The AP1 transcription factor Fosl2 promotes systemic autoimmunity and inflammation by repressing treg development

Renoux, Florian; Stellato, Mara; Haftmann, Claudia; Vogetseder, Alexander; Huang, Riyun; Subramaniam, Arun; Becker, Mike O; Blyszczuk, Przemyslaw; Becher, Burkhard; Distler, Jörg H W; Kania, Gabriela; Boyman, Onur; Distler, Oliver

doi:10.1016/j.celrep.2020.107826

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Renoux, F., Stellato, M., Haftmann, C., Vogetseder, A., Huang, R., Subramaniam, A., Becker, M. O., Blyszczuk, P., Becher, B., Distler, J. H. W., Kania, G., Boyman, O., & Distler, O. (2020). The AP1 transcription factor Fosl2 promotes systemic autoimmunity and inflammation by repressing treg development. Cell Reports, 31(13), 107826. https://doi.org/10.1016/j.celrep.2020.107826

Abstract

Regulatory T cells (Tregs) represent a major population in the control of immune homeostasis and autoimmunity. Here we show that Fos-like 2 (Fosl2), a TCR-induced AP1 transcription factor, represses Treg development and controls autoimmunity. Mice overexpressing Fosl2 (Fosl2$^{tg}$) indeed show a systemic inflammatory phenotype, with immune infiltrates in multiple organs. This phenotype is absent in Fosl2$^{tg}$ × Rag2$^{-/-}$