Abstract

Emerging evidence has suggested that CD8+ T had modulatory function on CD4+ T mediated autoimmune and inflammatory diseases. However, the underlying mechanisms remain unclear. In this study, we found that CD8+ T activation inhibited OVA323–339 antigen specific CD4+ T cells proliferation in vitro and in vivo. Further investigation demonstrated that this immunosuppression largely depended on the soluble factor from activated CD8+ T to modify the phenotype and functions of DCs. Moreover, not only the inhibitors for IDO or iNOS, but also IFN-γ neutralization markedly reversed this immunosuppression on OVA323–339 antigen specific CD4+ T cells proliferation. Interestingly, CD8+ T cells absence aggravated the pathological damage in lung in OVA-induced asthma model, but alleviated by CD8+ T transfer and activation. Thus, these findings suggested that activated CD8+ T population exerted feedback regulation in DCs modification, and then attenuated CD4+ T mediated immune response.

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