| First Author | Zhang Q | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 2040 | PubMed ID | 32973810 |
| Mgi Jnum | J:308197 | Mgi Id | MGI:6714381 |
| Doi | 10.3389/fimmu.2020.02040 | Citation | Zhang Q, et al. (2020) Critical Role of AdipoR1 in Regulating Th17 Cell Differentiation Through Modulation of HIF-1alpha-Dependent Glycolysis. Front Immunol 11:2040 |
| abstractText | We previously reported that adiponectin (AD) promotes naive T cell differentiation into Th17 cells and participates in synovial inflammation and the bone erosion process in patients with rheumatoid arthritis. Here, we use a T cell lineage adiponectin receptor 1 (AdipoR1) conditional knockout model to investigate the role of AdipoR1 in Th17 differentiation. RNA-sequencing (RNA-seq) demonstrated that AdipoR1 knockout reduced the expression of a variety of T cell related genes, with Rorc showing the greatest level of down-regulation. AdipoR1 deficiency inhibited Th17 cell differentiation in vitro and ameliorated joint inflammation in antigen-induced arthritis mice. Moreover, AdipoR1-deficent CD4(+)T cells displayed reduced Hypoxia-Inducible Factor-1alpha expression leading to glycolysis inhibition during naive CD4(+)T cell differentiation into Th17 cells. We describe a novel function of AdipoR1 in regulating Th17 cell differentiation through modulating HIF-1alpha-dependent glycolysis. |
