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Background The immune regulatory properties of semaphorin3A (sema3A) (both innate and adaptive) are well established in many in-vitro studies. When sema3A was incubated with active B cells from SLE patients, it could efficiently reduce the expression of TLR-9 in correlation with a significant reduction of relevant auto-antibodies. The injection of sema3A to a mice model of rheumatoid arthritis was proven to be highly beneficial, both in attenuating clinical symptoms and in decreasing inflammatory mechanisms. Objectives This study was designed in order to assess possible therapeutic benefits following the injection of sema3A to NZB/W mice. Results The injection of sema3A to young mice (at week 12) before disease onset, delayed the appearance of proteinuria. Here, the median time to severe proteinuria was 110 days, 95% CI: 88 to 131. However, in mice in which empty vector was injected, median time to severe proteinuria was 63 days, 95% CI: 0 to 139). Sema3A treatment, reduced significantly renal damage, namely, it prevented the development of immune deposits in the glomeruli. When sema3A was injected at the onset of proteinuria, aiming to treat rather than to prevent disease in these mice, survival was significantly increased and the deterioration of proteinuria was significantly delayed. Conclusion Semaphorin3A is highly beneficial in reducing lupus nephritis in NZB/w mice. It delays the appearance and deterioration of proteinuria, and increases survival rates in these mice. Further studies will establish the idea of applying sema3A in the treatment of lupus nephritis. |
