Abstract

Ultraviolet A (UVA) radiation can have dual affects on the immune system depending on dose. At doses of approximately 1.8 J cm(-2), UVA acts in an immunosuppressive manner, whilst at higher doses UVA can promote recovery and protection against UVB-induced immunosuppression in mice. We utilised a model of contact hypersensitivity (CHS) to investigate how different doses of UVA modulates CD8 T cell immunity against a hapten in vivo. Only 1.8 J cm(-2) UVA decreased the CHS response compared to unirradiated mice, but this did not correlate with an inhibition of primary effector CD8 T cells. A similar expansion of effector CD8 T cells in skin-draining lymph nodes and accumulation of IFN-gamma-producing CD8 T cells in the ear skin was observed between unirradiated and UVA-irradiated mice. However, dermal memory CD8 T cells examined 9 weeks post challenge showed decreased numbers in mice irradiated with 1.8 J cm(-2) UVA compared with unirradiated, 1.3 J cm(-2) and 3.4 J cm(-2) UVA-irradiated mice. Therefore, UVA does not inhibit the expansion, migration or IFN-gamma secretion of CD8 T cells during a primary immune response. However, exposure to immunosuppressive UVA causes a defect in CD8 T cell development that impairs the ability of cells to become long-term memory cells.

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