Bystander virus infection prolongs activated T cell survival.

摘要: In animals, T cells often die rapidly after activation, unless activation occurs in the presence of inflammatory factors. To understand how such activated survive to participate immune responses, we studied effects viral infection on responding an unrelated superantigen. Normal by superantigen uninfected mice died as a result their whereas that were during vaccinia survived longer vivo and culture. This bystander effect was independent magnitude initial cell response, induction Bcl-2 Bcl-x, proliferation, Fas killing. The failure predict fate indicates virus infections shape responses via mechanisms differ from those described previously. These may contribute ability induce autoimmunity.