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炎症性皮肤病中表皮细胞与T细胞的相互作用。

Interactions of epidermal cells and T cells in inflammatory skin diseases.

作者信息

Baadsgaard O, Fisher G J, Voorhees J J, Cooper K D

机构信息

Department of Dermatology, University of Copenhagen, Denmark.

出版信息

J Am Acad Dermatol. 1990 Dec;23(6 Pt 2):1312-6; discussion 1316-7. doi: 10.1016/0190-9622(90)70359-p.

Abstract

Multiple cell types and their factors and cytokines are involved in regulating the immune response in inflammatory skin diseases. Stimulatory and inhibitory factors interact to determine whether the immune response is regulated up or down. Normally, stimulatory signals are counteracted by inhibitory signals to prevent an immune reaction from being initiated. However, exogenous antigens and irritants or endogenous factors and altered immunogenic self-peptides can upset this balance. When that occurs, T cells are activated and an inflammatory skin reaction develops. Lymphokines released from such activated T cells can modify the phenotype and function of normal keratinocytes. They can induce the expression of adhesion molecules and receptors involved in antigen presentation. Furthermore, they can also stimulate keratinocyte proliferation. This may be important in development of the hyperplasia seen in inflammatory skin diseases, especially in psoriasis. Cytokines released from the activated keratinocytes can both stimulate and attract T cells to the epidermis and thereby continue the ongoing immune reaction.

摘要

多种细胞类型及其因子和细胞因子参与调节炎症性皮肤病中的免疫反应。刺激因子和抑制因子相互作用,以确定免疫反应是上调还是下调。正常情况下,刺激信号会被抑制信号抵消,以防止免疫反应的启动。然而,外源性抗原和刺激物或内源性因子以及改变的免疫原性自身肽会破坏这种平衡。当这种情况发生时,T细胞被激活,炎症性皮肤反应就会出现。从这些活化的T细胞释放的淋巴因子可以改变正常角质形成细胞的表型和功能。它们可以诱导参与抗原呈递的黏附分子和受体的表达。此外,它们还可以刺激角质形成细胞增殖。这在炎症性皮肤病尤其是银屑病中所见的增生发展中可能很重要。从活化的角质形成细胞释放的细胞因子既可以刺激T细胞并将其吸引到表皮,从而延续正在进行的免疫反应。

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