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 is a β-galactoside-binding lectin which is highly expressed in several types of immune cells. The role of endogenous Galectin-1 in contact hypersensitivity is not known. We found that Galectin-1-deficient mice display more sustained and prolonged skin inflammation than wild type mice after oxazolone treatment. Galectin-1-deficient mice have increased CD8 T cells and neutrophilic infiltration in the skin. After the sensitization phase, Galectin-1-depleted mice showed increased frequency of central memory CD8 T cells and IFNγ secretion by CD8 T cells. The absence of Galectin-1 does not affect migration of transferred CD4 and CD8 T cells from the blood to the lymph nodes or to the skin. Depletion of CD4 T lymphocytes as well as adoptive transfer experiments demonstrated that endogenous expression of Galectin-1 on CD8 T lymphocytes exerts a major role in the control of contact hypersensitivity model. These data underscore the protective role of endogenous Galectin-1 in CD8 but not CD4 T cells in the development of allergic contact dermatitis.
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