el-Ghorr A A, Norval M
Department of Medical Microbiology, University of Edinburgh Medical School, UK.
Immunology. 1997 Sep;92(1):26-32. doi: 10.1046/j.1365-2567.1997.d01-2292.x.
Prolonged exposure to ultraviolet light (UV) is known to lead to premature skin ageing, increased incidence of cataract and a high risk of developing skin cancers. UV-B irradiation, even if given as a single suberythemal dose, suppresses some immune responses, possibly reducing the production of T helper (Th) 1 cytokines [interleukin (IL)-2 and interferon-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 immunomodulation using IL-4 knockout (IL-4 -/-) mice and the parent strain Bb129. Suberythemal UV-B irradiation (1440 J/m2) led to a reduction in the density and antigen presenting ability of Langerhans' cells in the epidermis of both normal and IL-4 -/- mice. Exposure also induced an accumulation of CD4+ and CD8+ lymphocytes as well as dendritic cells in the lymph nodes draining the irradiated site in both strains. The proliferation 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 node cells of parent mice but was significantly suppressed in the IL-4 -/- mice. The contact hypersensitivity (CH) response to oxazolone was suppressed to the same extent by UV-B irradiation in both strains. In the parent mice, infected with herpes simplex virus (HSV) following UV-B exposure and challenged subsequently with inactivated virus, the delayed hypersensitivity (DH) response was suppressed by about 50% compared with unirradiated mice; no such suppression in DH occurred in irradiated IL-4 -/- mice infected with HSV. Thus, IL-4 may be an important mediator of the UV-B-induced suppression in DH but not in CH, where other cytokines may be involved or may compensate for the lack of IL-4.
已知长期暴露于紫外线（UV）会导致皮肤过早老化、白内障发病率增加以及患皮肤癌的高风险。即使给予单次亚红斑剂量的UV-B照射，也会抑制某些免疫反应，可能会减少小鼠体内辅助性T（Th）1细胞因子[白细胞介素（IL）-2和干扰素-γ]的产生，并增加Th2细胞因子（IL-4、IL-5和IL-10）的产生。我们使用IL-4基因敲除（IL-4 -/-）小鼠及其亲代品系Bb129研究了IL-4在UV-B诱导的免疫调节中的作用。亚红斑剂量的UV-B照射（1440 J/m2）导致正常小鼠和IL-4 -/-小鼠表皮中朗格汉斯细胞的密度和抗原呈递能力降低。照射还诱导了两种品系小鼠受照射部位引流淋巴结中CD4+和CD8+淋巴细胞以及树突状细胞的积聚。与亲代品系相比，IL-4 -/-小鼠中淋巴结细胞对有丝分裂原伴刀豆球蛋白A的增殖反应增强。UV-B照射后，亲代小鼠淋巴结细胞的这种增殖增加，但在IL-4 -/-小鼠中显著受到抑制。两种品系中，UV-B照射对恶唑酮的接触性超敏反应（CH）的抑制程度相同。在亲代小鼠中，UV-B照射后感染单纯疱疹病毒（HSV），随后用灭活病毒进行攻击，与未照射的小鼠相比，迟发型超敏反应（DH）受到约50%的抑制；在感染HSV的照射IL-4 -/-小鼠中未发生这种DH抑制现象。因此，IL-4可能是UV-B诱导的DH抑制的重要介质，但在CH中不是，在CH中可能涉及其他细胞因子或可能补偿IL-4的缺乏。
