Basic science answers to questions in clinical contact dermatitis.
Since the first clear demonstration in the 1970s of an immunologic linkage between UV-light exposure of laboratory mice and the development of skin cancers in these animals, much progress has been achieved in our understanding of the effects of UV light on the immune system. At the cellular level, two overlapping mechanisms have been expounded to explain UVB-induced immunosuppression: (1) altered cutaneous antigen presentation due to perturbations in Langerhans' cells and/or the recruitment of macrophage-like cells into skin, and (2) the initiated or up-regulated secretion by skin cells (particularly but not limited to keratinocytes) of soluble mediators of immunosuppression (alpha-melanocyte-stimulating hormone, interleukin 10, tumor necrosis factor alpha). An end result common to both mechanisms is inhibition of Th1-type immunity in favor of preserved or heightened Th2-type immunity. At the molecular level, two targets of UVB radiation are the subject of intense investigation. Circumstantial evidence has accumulated to implicate a direct effect of UVB on DNA (in antigen-presenting cells and/or cytokine-producing cells) as the triggering cause of UVB-evoked immunosuppression. On the other hand, UVB-triggered changes in cell membrane molecules (epidermal growth factor receptor, intercellular adhesion molecule 1, B7) have been correlated with temporally distal UV effects, including the activation of gene transcription pathways and the down-regulation of antigen presentation independent of DNA damage.
Cruz
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PD
Department of Dermatology, University of Texas Southwestern Medical Center, Dallas 75235-9069, USA.
D000818:Animals; D017449:Dermatitis, Allergic Contact / Q000209:etiology / Q000276:immunology; D006801:Humans; D007107:Immune System / Q000502:physiology*; D051379:Mice; D014466:Ultraviolet Rays / Q000009:adverse effects