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Objective To study the role of Schwann cells apoptosis in the pathogenesis of experimental autoimmune neuritis(EAN) in TNF receptor Ⅰ knock out(TNFR Ⅰ-/-)mice.Methods For induction of EAN,TNFRⅠ-/- and wild type C57BL/6 mice were immunized by subcutaneous injection into the back with the peripheral nerve P0 protein peptide 180-199;clinical scores of EAN were assessed and scored immediately before immunization(day 0) and thereafter every other day until day 46 post immunization(p.i.).On day 22 p.i.,Schwann cells were collected from the two groups and cultivated in vitro.The expressions of Fas and Annexin-Ⅴ(Annexin-Ⅴ+/PI-)on Schwann cells from TNFRⅠ-/-and wild type EAN were detected by flow cytometry.Results More light clinical signs of EAN were observed in the TNFRⅠ-/-mice(1.50?0.19) than in wild type mice(1.90?0.16);the percentage of Fas expression on Schwann cells was significantly decreased in TNFRⅠ-/-mice(88.03%?1.40%)as compared with wild type mice(94.70%?1.53%)(P
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Objective To establish the model of P2 peptide-induced experimental autoimmune neuritis(EAN)in rats and explore the roles of Th_1/Th_2 type eytokines in EAN.Methods Lewis rats were grouped into EAN rats and control rats.The EAN rats were immunized by injection into both hind footpads of inoculums containing 100 ?g or 200 ?g of P2_(57-81)peptide and FCA while the control rats were immunized with FCA only.Clinical scores were compared at the maximum of disease.Supernatant productions of IFN- ?, IL-4 and IL-10 secreted by lymphocytes and obtained on day 14 after the immunization were examined. Histopathological assessment of sciatic nerves was made.Results Peak clinical scores of P2_(57-81)200 ?g (3.6?0.3)group were significantly higher than P2_(57-81)100 ?g group(2.2?0.6,P
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Objective To establish P2 or P0 peptide-induced experimental autoimmune neuritis (EAN)in the Lewis rats and to explore the optimal type and doses of antigen inoculated to induce EAN and the associated cell-mediated immune mechanisms.Methods Lewis rats were classified into EAN and control groups.The EAN rats were immunized by injection into both hind footpads of inoculums containing 100 or 200 ?g of P2_(57-81)peptide or 200?g of P0_(180-199)peptide and Freund's complete adjuvant(FCA),and the control rats were immunized with FCA only.Clinical scores were compared when they were at peak time of paralysis.Lymphocyte proliferation assay,the ratio of CD_4~+ T cells to lymphatic monocytes and percentage of CD_4~+ CD_(25)~+ T cells to CD_4~+ T cells obtained on day 14 post-immunization were examined.Histopathalogical assessment of sciatic nerves was made.Results Peak clinical scores of P2_(57-81)200 ?g group were dramatically higher than those in P2_(57-81)100 ?g group and P0_(180-199)200 ?g group(both P
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Objective To investigate which subfamily genes of T cell receptor (TCR) V? expand predominantly during the course of experimental allergic neuritis (EAN). Methods Using RT-PCR and in situ hybridization techniques,the expression levels of TCR V? 2,6,8,10,14 in the peripheral blood,lymph nodes,peripheral nerves of group EAN and those of the control group were compared. Results In group EAN,the expression of TCR V? 6?8 mRNA increased at the early phage(41.1?1.1 and 74.4?1.9 vs 25.9?1.5 and 26.1?1.6) and became more significantly at the peak of the disease,and resolved to normal at the recovery phage in the lymph nodes.But they amounted up gradually from the early stage to the peak,and then decreased a little in the infiltrating T-lymphocytes in peripheral nerves,the difference was significant.In addition,the expression of TCR V? 8 was notably higher than that of TCR V? 6 in the levels of mRNA. Conclusion The subfamilies of TCRV? genes which restrict the development of EAN due to recognizing the specific antigens are TCRV? 8 and TCRV? 6. T lymphocytes specifically expressing TCR V?6?8 genes are activated and clonally proliferated in the lymph nodes,and then migrate to the involved peripheral nerves,which might induce a series of immune lesions consequently.