Walsh L J
Department of Dentistry, University of Queensland, Brisbane, Australia.
Immunol Cell Biol. 1995 Jun;73(3):226-33. doi: 10.1038/icb.1995.37.
In the 'sunburn' response in skin, dermal blood vessels are activated and traffic of dendritic Langerhans' cells altered. While these changes have been attributed to the cytokine TNF-alpha, the source of this acutely released TNF has not been identified. This report demonstrates that the 'sunburn' response, both in vivo and in vitro, is accompanied by rapid degranulation of cutaneous mast cells, with consequential release of intracellular stores of TNF. Epidermal keratinocytes were only minor contributors to local TNF production. Expression of the TNF-inducible CD62E (E-selectin/ELAM-1) and CD54 adhesion molecules on cutaneous endothelium occurred 2 h following mast cell degranulation, and this event was sensitive to blockade of mast cells with disodium cromoglycate. These results indicate that TNF release in skin in the acute sunburn response can largely be attributed to mast cells.
在皮肤的“晒伤”反应中,真皮血管被激活,树突状朗格汉斯细胞的迁移发生改变。虽然这些变化被认为是由细胞因子肿瘤坏死因子-α(TNF-α)引起的,但这种急性释放的TNF的来源尚未确定。本报告表明,无论是在体内还是体外,“晒伤”反应都伴随着皮肤肥大细胞的快速脱颗粒,从而导致细胞内储存的TNF释放。表皮角质形成细胞对局部TNF产生的贡献较小。肥大细胞脱颗粒2小时后,皮肤内皮细胞上可被TNF诱导的CD62E(E-选择素/ELAM-1)和CD54黏附分子表达增加,并且这一事件对用色甘酸钠阻断肥大细胞敏感。这些结果表明,急性晒伤反应中皮肤内TNF的释放很大程度上可归因于肥大细胞。