THE ROLE OF INTERLEUKIN-4 IN ULTRAVIOLET-B LIGHT-INDUCED IMMUNOSUPPRESSION

Prolonged exposure to ultraviolet light (UV) is known to lead to prema ture skin ageing, increased incidence of cataract and a high risk of d eveloping skin cancers. UV-B irradiation, even if given as a single su berythemal dose, suppresses some immune responses, possibly reducing t he production of T helper (Th) 1 cytokines [interleukin (IL)-2 and int erferon-gamma] and augmenting Th2 cytokines (IL-4, IL-5 and IL-10) in mice. We investigated the role of IL-4 in UV-B induced immunomodulatio n using IL-4 knockout (IL-4(-/-)) mice and the parent strain Bb129. Su berythermal UV-B irradiation (1440 J/m(2)) led to a reduction in the d ensity and antigen presenting ability of Langerhans' cells in the epid ermis of both normal and IL-IF-I-mice. Exposure also induced an accumu lation of CD4(+) and CD8(+) lymphocytes as well as dendritic cells in the lymph nodes draining the irradiated site in both strains. The prol iferation of lymph node cells in response to the mitogen concanavalin A was enhanced in the IL-4(-/-) mice compared with the parent strain. Following UV-B exposure, this proliferation was increased in lymph nod e cells of parent mice but was significantly suppressed in the IL-4(-/ -) mice. The contact hypersensitivity (CH) response to oxazolone was s uppressed to the same extent by UV-B irradiation in both strains. In t he parent mice, infected with herpes simplex virus (HSV) following UV- B exposure and challenged subsequently with inactivated virus, the del ayed hypersensitivity (DH) response was suppressed by about 50% compar ed with unirradiated mice; no such suppression in DH occurred in irrad iated IL-4(-/-) mice infected with RSV. Thus, IL-4 may be an important mediator of the UV-B-induced suppression in DH but not in CH, where o ther cytokines may be involved or may compensate for the lack of IL-4.