Rattis F M, Péguet-Navarro J, Courtellemont P, Redziniak G, Schmitt D
Laboratoire Peau Humaine et Immunité, INSERM U346, Hôpital E. Herriot, Lyon, France.
Cell Immunol. 1995 Aug;164(1):65-72. doi: 10.1006/cimm.1995.1143.
The effects of ultraviolet B radiation (UBV) on the immune function of human epidermal Langerhans cells (LC) were studied by using the mixed epidermal cell-lymphocyte reaction (MELR). Exposure of both enriched LC suspensions (eLC, 8-20% LC) and purified LC suspensions (pLC, 70-90% LC) to increasing doses of UVB radiation (25 to 200 J/m2) decreased the proliferative T cell response in a very similar dose-dependent way, suggesting that keratinocytes did not play a major role in the UVB-induced inhibition of MELR. Supernatants from irradiated cultured eLC or pLC failed to inhibit T cell proliferation induced by untreated pLC. Furthermore, addition of irradiated eLC to untreated pLC did not affec the allogeneic T cell response. Taken together, these results provide evidence that in vitro UVB-induced immunosuppression was not mediated by inhibitory soluble factors that could affect either LC allostimulatory property or T cell proliferative response. UVB irradiation of human LC inhibited the capacity of these cells to induce CD4+ as well as CD8+ T cell proliferation. UVB-irradiated LC also induced a decreased T cell response to recall antigen or mitogen. Moreover, addition of exogeneous cytokines such as IL-1 beta, IL-1 alpha, or IL-2 did not reverse the defective function of UVB-irradiated LC in MELR. The inhibitory effect of UVB radiation on human LC was not related to a decreased HLA-DR expression. Because cultured LC appeared to be less sensitive than freshly isolated LC to UVB-induced suppressive effects, the deleterious effects of UVB radiation on human LC allostimulatory properties may be associated with an impaired development of LC accessory function.
采用混合表皮细胞 - 淋巴细胞反应(MELR)研究了紫外线B辐射(UVB)对人表皮朗格汉斯细胞(LC)免疫功能的影响。将富集的LC悬液(eLC,LC含量8 - 20%)和纯化的LC悬液(pLC,LC含量70 - 90%)暴露于递增剂量的UVB辐射(25至200 J/m²)下,均以非常相似的剂量依赖性方式降低了增殖性T细胞反应,这表明角质形成细胞在UVB诱导的MELR抑制中未起主要作用。照射后的培养eLC或pLC的上清液未能抑制未处理的pLC诱导的T细胞增殖。此外,将照射后的eLC添加到未处理的pLC中并不影响同种异体T细胞反应。综上所述,这些结果证明,体外UVB诱导的免疫抑制不是由可影响LC同种异体刺激特性或T细胞增殖反应的抑制性可溶性因子介导的。UVB照射人LC抑制了这些细胞诱导CD4⁺以及CD8⁺T细胞增殖的能力。UVB照射的LC还诱导T细胞对回忆抗原或丝裂原的反应降低。此外,添加外源性细胞因子如IL - 1β、IL - 1α或IL - 2并不能逆转UVB照射的LC在MELR中的功能缺陷。UVB辐射对人LC的抑制作用与HLA - DR表达降低无关。由于培养的LC似乎比新鲜分离的LC对UVB诱导的抑制作用更不敏感,UVB辐射对人LC同种异体刺激特性的有害影响可能与LC辅助功能的发育受损有关。