Krutmann J, Schwarz T, Kirnbauer R, Urbanski A, Luger T A
Department of Dermatology II, University of Vienna, Austria.
Photochem Photobiol. 1990 Oct;52(4):783-8. doi: 10.1111/j.1751-1097.1990.tb08682.x.
Ultraviolet B (UVB) radiation (280-320 nm) is capable of suppressing selected cell mediated immune responses by inhibiting the function of antigen presenting/accessory cells. Human keratinocytes and carcinoma cell lines (A431) upon UVB radiation or treatment with PMA secrete a suppressor factor, which blocks IL 1 activity (hEC-contra-IL 1). Therefore, the capacity of this UVB-inducible cytokine to modulate human accessory cell function was tested. Human peripheral blood mononuclear cells were stimulated with the mitogenic anti-CD3 monoclonal antibody OKT3 and thymidine incorporation into proliferating T-cells was measured as an index for monocyte accessory cell activity. Addition of hEC-contra-IL 1 which was purified by HPLC chromatography partially decreased OKT3 induced T-cell proliferation in a dose dependent manner. Human EC-contra-IL 1, however, failed to inhibit blastogenesis when T-cells depleted of accessory cells were stimulated in an accessory cell independent fashion via OKT3 attached to the bottom of microtiter plates. Recombinant human (rh) IL 1, but not rhIL 6 was able to reconstitute hEC-contra-IL 1 suppressed blastogenesis in a dose dependent manner. Furthermore, the combined addition of h-EC-contra-IL 1 and an antibody against rhIL 6 to cultures resulted in an additive inhibitory effect which could not be observed when hEC-contra-IL 1 was added together with a monoclonal antibody against rhIL 1 alpha/beta. These studies indicate that hEC-contra-IL 1 is capable of suppressing human accessory cell function by specifically blocking IL 1 activity. This property of hEC-contra-IL 1 points to a novel mechanism by which UVB radiation may modulate human accessory cell function in an indirect manner.
紫外线B（UVB）辐射（280 - 320纳米）能够通过抑制抗原呈递/辅助细胞的功能来抑制特定的细胞介导免疫反应。人角质形成细胞和癌细胞系（A431）在UVB辐射或用佛波酯（PMA）处理后会分泌一种抑制因子，该因子可阻断白细胞介素1（IL - 1）的活性（人表皮细胞对抗IL - 1）。因此，对这种UVB诱导的细胞因子调节人辅助细胞功能的能力进行了测试。用人促有丝分裂抗CD3单克隆抗体OKT3刺激人外周血单个核细胞，并测量增殖T细胞中胸苷掺入量，以此作为单核细胞辅助细胞活性的指标。添加经高效液相色谱法纯化的人表皮细胞对抗IL - 1，可部分地以剂量依赖方式降低OKT3诱导的T细胞增殖。然而，当通过附着在微量滴定板底部的OKT3以辅助细胞非依赖方式刺激去除辅助细胞的T细胞时，人表皮细胞对抗IL - 1未能抑制其母细胞形成。重组人（rh）IL - 1而非rhIL - 6能够以剂量依赖方式恢复人表皮细胞对抗IL - 1抑制的母细胞形成。此外，将人表皮细胞对抗IL - 1和抗rhIL - 6抗体联合添加到培养物中会产生相加抑制作用，而当人表皮细胞对抗IL - 1与抗rhIL - 1α/β单克隆抗体一起添加时则未观察到这种作用。这些研究表明，人表皮细胞对抗IL - 1能够通过特异性阻断IL - 1活性来抑制人辅助细胞功能。人表皮细胞对抗IL - 1的这一特性指出了UVB辐射可能以间接方式调节人辅助细胞功能的一种新机制。
