| First Author | Ikegami I | Year | 2019 |
| Journal | Biochem Biophys Res Commun | Volume | 514 |
| Issue | 4 | Pages | 1167-1171 |
| PubMed ID | 31103264 | Mgi Jnum | J:291746 |
| Mgi Id | MGI:6443158 | Doi | 10.1016/j.bbrc.2019.05.057 |
| Citation | Ikegami I, et al. (2019) Bob1 enhances RORgammat-mediated IL-17A expression in Th17cells through interaction with RORgammat. Biochem Biophys Res Commun 514(4):1167-1171 |
| abstractText | POU domain class 2-associating factor 1 (also called Bob1), which is mainly expressed in B cells, regulates B cell homeostasis and controls humoral immune responses. Although Bob1 is known to function reliably in T cell subsets including follicular helper T cells, Th1 cells and Th2 cells, it is unknown whether Bob1 functions in other T cell subsets. In this study, we found that Bob1 knock out (KO) mice are resistant to experimental autoimmune encephalomyelitis (EAE) induced by MOG35-55 peptide and that Bob1 KO T cells are defective in Th17 differentiation. Importantly, Bob1 interacts with retinoid acid receptor-related orphan receptor (ROR) gamma t (RORgammat), a signature transcription factor for Th17cells, through the ligand-binding domain of RORgammat, thereby enhancing IL-17A transcription activity. IL-17A induction by Bob1 requires the ability for its formation of a DNA-Oct1-Bobl ternary complex. Thus, our findings demonstrate that Bob1 enhances IL-17A expression in vivo and in vitro by interacting with RORgammat in Th17cells, suggesting that Bob1 plays a pivotal role in Th17-mediated autoimmune disease. |
