BACKGROUND: Galectins are members of a β-galactoside-binding animal lectin family. Recombinant galectin-9 is a negative regulator of Th1 cells through the Tim3 inhibitory signaling pathway, but the function of endogenous galectin-9 in the immune response is not well studied. Here we examined the role of endogenous galectin-9 in T cells by a mouse model of contact hypersensitivity (CHS), mediated by T cells. RESULTS: CHS response was less severe in galectin-9-deficient (Gal-9 -/-) mice than in Gal-9 +/+ mice by checking the ear thickness change. CD4+ T cells from Gal-9 -/- mice secreted less IFN-γ, IL-17, IL-4 and IL-13 than those from Gal-9 +/+ mice when stimulated by anti-CD3/anti-CD28 mAbs in vitro. CD4+ T cells from Gal-9 -/- mice sensitized with dinitrofluorobenzene topically secreted less IL-17, but not other three cytokines, than those from comparably sensitized Gal-9 +/+ mice. The adoptive transfer with sensitized CD4+ T cells from Gal-9 -/- mice evoked less severe CHS response than those from Gal-9 +/+ mice. Further, CD4+ T cells from Gal-9 -/- mice contained a lower amount of phosphorylated IκBα than those from Gal-9 +/+ mice, when activated by anti-CD3/anti-CD28. CONCLUSIONS: Galectin-9-deficient mice exhibit less CHS response, which might be related to lower IκBα phosphorylation and lower cytokine production in CD4+ T cells. Additional studies of the function of endogenous Gal-9 may provide a new insight on treatment of allergic contact dermatitis.
- Copyright © 2013 by The American Association of Immunologists, Inc.