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Background: This paper examines a new material composed of polylactic and polyglycolic acids mixed with destrane easy to handle in bone defect reconstruction in periodontology and implantology: its name is fisiograft., Methods: According to the European directives, fisiograft was checked for some biological tests selected for its specific use. In particular, tests of cytotoxicity, genotoxicity, sensitization and implantation in rabbit's femurs were carried out., Results: The results show that the composite material is not cytotoxic when it is in direct and indirect contact with murine fibroblasts. It is not genotoxic and not allergenic. The implantation in rabbit, already after 30 days, shows that around the material there is a rapid bone growth and the material is reabsorbing. The degradation is suitable for its clinical use., Conclusions: Fisiograft showed to be biocompatible, easy to handle and its degradation kinetics in bone is appropriate.

The involvement of thyroid autoimmunity in the pathogenesis of sporadic congenital hypothyroidism is still incompletely understood. While antithyroglobulin and anti-thyroperoxidase antibodies are harmless, the transplacental passage of TSH receptor antibodies with blocking activity from a mother with autoimmune thyroiditis to the fetus is responsible of transient neonatal hypothyroidism in the baby. This is however a rare condition. Thyroid growth blocking antibodies have been described in healthy mothers of children with permanent congenital hypothyroidism due to thyroid dysgenesis, but this observation was not confirmed in other studies including our own. Antibodies producing cell mediated cytotoxicity (ADCC), either transferred from the mother or due to an autoimmune thyroiditis developing in utero, might be involved in the pathogenesis of permanent congenital hypothyroidism. However, this hypothesis requires confirmation in more extensive studies.

Respiratory infections are the major cause of disease in childhood in the industrialized areas of the world. This essentially depends on two factors: immunological immaturity and immunological naivety. In most cases a virus has been considered the causative agent in respiratory infection. A defect in immune responses has been described in children with recurrent respiratory infections and in particular a decrease in CD4/CD8 T lymphocyte ratio or in IL-2 and IFN-gamma production. Our results show that Natural Killer (NK) cell activity is defective in children with recurrent respiratory infections. That is particularly noteworthy since NK cells play an important role in host defense against viral infections. At present it is difficult to understand whether the NK defect is a primary defect or it is secondary to viral infections. Further studies will help to clarify whether NK decreased activity depends on a cell damage directly caused by virus or it depends on the decreased levels of cytokines.

NK Lymphocytes were first identified by their cytotoxic and cytolytic activity against tumor cells. However there is now increasing evidence that these cells are also mediators of natural resistance against viruses, fungi, protozoa and bacteria. The purpose of this review is to summarize the data on the antimicrobial activity of NK cells and to discuss the influence of corticoids and of other molecules interfering with innate resistance against pathogenic micro-organisms.

Tumor infiltrating lymphocytes (TIL) play an important role in the host immune response to cancer. When these cells are reinfused into cancer patients after in vitro expansion with lymphokines such as interleukin 2 (rIL-2), they often induce regression of tumor metastases. We obtained TIL of enzymatic digestion of 7 human solid tumors and then cultured them with rIL-2 and interleukin 4 (IL-4) at different concentrations for about 36 days. Immunophenotypic analysis was performed at the end of the second and fourth week; cytotoxic activity against autologous and heterologous targets was assessed on the 30th day of culture. The best lymphocytic growth was observed when we used rIL-2 and IL-4 for the first two weeks of culturing and then continued with rIL-2 alone. CD3 and CD56 cells formed the majority of TIL in all cultures. In 4 cases CD4 cells predominated at the initial stage of culturing, with CD8 cells gradually increasing and finally inverting the CD4/CD8 ratio. Autologous cytotoxicity (3/4 cases) appeared to be better in those patients in whom the CD4/CD8 ratio was inverted. These data enable identification of the combination of lymphokines that will will best provide expansion of live TIL active against tumoral cells. This procedure must be followed before in vivo reinfusion of expanded lymphocytes is carried out.

Using two different anaesthetic techniques, the author have investigated the cytotoxicity in process during abdominal surgery. In these investigations, no significant differences have been demonstrated in the behaviour of the NK with the two techniques adopted. The increase noted in traceable to the mobilization of the N.K. of the extra vascular deposits. The increase of the cytotoxic activity is probably traceable to the action of the endogenous opiate substances.

An antigenically altered DTIC-treated tumor subline was tested for sensitivity to the cytotoxic activity of murine Natural Killer (NK) cells in comparison to that of the original (parental) tumor. Direct lysis assays and "cold" inhibition procedures showed that the DTIC-subline is consistently less susceptible to lysis that the parental tumor.

We have investigated the possible role of cell-mediated immunity in the pathogenesis of liver disease associated with alpha 1-antitrypsin (AAT) deficiency in 16 children with PiZZ phenotype, who presented with liver disease in infancy. Peripheral blood lymphocytes from 13 patients were incubated with autologous hepatocytes in a microcytotoxicity assay. There was a clear trend for cytotoxicity to increase with age and thus significantly increased cytotoxicity was found in four cases older than 2 years, while intermediate values were recorded in three children between 6 months and 2 years and normal values in children younger than 6 months. Fractionation of PBL into T and non-T-enriched subsets showed that both were involved in the cytotoxic reaction. A purified liver membrane lipoprotein preparation (LSP) inhibited both T and non-T-cell cytotoxicity suggesting that LSP is a major target antigen in this system. Sensitization to LSP was also present in 2 of the 3 children studied using a recently developed T-lymphocyte migration inhibitory factor (T-LIF) test. Control experiments performed in infants with neonatal hepatitis syndrome, but with normal Pi phenotype showed consistently increased cytotoxicity values. Cell-mediated immune reactions directed against autologous hepatocytes develop late in the course of the liver disease associated with AAT deficiency. While this reaction cannot be involved in the pathogenesis of the initial liver lesion, it may contribute to perpetuation of liver damage.

Since Burnet expounded the theory of immune surveillance, various cells have been indicated as the "effectors" of the body immunological defence against tumours. Until recently, the ability to lyse tumour target cells was assigned to macrophages and the so-called thymus-dependent lymphocytes, known as killer T cells. The discovery of natural killer cells in mice recently has widened the number of effectors and the field of research in this sector. An examination is made of the features and main properties of these cell groups, and some questions are posed concerning their ability to cooperate in anti-neoplastic immunological defence.

Authors reconsider the present state of knowledge about immunology of laryngeal cancer. Authors, besides, analyse, in a critical way, problems concerning immunological monitoring of patients bearing solid carcinomas. They conclude that, up to date, it is impossible to have a biological test which can concretely show the patient's immune state.

In this study we have examined whether resident peritoneal macrophages could be activated in vitro by immune T lymphocytes obtained from mice which were immunized with live Trichomonas vaginalis (T. vaginalis). T lymphocytes obtained from mice previously sensitized against T. vaginalis, showed a significant proliferative response when cultured in vitro in the presence of T. vaginalis. Resident peritoneal macrophages obtained from untreated syngenic Balb/c mice revealed an increasing cytotoxic activity against the protozoa when seeded with increasing concentrations of purified immune T lymphocytes and a constant number of H3 thymidine-labeled T. vaginalis. This cytotoxicity was detectable after 24 h of culture and peaked after 48 h. Supernatants obtained from cocultures of macrophages, immune T lymphocytes and T. vaginalis contained gamma-Interferon and TNF alpha/beta.

NK activity and cells with NK phenotype (CD16+) were studied in 21 patients with HIV infection. In particular 8 patients with full-blown AIDS, 6 with AIDS related complex (ARC), 7 asymptomatic seropositive for anti-HIV antibodies were evaluated. Six subjects seronegative for anti-HIV antibodies from groups at risk for HIV infection were evaluated as well. NK activity was significantly reduced in AIDS and ARC patients but normal in asymptomatic seropositive subjects and in seronegative subjects at risk. NK cells (CD16+) were normal in AIDS patients, and in asymptomatic seropositive subjects, increased in ARC patients and in the subjects at risk. No statistical correlation was evident between the NK activity and the number of CD16+ cells in individual patients. The percentage of CD16+ cells coexpressing the HLA-DR marker i.e. CD16+ HLADR+ cells was significantly elevated only in ARC patients, and normal in the others. NK activity is the first line of defense against an invading virus and plays an important role in the immune surveillance of neoplasms. Therefore the reduced NK activity in AIDS and ARC patients can be consistent with the development of viral infections and unusual neoplasms frequently observed in such patients. The lack of correlation between defective NK activity and normal or increased number of cells with NK phenotype seems to indicate the existence of a more profound alteration in the function of NK cells rather than a simple numeric variation.

The lymphocytotoxicity to rabbit hepatocytes either direct or serum induced was evaluated in chronic active hepatitis (CAH). We obtained the following results: a) the direct lymphocytotoxicity obtained in CAH patients significantly correlated with the cytotoxicity induced by CAH sera in normal lymphocytes; b) no difference could be recorded in CAH HBsAG positive or negative; c) the target antigen of the immune reaction seems to be the liver specific lipoprotein.

It has been known for some years that rats developing a granulomatous inflammation following the intraperitoneal injection of fragments of a polyester suture thread (Mersilene, M) reject a graft of 10(8) Yoshida's ascites hepatoma cells, which on the contrary rapidly grow in M-uninjected animals, originating an ascites tumor and killing the rats in a few days. In this paper granulomatous (TM) and normal (control, C) small pieces of peritoneum (omentum, mesentery and parietal) have been cultivated for 15 h in Eagle-Dul becco's medium together with 10(5) 51Cr-labelled hepatoma cells: the release of the label, an index of cell lysis, was considerably higher in the TM cultures, suggesting a cytotoxic activity of some components of the granulomas. Differences have been observed in the amount of radioisotope released among the TM cultures, suggesting that the particular composition of the cell population may be relevant to the cytotoxicity versus the hepatoma cells.

The cytotoxic activity of Hodgkin serum on some isolated T and B lymphocyte populations of 10 normal subjects, 10 patients with Hodgkin disease in the acute phase and 10 patients with Hodgkin disease but in clinical and biohumoral remission was studied. The effect of citotoxic serum variously affects the two different lymphocyte populations, particularly inhibiting LIF activity of T lymphocytes, while stimulating LIF activity of B lymphocytes. The possible causes of this phenomenon are set forth as well as their clinical implications.