AIM2 promotes TH17 cells differentiation by regulating RORγt transcription activity
| Autor: | Jefferson Antônio Leite, Luísa Menezes, Eloisa Martins, Tamara Silva Rodrigues, Lucas Tavares, Anna Ebering, Carsten Schelmbauer, Guilherme C. Martelossi Cebinelli, Valeriya Zinina, Artemiy Golden, Natalia Soshnikova, Dario S. Zamboni, Fernando Q. Cunha, Magdalena Huber, João Santana Silva, Ari Waisman, Daniela Carlos, Niels Olsen Saraiva Câmara |
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| Jazyk: | angličtina |
| Rok vydání: | 2023 |
| Předmět: | |
| Zdroj: | iScience, Vol 26, Iss 11, Pp 108134- (2023) |
| Druh dokumentu: | article |
| ISSN: | 2589-0042 99703394 |
| DOI: | 10.1016/j.isci.2023.108134 |
| Popis: | Summary: AIM2 is an interferon-inducible HIN-200 protein family member and is well-documented for its roles in innate immune responses as a DNA sensor. Recent studies have highlighted AIM2’s function on regulatory T cells (Treg) and follicular T cells (Tfh). However, its involvement in Th17 cell differentiation remains unclear. This study reveals that AIM2 promotes Th17 cell differentiation. AIM2 deficiency decreases IL-17A production and downregulates key Th17 associated proteins (RORγt, IL-1R1, IL-23R). AIM2 is located in the nucleus of Th17 cells, where it interacts with RORγt, enhancing its binding to the Il17a promoter. The absence of AIM2 hinders naive CD4 T cells from differentiating into functional Th17 cells and from inducing colitis in Rag1−/− mice. This study uncovers AIM2’s role as a regulator of Th17 cell transcriptional programming, highlighting its potential as a therapeutic target for Th17 cell-mediated inflammatory diseases. |
| Databáze: | Directory of Open Access Journals |
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