Journal
JOURNAL OF IMMUNOLOGY
Volume 204, Issue 5, Pages 1158-1172Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1901114
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Funding
- Ministry of Science and Technology, Taiwan [MOST 106-2320-B-400-032-MY3, MOST 106-2321-B-400-014, MOST 107-2321-B-400-016, MOST 108-2321-B-400-018]
- Tri-Service General Hospital [TSGH-C107-008-S02, TSGH-C108-007-008-S02, VTA107-T-1-1, VTA108-T-1-2]
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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.
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