Oral Salmonella expressing Colonization Factor Antigen I stimulates the rapid induction of Galectin-1 on induced Treg cells (P4204)

Abstract

Abstract Galectin-1 (Gal-1) is one of the 15 Galectin family members that bind to β-galactoside. Gal-1 binding to various cell surface glycoproteins leads to deletion of T effector functions. Gal-1 engagement to CD43 on APCs converts these cells to tolerogenic supporting the generation of Treg cells. Our previous work have shown that oral Salmonella-CFA/I strain H696 (expresses CFA/I fimbriae from enterotoxigenic E. coli) induces a highly suppressive Foxp3+ CD25+CD4+ Treg cells capable of suppressing the development of experimental autoimmune encephalomyelitis (EAE). Gal-1 expression was rapidly induced within 3 days by both Foxp3+ Treg cells obtained from Salmonella-CFA/I-immunized mice unlike mice vaccinated with isogenic Salmonella vaccine (strain H647) control. To assess the function of Gal-1, isolated Treg cells from H696- and H647-vaccinated mice were assessed for their ability to suppress OT-2 OVA-specific effector T cell proliferation following r estimulation with OVA peptide. Upon neutralization of Gal-1, Salmonella-CFA/I-induced Treg cells were unable to suppress OT-2 cell proliferation; similar neutralization of Salmonella vector-derived Treg cells had no effect. Kinetic analysis of Gal-1 expression by dendritic cells (DCs) following H696 imminization also showed early induction of Gal-1 suggesting the importance of Gal-1 to induce tolerogenic T cells and DCs. These results suggest Gal-1 is a major effector molecule for the Salmonella-CFA/I-induced Treg cells.</jats:p