Abstract
The transcription factor interferon regulatory factor 5 (IRF-5) plays an important function in innate immunity and in initiating pro-inflammatory responses against pathogens. IRF-5 is constitutively expressed in several cell types, including plasmacytoid dendritic cells, monocytes, and B cells. We have previously reported that IRF-5 is also expressed in Tcells during infection. The role of IRF-5 in Tcells is yet unknown. Here, we demonstrate that IRF-5 is increasingly expressed in interferon (IFN)-γ+ CD4 Tcells over the course of L.donovani infection. This transcription factor is induced by apoptotic material via Toll-like receptor 7 (TLR7) and promotes the expression of death receptor 5 (DR5). IRF-5 activation sensitizes CD4 Tcells to cell death. Because tissue disruption and chronic inflammation are common characteristics of persistent infections, activation of IRF-5 in CD4 Tcells may represent a common pathway that leads to suppression of protective CD4 Tcell responses, favoring the establishment of chronic infection.
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