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- W2116092893 abstract "Chronic infections result in T-cell exhaustion, a state of functional unresponsiveness. To control the infection, it is important to salvage the exhausted T cells. In this study, we delivered signals through Toll-like receptor 2 (TLR-2) to reinvigorate functionality in chronically activated T-helper type 1 (Th1) cells. This process significantly augmented the expression of T-bet, interferon γ, interleukin 2, and the antiapoptotic molecule Bcl-2, whereas it dampened the display of the exhaustion markers programmed death receptor 1 (PD-1) and lymphocyte activation gene 3 (Lag-3). Additionally, TLR-2 signaling bolstered the ability of chronically stimulated Th1 cells to activate B cells. Finally, the results were substantiated by observing reduced lung pathology upon administration of TLR-2 agonist in the chronic infection model of tuberculosis. These data demonstrated the importance of TLR-2 in rescuing chronically activated Th1 cells from undergoing exhaustion. This study will pave a way for targeting TLR-2 in developing therapeutic strategies to treat chronic diseases involving loss of Th1 cell function." @default.
- W2116092893 created "2016-06-24" @default.
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- W2116092893 date "2014-08-25" @default.
- W2116092893 modified "2023-10-14" @default.
- W2116092893 title "Triggering Through Toll-like Receptor 2 Limits Chronically Stimulated T-helper Type 1 Cells From Undergoing Exhaustion" @default.
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- W2116092893 doi "https://doi.org/10.1093/infdis/jiu472" @default.
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