IRF-5 Promotes Cell Death in CD4 T Cells During Chronic Infection (IMAGE)
Caption
The study presented by Professor Simona Stager's team points to a mechanism involving the TLR7 receptor (Toll-like Receptor 7), usually activated in innate immune system cells by pathogen recognition. In the case of chronic inflammation, the cellular residues present after tissue destruction activate TLR7 in Th1 cells. Activation of TLR7 induces expression and activation of IRF-5, which in turn increases expression of DR5 (Death Receptor 5) and caspase 8, two signaling elements leading to cell death. Thus, chronic inflammation induces the death of protective CD4 T cells via the TLR7-IRF-5 cellular pathway.
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