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Publication : Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection.

First Author  Villegas-Mendez A Year  2011
Journal  J Immunol Volume  187
Issue  6 Pages  2885-97
PubMed ID  21880980 Mgi Jnum  J:179223
Mgi Id  MGI:5301477 Doi  10.4049/jimmunol.1100241
Citation  Villegas-Mendez A, et al. (2011) Heterogeneous and tissue-specific regulation of effector T cell responses by IFN-gamma during Plasmodium berghei ANKA infection. J Immunol 187(6):2885-97
abstractText  IFN-gamma and T cells are both required for the development of experimental cerebral malaria during Plasmodium berghei ANKA infection. Surprisingly, however, the role of IFN-gamma 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-gamma(-/-) 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-gamma, but the contraction phase of the T cell response was significantly attenuated. Splenic T cell activation and effector function were essentially normal in IFN-gamma(-/-) mice; however, the migration to, and accumulation of, effector CD4(+) and CD8(+) T cells in the lung, liver, and brain was altered in IFN-gamma(-/-) mice. Interestingly, activation and accumulation of T cells in various nonlymphoid organs was differently affected by lack of IFN-gamma, suggesting that IFN-gamma 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 on active IFN-gamma-dependent environmental signals--leading to T cell apoptosis--rather than upon intrinsic alterations in T cell programming. To our knowledge, this is the first study to fully investigate the role of IFN-gamma in modulating T cell function during P. berghei ANKA infection and reveals that IFN-gamma is required for efficient contraction of the pool of activated T cells.
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