Galectin-3 exacerbates autoimmune diabetes by limiting regulatory T cell differentiation and function.

ABSTRACT: Galectin-3, a β-galactoside-binding lectin, has been implicated in several inflammatory and autoimmune diseases. However, the significance of circulating Galectin-3 in type 1 diabetes (T1D) remains unclear. Here, we report that compared to healthy controls, patients with T1D and their first-degree relatives (FDRs) exhibited significantly increased serum Galectin-3 levels primarily produced and secreted by monocytes/macrophages. Pharmacological inhibition (TD139) as well as knockout of Galectin-3 gene both attenuated Galectin-3-mediated suppression of regulatory T cells (T_reg cells) and protected from insulitis and diabetes onset in NOD mice. Mechanistically, Galectin-3 bound to and activated lymphocyte activation gene 3 (LAG3), a receptor expressed on activated T cells, subseque

SUBMITTER: Xie L 

PROVIDER: S-EPMC12757048 | biostudies-literature | 2026 Jan

REPOSITORIES: biostudies-literature