IRF-5 Promotes Cell Death in CD4 T Cells during Chronic Infection.

Cell Rep

INRS-Institut Armand-Frappier, 531 Boulevard des Prairies, Laval, QC H7V 1B7, Canada. Electronic address:

Published: July 2018

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 T cells during infection. The role of IRF-5 in T cells is yet unknown. Here, we demonstrate that IRF-5 is increasingly expressed in interferon (IFN)-γ CD4 T cells 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 T cells to cell death. Because tissue disruption and chronic inflammation are common characteristics of persistent infections, activation of IRF-5 in CD4 T cells may represent a common pathway that leads to suppression of protective CD4 T cell responses, favoring the establishment of chronic infection.

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http://dx.doi.org/10.1016/j.celrep.2018.06.107DOI Listing

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