CD4+CD25+ regulatory T-cell (Treg) was found to be a suppressive subset of T-cell, in 1995, by Japanese immunologist Dr. Sakaguchi. Treg inhibits effector T cells by direct contact with its target cells. Or it surpresses target cells by its secreting immuno-suppressive cytokines such as TGF-βor IL-10. Current understanding of Treg’s roles in maintaining the balance between immunity against pathogens and tolerance has been greatly expanded by its double-faced function in immunity against HIV. With its surpressive function, Treg may be disarmed in HIV infection, which results in an overactivated immune system. While some research showes that the quantity of Treg cells has been remarkablely expanded in primary infection. Treg dysfunctions both HIV-specific helper T cells and CTLs. Depleting Treg from CD4+ T cell leads to a reconstitution of strong immunity against HIV. On our established animal model, a SIV-Chinese rhesus macacaque one, we made a study on Treg in SIV-infected rhesus monkeys. One week post infection, proviral DNA in PBMC could be detected by nested-PCR. CD4+ T cells decreased greatly, while CD8+ T cells increased in quantity. And we found SIV-p27 specific antibodies lagged two weeks or so behind some SIV-specific antibodies. However, the latter peaked, quickly after which they dropped even to undetectable level. But p27 antibodies maintained at high level throughout this period. The underlying mechanism remains unknown. And we expect to find out if p27 antibodies will help the hosts to control the replication of SIV more effectively. Both the absolute quantity and the relative quantity of Treg in CD4+ T cells increased dramatically in primary and chronic SIV-infection. Moreover, it seemed that those Tregs had not been negatively affected in its immuno- suppressive abilities in downregulating IFN-γ and IL-2 secretion of CD4+CD25- T cells. CCR5, one of the co-receptor of HIV/SIV infection, is also expressed on the surface of Tregs. So it is presumed that Treg could be targets cell of SIV. But references in this topic could rarely be found in journals. In our study, we detected proviral DNA in Tregs. It was shown that Tregs might be more easily infected than CD4+CD25- T cells (not including memory T cells). But many details are far from being clear. We screened for the differences mRNA expressions in several tissues of SIV-infected monkeys. And we found that the transcription level of FoxP3 mRNA had been upregulated in the abdominal lymph nodes. Meanwhile, immuno-suppressive cytokines TGF-βand IL-10 increased at transcription level. TGF-β could suppress indirectly target cells through its crosstalk with dendritic cells. IL-10 could suppress target cells directly. So SIV-specific immunity might be dysfunctioned by Tregs.
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