Cellular immunology

CD8(+) T activation attenuates CD4(+) T proliferation through dendritic cells modification.

PMID 26022412


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 OVA(323-339) 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 OVA(323-339) 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.