Galectin-1 Expression in CD8+ T Lymphocytes Controls Inflammation in Contact Hypersensitivity

Allergic contact dermatitis, also known as contact hypersensitivity, is a frequent T-cell-mediated inflammatory skin disease characterized by red, itchy, swollen, and cracked skin. It is caused by the direct contact with an allergen and/or irritant hapten. Galectin-1 (Gal-1) is a b-galactoside-binding lectin, which is highly expressed in several types of immune cells. The role of endogenous Gal-1 in contact hypersensitivity is not known. We found that Gal-1-deficient mice display more sustained and prolonged skin inflammation than wild-type mice after oxazolone treatment. Gal-1-deficient mice have increased CD8+ T cells and neutrophilic infiltration in the skin. After the sensitization phase, Gal-1-depleted mice showed an increased frequency of central memory CD8+ T cells and IFN-g secretion by CD8+ T cells. The absence of Gal-1 does not affect the migration of transferred CD4+ and CD8+ T cells from the blood to the lymph nodes or to the skin. The depletion of CD4+ T lymphocytes as well as adoptive transfer experiments demonstrated that endogenous expression of Gal-1 on CD8+ T lymphocytes exerts a major role in the control of contact hypersensitivity model. These data underscore the protective role of endogenous Gal-1 in CD8+ but not CD4+ T cells in the development of allergic contact dermatitis.

Automated summary

Allergic contact dermatitis is a common T-cell-mediated inflammatory skin disease characterized by red, itchy, swollen, and cracked skin. The absence of endogenous Gal-1 in CD8+ T cells plays a protective role in controlling the development of allergic contact dermatitis, as Gal-1-deficient mice display more sustained and severe skin inflammation after treatment.