The effect of UV-B irradiation on primary and secondary HSV-1 infections in interleukin-4 knockout mice.

Ultraviolet B (UV-B) irradiation suppresses cell-mediated immunity and may lead to increased susceptibility to infectious diseases. Limited evidence suggests that exposure promotes a T helper (Th) 2 type of cytokine response with abrogation of a Th1 response. Several putative mediators of UV-induced immunosuppression have been identified, of which interleukin-4 (IL-4), an example of a Th2 cytokine, is one. Primary and secondary epidermal infections with herpes simplex virus (HSV) type 1 in IL-4 knockout (IL-4-/-) mice and the parent strain Bb 129 strain (IL-4+/+) were investigated using clinical features, phenotyping of cells from lymph nodes draining the sites of infection and lymphoproliferation assays. The IL-4-/- mice were more susceptible to both primary and secondary HSV infections than the parent mice. The percentage of lymph node dendritic cells (DC) expressing Ia was 45 in the IL-4+/+ mice but only 18 in the IL-4-/- strain, and the lymph node cells from infected IL-4-/- mice were less able to respond in vitro to HSV than those from the parent strain. Following suberythemal UV-B irradiation, more severe primary and secondary lesions resulted in both strains. There were fewer lymph node DC expressing Ia in both strains and this change was accompanied by suppression of the lymphoproliferation induced by HSV which was due to an effect on DC function rather than on the proliferative ability of the responding lymphocytes. UV-B exposure had no effect on ICAM-1 or B7.2 expression on the DC. Thus IL-4 seems to protect mice against HSV infection, and no evidence was obtained for the involvement of IL-4 in the UV-induced immunomodulation which results in more severe cutaneous HSV infections.