| First Author | Fabié A | Year | 2018 |
| Journal | Cell Rep | Volume | 24 |
| Issue | 5 | Pages | 1163-1175 |
| PubMed ID | 30067973 | Mgi Jnum | J:270775 |
| Mgi Id | MGI:6278707 | Doi | 10.1016/j.celrep.2018.06.107 |
| Citation | Fabie A, et al. (2018) IRF-5 Promotes Cell Death in CD4 T Cells during Chronic Infection. Cell Rep 24(5):1163-1175 |
| abstractText | 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)-gamma(+) 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. |
