Persistent gamma-herpesvirus infection induces a CD4 T cell response containing functionally distinct effector populations.
Persistent gamma-herpesvirus infection induces a CD4 T cell response containing functionally distinct effector populations.
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DOI：
10.4049/jimmunol.0902935
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发表时间：
2010-04-01
期刊：
影响因子：
--
通讯作者：
Flaño E
中科院分区：
文献类型：
--
作者：
Stuller KA;Cush SS;Flaño E
The direct effector mechanisms of CD4 T cells during γ-herpesvirus 68 (γHV68)-persistent infection are less well understood than those of their CD8 T cell counterparts, although there is substantial evidence that CD4 T cells are critical for the control of persistent γ-herpesvirus infection. Our results show that in γHV68-persistently infected mice, CD4 T cells are not cytokine polyfunctional, but there is a division of labor in the CD4 T cell compartment in which CD4 T cells polarize toward two distinct populations with different effector functions: IFN-γ producers and CD107+ cytolytic effectors. These two CD4 T cell effector populations degranulate and produce IFN-γ during steady state without need for exogenous antigenic restimulation, which is fundamentally different from that observed with γHV68-specific CD8 T cells. By using anti–IFN-γ Ab depletions and IFN-γ–deficient mice, we show that CD4 T cell-mediated cytotoxicity in vivo is not dependent on IFN-γ activity. In addition, our data show that purified CD4 T cells isolated from γHV68-latently infected mice have the capacity to inhibit γHV68 reactivation from latency. Our results support the concept that CD4 T cells are critical effectors for the control of γ-herpesvirus latent infection, and they mediate this effect by two independent mechanisms: IFN-γ production and cytotoxicity.
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