@article{open1653,
          volume = {211},
          number = {3},
           month = {February},
          author = {Sathi Babu Chodisetti and Uthaman Gowthaman and Pradeep K Rai and Aurobind Vidyarthi and Nargis Khan and J N Agrewala},
            note = {Copyright of this article belongs to Oxford University Press},
           title = {Triggering through Toll-like receptor 2 limits chronically stimulated T-helper type 1 cells from undergoing exhaustion.},
       publisher = {Oxford University Press},
            year = {2015},
         journal = {The Journal of infectious diseases},
           pages = {486--96},
        keywords = {LR-2; Th1 cells; chronic infection; exhaustion markers; tuberculosis},
             url = {http://crdd.osdd.net/open/1653/},
        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 {\ensuremath{\gamma}}, 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.}
}