that IFN-β 1a therapy leads to the upregulation of RIG-1, but not MDA5, in the total MS patients and the female group. MS patients suffer from insufficient expression of MDA5 and RIG-1, and IFN-β 1a therapy results in the upregulation of RIG-1 in the patients, especially in the female patients. Thus, it seems that IFN-β 1a not only decreased pathogenic inflammatory responses but also modulated the expression of RIG-1 to protect the patients from infectious diseases and upregulation of IFN-I in a positive feedback.

Since the first production of monoclonal antibodies about 35 years ago, researchers have found them useful in the treatment and diagnosis of various diseases such as cancer. By developing different types of monoclonal antibodies such as humanized, drug conjugated, or bispecific ones, researchers, have achieved remarkable success in treating several complicated and challenging diseases, targeting specific antigens or receptors makes monoclonal antibodies the right choice to inhibit signaling pathways like programmed death-ligand 1 (PD-L1) or programmed death1 (PD-1) and changing cell behavior. As one of the most common types of malignancies among women, breast cancer is one of the most critical conditions which different types of monoclonal antibodies were designed and produced to treat. Therefore, we reviewed these antibodies in breast cancer, their targets, and their efficacy and toxicity, with more focus on recent PD-L1or PD-1 inhibitor antibodies in breast cancer and beyond.

Background: Sexually transmitted infections (STIs) are a subject of great concern in public health, particularly in the field of reproductive medicine. Objectives: This study aimed to detect the presence of two sexually-transmitted bacteria, C. trachomatis and N. gonorrhoeae, in the semen samples of infertile men referred to a medical diagnostic laboratory in Rafsanjan city by PCR and also to investigate their possible effects on semen parameters. Methods: Semen samples of 309 infertile men who were asymptomatic for genital tract infections were evaluated using the PCR method. In addition, the analysis of semen parameters was performed according to the WHO guidelines. Results: The average age of the participants was 32.67 ± 17.02 years and 11.65% of cases were positive at least for one of the two tested bacteria; 11.32% for C. trachomatis and only 0.32% for N. gonorrhoeae. Furthermore, there was a direct significant correlation between chlamydia infection and at least two variables of sperm quality; activity, and live ratio (P < 0.05). Conclusions: The results demonstrated that C. trachomatis are widespread among males, and this infection may lead to an effect on semen parameters such as activity and live ratio.

Background: Methicillin-resistant Staphylococcus aureus (MRSA) is a multidrug-resistant microorganism and the predominant nosocomial pathogen all over the world. The potential benefits of probiotic lactobacilli against pathogenic bacteria have been shown in many studies. Objectives: This study aimed to investigate the effect of cell-free culture supernatant (CFS) of probiotic Lactobacillus spp, including Lactobacillus reuteri, L. plantarum, and L. fermentum, on virulence factor gene expression of MRSA. Methods: Lactobacilli were cultured in MRS and the cells were harvested by centrifuging at 10,000 × g for 10 min at 4°C. The pellet was discarded and 1/2 and 1/4 CFS concentrations from Lactobacillus spp were added to the medium (MHB) containing 107 CFU/mL of the MRSA strain. A quantitative polymerase chain reaction (qPCR) was performed to measure the expression of virulence factors at the transcriptional level. Results: The results showed that lactobacilli CFS had no obvious inhibitory effects on the growth of S. aureus. The qPCR assay showed that the expression levels of sea, sae, agr A, tst, spa, and spi genes reduced at different levels, depending on the concentration of CFS and the species of lactobacilli so that the maximum significant down-regulation rate was observed in the sea and tst genes (up to 23.5 folds in the presence of 1/2 concentration of L. reuteri CFS after 12 h incubation). Conclusions: Cell-free culture supernatants of probiotic bacteria can down-regulate the virulence genes. Consequently, toxins and enzymes are less produced by S. aureus as a food-borne pathogen. Therefore, the presence of CFS in the food probably reduces diarrhea and vomiting caused by S. aureus.

Introduction: Inflammation is a risk factor for dental complications. Inflammasomes are a set of intracellular sensors which participate in the induction of inflammation. As the main factors involved in the induction of pulp inflammation in the carious teeth are yet to be clarified, this study was aimed to evaluate NLRP1 and NLRC4 expression levels in the inflamed and healthy pulps. Materials and Methods: Fifty inflamed and fifty healthy pulps were evaluated regarding the multiRNA levels of NLRP1 and NLRC4 using real-time polymerase chain reaction technique. Results: Results demonstrated that expression of NLRP1 (P = 0.985) and NLRC4 (P = 0.581) did not significantly differ in inflamed in comparison to healthy pulps. NLRP1 (P = 0.989) and NLRC4 (P = 0.170) did not change in males when compared with females in inflamed pulps. Furthermore, NLRP1 (P = 0.133) and NLRC4 (P = 0.642) were not altered in males in comparison to females in healthy pulps. Conclusion: Although NLRP1 and NLRC4 are the main inflammasomes, it appears that they are not the responsible molecules involved in the human pulp inflammation in the carious teeth.

Objectives: Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules. Methods: S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy. Results: S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB. Conclusions: It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-independent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions.

Background: Nisin is a member of the group of anti-microbial peptides which are considered as bacteriocins, but it possesses a vast range of activities. Astrocytoma is among the most prevalent types of brain tumor globally. Considering all facts about this peptide, the aim of the present study was the evaluation of any impact of nisin on proliferation and apoptosis of an astrocytoma cell line (SW1088). Methods: The SW1088 cell line was purchased from the Pasteur Institute of Iran and treated with various concentrations of Nisin. Nisin-induced cell toxicity and apoptosis were detected by both MTT assay and annexin V-FITC /propidium iodide (PI) staining. Result: In current study we observed that the cell death and apoptosis were significantly increased following nisin treatment, as compared to the control group. Conclusion: These results open a new window for establishment promising approaches with the concept of anti-cancer therapy by nisin in the future.

Objective: This research aimed to study the anti-aging and anti-inflammatory effects of low and high doses of the β-D-mannuronic (M2000) on gene expression of enzymes involved in oxidative stress (including SOD2, GST, GPX1, CAT, iNOS, and MPO) in peripheral blood mononuclear cells (PBMCs) of healthy donors under in vitro conditions. Methods: The PBMCs were separated and the RNAs were then extracted and the cDNAs synthesized, and expression levels of the mentioned genes were detected by qRT-PCR. Results: Our results indicated that the high dose of this drug could significantly reduce the expression level of the SOD2 gene compared to the lipopolysaccharide (LPS) group (p < 0.0001). Moreover, it was found that the high dose of this drug could significantly decrease the expression level of the GST gene compared to the LPS group (p < 0.0001). However, no significant reductions were observed in expression levels of the CAT and GPX1 genes compared to the LPS group. Furthermore, our data revealed that the level of iNOS and MPO gene expression was significantly reduced, in both doses of M2000, respectively, compared to the LPS group (p < 0.0001). Conclusion: This research showed that M2000 as a novel NSAID with immunosuppressive properties could modify oxidative stress through lowering expression levels of the SOD2, GST, iNOS, and MPO genes compared to the healthy expression levels, with a probable reduction of the risk of developing inflammatory diseases related to age and aging.

Background: The hepatocellular carcinoma is believed to be the third cause of death due to cancer, worldwide. A new derivative of the (2R,4S)-N-(2,5-difluorophenyl)-4-hydroxy-1-(2,2,2-trifluoroacetyl) pyrrolidine-2-carboxamide compound were synthesized, employing a facile one-pot reaction of trans-4-hydroxy proline and N-(2,5-difluorophenyl)-2,2,2-trifluoroacetimidoyl chloride in the presence of TiO2 as catalysts and sodium hydrogen carbonate. Objectives: Therefore, in the present study we aimed to explore whether if the above new derivative pyrrolidine-2-carboxamide can affect cellular viability and apoptosis in cancerous HepG2 cell line. Methods: HepG2 cells were cultured in RPMI 1640 medium containing fetal bovine serum. Cultured cells were then treated with 7.8 µM to 125 µM of pyrrolidine-2-carboxamide. The toxicity of the compound was assayed by MTT method and detection of annexin V signal, using a flowcytometry system. Results: We found the pyrrolidine-2-carboxamide derived inhibition of HepG2 cells following a dose and time dependent fashion. The highest numbers of dead cells were observed in 125 µM dose, after 48 hours of treatment. Flow cytometric analysis also revealed that massive numbers of apoptotic cells were detectable in response to treatment with this pyrrolidine derivative. Conclusions: Overall, according to the data presented here, the pyrrolidine-2-carboxamide could possibly control cellular viability/apoptosis. Thus it can potentially be concerned as a useful therapeutic tool for hepatocellular carcinoma treatment.

Interferon-β 1a (IFN-β 1a) is a common strategy therapy for multiple sclerosis (MS) with unknown mechanisms. S100A12 (S100 calcium-binding protein A12) is a damage-associated molecular pattern molecule which binds to its receptor, RAGE (receptor for advanced glycation end products), and activates nuclear factor-κB (NF-κB). NF-κB is transcribed from proinflammatory molecules, which may participate in the pathogenesis of MS. Therefore, the aims of this study were to compare mRNA levels of S100A12, RAGE, and NF-κB in newly diagnosed MS patients with healthy controls and determine whether IFN-β 1a therapy affects the expression of the molecules.S100A12, RAGE, and NF-κB mRNA levels in 30 new cases of untreated MS patients and 35 healthy controls were evaluated using the real-time PCR technique. The mRNA levels were also evaluated in the MS patients after 6 months of IFN-β 1a therapy.S100A12, RAGE, and NF-κB mRNA levels were significantly decreased in the new cases of untreated MS patients in comparison to healthy controls. IFN-β 1a therapy results in upregulation of RAGE in MS patients, but not S100A12 and NF-κB.It appears that S100A12 participates in the pathogenesis of MS, and it seems that IFN-β 1a modulates immune responses in an S100A12-independent manner. Based on the reported anti-inflammatory effects of RAGE, it seems that RAGE may be considered as a mechanism by IFN-β 1a to modulate immune responses. NF-κB is produced permanently in the human cells and is inactive in the cytoplasm; therefore, the effects of IFN-β 1a may be related to its functions rather than expressions.

Aim S100 calcium-binding protein A1 (S100A12) is a pro-inflammatory molecule which is secreted during inflammation and induces chemotaxis and the production of pro-inflammatory cytokines via interaction with receptor for advanced glycation endproducts (RAGE) and subsequent, activation of nuclear factor-κB (NF-κB). The present study was designed to determine the expression levels of S100A12, RAGE, and NF-κB in the inflamed pulp of carried teeth. Methods In the present study, mRNA from 50 inflamed pulp and 50 healthy pulp were used for expression studies using real-time polymerase chain reaction. The expression levels of S100A12, RAGE, and NF-κB were compared between inflamed and healthy tissues. Results The results revealed that the expression of S100A12, but not of RAGE or NF-κB, was significantly decreased in inflamed pulp when compared to healthy pulp. mRNA levels of RAGE were also increased in the inflamed pulp taken from men when compared with women. Conclusion The results suggest that S100A12 does not participate in the induction of inflammation in dental pulp. However, RAGE can participate in the inflammation in the pulp of males.

Summary Background and aims TRIF is one of the main intracellular adaptor proteins required for TLR3 and 4 signaling. Abnormal gene expression of TRIF may lead to abrogated immune responses against viral infections including hepatitis B infection. The aim of this study was to identify the mRNA levels of TRIF in PBMCs isolated from chronic HBV (CHB) infected patients. Material and methods mRNA was isolated from 63 CHB patients and 60 healthy controls and transcript levels of TRIF were examined in parallel with beta-actin (as housekeeping gene) using Real-Time PCR techniques. Results Our results demonstrated that expression of TRIF was significantly decreased in PBMCs isolated from CHB patients when compared to healthy controls. Conclusions Based on the results reported here, it seems that CHB patients are unable to express appropriate levels of the TRIF gene, which may attenuate TLR3 and 4 signaling subsequent to HBV infection. Our results suggest a possible mechanism, which may explain why hepatitis B infection is stable in CHB patients.

Chlamydia species are obligate intracellular pathogens causing different infectious diseases particularly asymptomatic genital infections and are also responsible for a wide range of complications. Previous studies showed that there are different immune responses to Chlamydia species and their infections are limited to some cases. Moreover, Chlamydia species are able to alter immune responses through modulating the expression of some immune system related molecules including cytokines. Toll like receptors (TLRs) belonge to pathogen recognition receptors (PRRs) and play vital roles in recognition of microbes and stimulation of appropriate immune responses. Therefore, it appears that TLRs may be considered as important sensors for recognition of Chlamydia and promotion of immune responses against these bacterial infections. Accordingly, TLR4 detects several microbial PAMPs such as bacterial lipopolysacharide (LPS) and subsequently activates transcription from pro-inflammatory cytokines in both MYD88 and TRIF pathways dependent manner. The purpose of this review is to provide the recent data about the status and major roles played by TLR4 in Chlamydia species recognition and promotion of immune responses against these infections and also the relationship between TLR4 activities and pathogenesis of Chlamydia infections.

Background: Multiple Sclerosis (MS) is a common autoimmune system disease which affects the central nervous system. It has been documented that interleukin-25 (IL-25) plays key roles in suppressing Th1 responses, which is increased during MS. Objectives: The aim of this study was to investigate the c424C/A polymorphism within the IL-25 gene in MS patients in comparison to healthy controls. Patients and Methods: In this case-control study, 74 patients with MS and 75 healthy controls were selected. Polymerase Chain ReactionRestriction Fragment Length Polymorphism (PCR-RFLP) was used in order to determine c424C/A polymorphism within the IL-25 gene. Results: The results showed that there was no statistical significant difference in distribution of genotype (AA, AC and CC) and allele (A and C) frequencies between MS patients and healthy controls (P = 0.901 and P = 0.728, respectively). Conclusions: In conclusion, it appears that the c424C/A polymorphism within the IL-25 gene has no significant relationship with MS, and this polymorphism is probably not associated with MS complications, its onset and gender distribution.

Investigations revealed substantial parts accomplished by chemokines specifically eotaxins and their specific receptors. They are functionally involved in the modulation of the pathologic state of tissue inflammation which is as a result of allergic reactions. Chemokines as small proteins with approximately 8-10 kDa molecular weight are considered and fit in the bigger family of cytokines, containing basic heparin-binding polypeptide mediators. Chemokines actively interfere in the processes of selective, oriented leukocyte (including eosinophil) recruitment. As eminent from their name, more specifically, eotaxins are specialized for eosinophils' oriented locomotion toward allergic inflamed regions. To date, three members are defined for eotaxin subfamily as follows: eotaxin-1 (CCL11), eotaxin-2 (CCL24), and eotaxin-3 (CCL26), all of them bind to and activate CCR3 but have a low level of homology and appear to exhibit different physiological potentials. Allergy is described as a clinical state in which a pathologic hypersensitivity reaction is always initiated throughout an immunologic mechanism; similar to other immunologic reactions, an allergic reaction could also either be antibody or cell mediated. This type of allergic reactions occurs in all age groups and damages several different organs, having a significant impact on the emotional and social health of patients and their families and relatives. Concerning introductory comments introduced above, the authors of the present review attempted to collect and provide the latest evidences and information regarding the correlation between expression of eotaxin family members and allergy, in a wider extent, in two important allergic disorders: atopic asthma (AA) and atopic dermatitis (AD). Overall, concerning the most recent articles published within the database in the life sciences literature regarding the fundamental role(s) played by eotaxins in the pathogenesis of AA and AD, the authors of the current article propose that eotaxins (CCL11, CCL24, and CCL26) play key role(s) during symptomatic inflammatory responses raised in response to allergic crisis of these two clinical states.

Background Chemokines play important roles in immune system activation against microbial infections. Objectives The current study aimed to evaluate seminal levels of CXC chemokines CXCL1, CXCL9, CXCL10 and CXCL12 in Chlamydia trachomatis infected patients. Materials and methods The C. trachomatis infection was determined employing Polymerase Chain Reaction (PCR)-based methods. Seminal concentrations of CXCL1, CXCL9, CXCL10 and CXCL12 were measured by Enzyme-Linked Immunosorbent Assay (ELISA). Results The current study results demonstrated that the semen levels of CXCL1 and CXCL9, but not CXCL10 and CXCL12, significantly increased in C. trachomatis infected patients compared to the healthy controls. Conclusions Based on the current study results, it may be concluded that both CXCL1 and CXCL9 play more important roles than CXCL10 and CXCL12 in induction of immune responses against C. trachomatis and could possibly be considered as future targets for immunotherapy of C. trachomatis infection.

Allergic rhinitis is a nasal hypersensitivity and allergic disease which leads to inflammation of nasal mucosa. Previous investigations revealed that innate immune receptors play a key role in the pathogenesis of inflammatory diseases including allergic diseases. Toll-like receptors (TLRs), which are important innate immune receptors, play crucial roles in the recognition of foreign antigens, including allergens, and subsequently for the induction of immune responses such as inflammation. There are several controversial reports regarding the roles of TLR4 in the pathogenesis of allergic rhinitis. This review presents current information regarding the roles of TLR4 in the pathogenesis of allergic rhinitis and the plausible mechanisms which lead to the expression and function of TLR4 in this disease.

Background Mycobacterium tuberculosis is a pulmonary pathogen responsible for tuberculosis. Tuberculosis (TB) is characterized histologically by granulomas at the site of disease activity. Primary pathologic feature of TB is formation of a granuloma, and chemokines are known to play an important role in the formation of granulomas during infection. Therefore, the aim of this study was to evaluate the serum levels of CCL11, CCL24, and CCL26 in the TB patients in comparison to healthy controls. Methods The population of this cross-sectional study included 300 patients suffering from TB and 100 healthy controls. Concentrations of CCL11, CCL24, and CCL26 were measured by enzyme linked immunosorbent assay (ELISA) technique. The results were analyzed using SPSS software package version 18. Differences were considered significant where p was less than 0.05. Results The results showed significant elevated serum levels of CCL11, CCL24, and CCL26 in TB patients compared to controls. Conclusions According to the present results it can be concluded that CCL11, CCL24, and CCL26 (which are produced by Th2 cells and other cells which induce Th2 development) are increased in TB patients; hence, it seems that TB suppresses Th1 and the classic function of macrophages subsequently by inducing the chemokines' expression.

Toxoplasma species are obligate intracellular protozoan which are responsible for induction of several forms of Toxoplasmosis in humans. The mechanisms responsible for the progression of the prolonged forms of Toxoplasmosis and associated pathologies are yet to be identified. However, previous studies proposed that immunological and genetic parameters may play important roles in the etiology and complexity of Toxoplasmosis. Pathogen recognition receptors (PRRs) recognize microbial antigens and induce immune responses against parasites, including toxoplasma species. Toll like receptors (TLRs) are PRRs which recognize toxoplasma as a pathogenic parasite and activate immune cells. It has been reported that the TLR4 is a critical innate immune cell receptor in toxoplasma detection and subsequently activates immune responses using either MYD88 or TRIF pathways. This review collates recent information regarding the role of TLR4 and its related signaling molecules with Toxoplasmosis.

Absent in Melanoma 2 (AIM2) is an intracellular microbial dsDNA sensor which plays an important role in production of proinflammatory cytokines through Apoptosis associated Speck-like protein containing a Caspase activation and recruitment domain (ASC) and Caspase-1. Micro-RNAs (miRNAs) play important roles in regulation of immune related genes. However, there is little information regarding the effects of miRNAs on the AIM2 and ASC expression.To determine the mRNA levels of AIM2 and ASC in Jurkat cell line following introducing miRNA-143 (miR-143).MiR-143, a scrambled sequence and PBS were introduced separately, to the Jurkat cell lines and the mRNA levels of AIM2 and ASC were examined in parallel with beta-actin and GAPDH (as housekeeping genes) using Real-Time PCR technique.The mRNA levels of AIM2 and ASC were significantly increased in the miR-143 transfected Jurkat cells when compared to the scrambled sequence or PBS treated cells.miR-143 can lead to increased expression of AIM2 and ASC mRNAs. Considering the significance of AIM2 and ASC in DNA sensing and inflammosome formation, it can be considered as a therapeutic agent for the treatment of chronic infectious diseases, especially viral infections.

Alopecia Areata (AA) is a non-scarring, autoimmune disorder which causes hair loss. Inflammatory reactions are involved in hair loss of the scalp and/or body. The involvement of chemokine receptors in the pathogenesis of AA is well defined among which, CXCL1 acts on neutrophils and CXCL9, CXCL10 and CXCL12 serve as T lymphocytes recruiters.To study the serum levels of ELR+ and ELR- CXCL1, CXCL9, CXCL10 and CXCL12 in the patients suffering from AA and healthy controls.The study population consisted of 30 patients suffering from AA and 30 healthy controls. Serum concentrations of CXCL1, CXCL9, CXCL10 and CXCL12 were measured using enzyme-linked immunosorbent assay (ELISA).Current results showed that AA patients had significantly elevated serum levels of CXCL9 and CXCL10 in comparison to controls (p0.001). These results also demonstrated that serum levels of CXCL1 and CXCL12 were significantly decreased in AA patients compared to control (p0.001).CXCL9 and CXCL10 are elevated in the AA patients and may be involved in the recruitment of T lymphocytes to the inflamed tissues. Moreover, due to the significant role played by these chemokines in angiogenesis/angiostatis phenomenon they could be considered as useful biomarkers in AA diagnosis and therapy.