Baadsgaard O
Department of Dermatology, Gentofte Hospital, University of Copenhagen, Denmark.
Arch Dermatol. 1991 Jan;127(1):99-109.
Ultraviolet exposure of human skin deletes the function of antigen-presenting Langerhans cells normally resident within the epidermis. Langerhans cells are capable of activating T-lymphocytes by presenting antigens (such as nickel or tumor antigens) to T-lymphocytes. Such activated T-lymphocytes may be involved in the development of contact dermatitis and the immune surveillance of immunogenic skin cancers. Deletion of the function of Langerhans cells does not result in abrogated epidermal antigen presentation since ultraviolet irradiation simultaneously induces the appearance of another epidermal antigen-presenting cell population that is distinct from the Langerhans cell population and seems to induce suppression of the immune response. Suppression of the immune response following ultraviolet irradiation in murine models is critical for growth of immunogenic ultraviolet-induced skin neoplasm. Thus, ultraviolet irradiation of human skin may facilitate the growth of human neoplasms, and the spreading of skin-associated infections due to induction of suppressor T cells.
人体皮肤暴露于紫外线会使正常驻留在表皮内的抗原呈递朗格汉斯细胞的功能丧失。朗格汉斯细胞能够通过向T淋巴细胞呈递抗原(如镍或肿瘤抗原)来激活T淋巴细胞。这种被激活的T淋巴细胞可能参与接触性皮炎的发展以及免疫原性皮肤癌的免疫监视。朗格汉斯细胞功能的丧失并不会导致表皮抗原呈递被废除,因为紫外线照射同时会诱导另一种与朗格汉斯细胞群体不同的表皮抗原呈递细胞群体出现,并且似乎会诱导免疫反应的抑制。在小鼠模型中,紫外线照射后免疫反应的抑制对于免疫原性紫外线诱导的皮肤肿瘤的生长至关重要。因此,人体皮肤的紫外线照射可能会促进人类肿瘤的生长,并由于抑制性T细胞的诱导而导致皮肤相关感染的传播。