| First Author | Chen HY | Year | 2020 |
| Journal | J Immunol | Volume | 204 |
| Issue | 5 | Pages | 1158-1172 |
| PubMed ID | 31969388 | Mgi Jnum | J:285613 |
| Mgi Id | MGI:6392178 | Doi | 10.4049/jimmunol.1901114 |
| Citation | Chen HY, et al. (2020) Intracellular Galectin-9 Enhances Proximal TCR Signaling and Potentiates Autoimmune Diseases. J Immunol 204(5):1158-1172 |
| abstractText | Galectin-9 is a risk gene in inflammatory bowel disease. By transcriptomic analyses of ileal biopsies and PBMCs from inflammatory bowel disease patients, we identified a positive correlation between galectin-9 expression and colitis severity. We observed that galectin-9-deficient T cells were less able to induce T cell-mediated colitis. However, several mouse-based studies reported that galectin-9 treatment induces T cell apoptosis and ameliorates autoimmune diseases in an exogenously modulated manner, indicating a complicated regulation of galectin-9 in T cells. We found that galectin-9 is expressed mainly inside T cells, and its secreted form is barely detected under physiological conditions. Endogenous galectin-9 was recruited to immune synapses upon T cell activation. Moreover, proximal TCR signaling was impaired in galectin-9-deficient T cells, and proliferation of these cells was decreased through an intracellularly modulated manner. Th17 cell differentiation was downregulated in galectin-9-deficient T cells, and this impairment can be rescued by strong TCR signaling. Taken together, these findings suggest that intracellular galectin-9 is a positive regulator of T cell activation and modulates the pathogenesis of autoimmune diseases. |
