Shankar G, Pickard-Elias S, Burnham K
Department of Microbiology and Molecular Genetics, Oklahoma State University, Stillwater 74078, USA.
Cell Immunol. 1996 Aug 1;171(2):240-5. doi: 10.1006/cimm.1996.0199.
The purpose of this study was to examine the role of cytokines in staphylococcal enterotoxin-A (SEA)-induced epidermal Langerhans cell (LS) depletion. This was accomplished by analyzing the effect of SEA on cytokine secretion by cultured epidermal cell populations by means of ELISA and by assessing the capacity of cytokines and cytokine-specific antibodies to affect epidermal LC density (as measured by immunoperoxidase staining of epidermal cells bearing surface Ia). The results of this study indicate that SEA induces the secretion of IL-1 alpha and TNF alpha by epidermal cells, that these cytokines induce LC depletion from epidermis, and that antibodies specific for these agents inhibit the depletion of LC by SEA. Taken together, these findings suggest that IL-1 alpha and TNF alpha may play essential roles in SEA-mediated depletion of LC from murine epidermis.
本研究的目的是探讨细胞因子在葡萄球菌肠毒素A（SEA）诱导的表皮朗格汉斯细胞（LC）耗竭中的作用。这是通过ELISA分析SEA对培养的表皮细胞群体细胞因子分泌的影响，并通过评估细胞因子和细胞因子特异性抗体影响表皮LC密度的能力（通过对表达表面Ia的表皮细胞进行免疫过氧化物酶染色来测量）来实现的。本研究结果表明，SEA诱导表皮细胞分泌IL-1α和TNFα，这些细胞因子诱导表皮LC耗竭，并且针对这些因子的特异性抗体抑制SEA介导的LC耗竭。综上所述，这些发现表明IL-1α和TNFα可能在SEA介导的小鼠表皮LC耗竭中起重要作用。
