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- W4313379435 abstract "Abstract CD4 T cells are critical for control of persistent infections; however, the key signals that regulate CD4 T help during infection remain incompletely defined. Here we show that during lymphocytic choriomeningitis virus (LCMV) clone 13 infection, glucocorticoid-induced TNFR (GITR)-deficient mice exhibit defective CTL responses and viral control. Differences in CTL responses and viral control between GITR+/+ and GITR-/- mice were lost when CD4 T cells were depleted. Furthermore, mixed bone marrow chimeric mice and transfer of LCMV-specific CD4 or CD8 T cells demonstrated that these effects of GITR are CD4 T cell-intrinsic. GITR is dispensable for initial CD4 T cell proliferation and differentiation, but supports the post-priming accumulation of IL-2+ Th1 cells to facilitate CTL expansion and early viral control. In vivo GITR-dependent activation of p65 NF-kB and S6 ribosomal protein was detected at day 3 p.i., a time at which GITR-L is maximally expressed on macrophages. Defects in CD4 T cell accumulation in GITR-deficient T cells were apparent starting at day 5 p.i. Consistently, we pinpoint IL-2-dependent CD4 T cell help for CTLs to between days 4-8 p.i. GITR also increases the ratio of T follicular helper to T follicular regulatory cells, thereby enhancing LCMV-specific IgG production. Together, these findings identify a CD4 T cell-intrinsic role for GITR in sustaining early CD8 and late humoral responses to collectively promote control of chronic LCMV clone 13 infection." @default.
- W4313379435 created "2023-01-06" @default.
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- W4313379435 date "2015-05-01" @default.
- W4313379435 modified "2023-09-27" @default.
- W4313379435 title "GITR sustains IL-2+ CD4 helper T cells to facilitate early control of a chronic viral infection (IRC7P.422)" @default.
- W4313379435 doi "https://doi.org/10.4049/jimmunol.194.supp.128.3" @default.
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