IRF4 activity is required in established plasma cells to regulate gene transcription and mitochondrial homeostasis
- Author(s)
- Low, MSY; Brodie, EJ; Fedele, PL; Liao, Y; Grigoriadis, G; Strasser, A; Kallies, A; Willis, SN; Tellier, J; Shi, W; Gabriel, S; O'Donnell, K; Pitt, C; Nutt, SL; Tarlinton, D;
- Details
- Publication Year 2019-11-26,Volume 29,Issue #9,Page 2634-2645 e5
- Journal Title
- Cell Reports
- Publication Type
- Journal Article
- Abstract
- The transcription factor interferon regulatory factor 4 (IRF4) is critical for the development, maintenance, and function of plasma cells. The mechanism by which IRF4 exerts its action in mature plasma cells has been elusive due to the death of all such cells upon IRF4 loss. While we identify apoptosis as a critical pathway for the death of plasma cells caused by IRF4 loss, we also determine that IRF4 did not regulate the intrinsic apoptotic pathway directly. By using an inducible IRF4 deletion system in the presence of the overexpression of anti-apoptotic BCL2, we identify genes whose expression is coordinated by IRF4 and that in turn specify plasma cell identity and mitochondrial homeostasis.
- Publisher
- Elsevier
- Research Division(s)
- Immunology; Bioinformatics; Blood Cells And Blood Cancer
- PubMed ID
- 31775034
- Publisher's Version
- https://doi.org/10.1016/j.celrep.2019.10.097
- Open Access at Publisher's Site
https://doi.org/10.1016/j.celrep.2019.10.097- NHMRC Grants
- NHMRC/1054925,
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 2019-12-05 01:26:20
Last Modified: 2020-02-11 09:01:48