Leung D Y, Hauk P, Strickland I, Travers J B, Norris D A
Department of Paediatrics, National Jewish Medical and Research Center, Denver, CO 80206, USA.
Br J Dermatol. 1998 Dec;139 Suppl 53:17-29. doi: 10.1046/j.1365-2133.1998.1390s3017.x.
Although it is well established that immune mechanisms contribute to the pathogenesis of chronic inflammatory skin diseases such as atopic dermatitis (AD) and psoriasis, the actual events that trigger the immunological pathways resulting in these skin diseases are not well understood. Colonization and infection with Staphylococcus aureus and streptococci has been reported to exacerbate AD and psoriasis. Recent studies demonstrating that bacterial toxins can act as superantigens provide mechanism(s) by which S. aureus and streptococci could mediate an inflammatory skin lesion that consists predominantly of activated T-cells and monocytes. This review will explore the diverse mechanisms by which bacterial superantigens can induce skin inflammation following systemic or local infection. These observations provide a new direction for the development of novel approaches for the treatment of skin inflammation.
尽管免疫机制在诸如特应性皮炎（AD）和银屑病等慢性炎症性皮肤病的发病机制中发挥作用已得到充分证实，但引发导致这些皮肤病的免疫途径的实际事件仍未完全明确。据报道，金黄色葡萄球菌和链球菌的定植与感染会加重AD和银屑病。最近的研究表明，细菌毒素可作为超抗原，这为金黄色葡萄球菌和链球菌介导主要由活化T细胞和单核细胞组成的炎症性皮肤病变提供了一种机制。本综述将探讨细菌超抗原在全身或局部感染后诱导皮肤炎症的多种机制。这些观察结果为开发治疗皮肤炎症的新方法提供了新方向。
