Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.
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DOI：
10.4049/jimmunol.1100241
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发表时间：
2011-09-15
期刊：
影响因子：
--
通讯作者：
Couper KN
中科院分区：
文献类型：
--
作者：
Villegas-Mendez A;de Souza JB;Murungi L;Hafalla JC;Shaw TN;Greig R;Riley EM;Couper KN
IFN-γ and T cells are both required for the development of experimental cerebral malaria during P. berghei ANKA infection. Surprisingly, however, the role of IFN-γ in shaping the effector CD4+ and CD8+ T cell response during this infection has not been examined in detail. To address this, we have compared the effector T cell responses in wild-type and IFN- γ−/− mice during P. berghei ANKA infection. The expansion of splenic CD4+ and CD8+ T cells during P. berghei ANKA infection was unaffected by the absence of IFN-γ but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN- γ−/− mice, however, the migration to, and accumulation of, effector CD4+ and CD8+ T cells in the lung, liver and brain was altered in IFN- γ−/− mice. Interestingly, activation and accumulation of T cells in various non-lymphoid organs was differently affected by lack of IFN-γ, suggesting that IFN- γ influences T cell effector function to varying levels in different anatomical locations. Importantly, control of splenic T cell numbers during P. berghei ANKA infection depended upon active IFN- γ-dependent environmental signals – leading to T cell apoptosis - rather than upon intrinsic alterations in T cell programming. This is the first study to fully investigate the role of IFN- γ in modulating T cell function during P. berghei ANKA infection and reveals that IFN-γ is required for efficient contraction of the pool of activated T cells.
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