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Immunopathogenesis and role of T cells in psoriasis.

机译:免疫发病机制和T细胞在牛皮癣中的作用。

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摘要

Psoriasis is a T cell-dependent autoimmune disease of the skin and joints. Disease manifestation is orchestrated by proinflammatory CD4-positive T helper cells producing either interferon-gamma (Th1) or interleukin (IL)-17 (Th17). These Th1 and Th17 cells interact with dermal dendritic cells, macrophages, mast cells, and neutrophils. Together, they cause an inflammation that mainly involves interferon-gamma, tumor necrosis factor, IL-8, IL-12, IL-17, IL-19, and IL-23. New therapeutics either are directed against T cells, tumor necrosis factor, and IL-12/IL-23 or deviate immune responses into a protective IL-4-dominated Th2 phenotype.
机译:牛皮癣是皮肤和关节的T细胞依赖性自身免疫性疾病。疾病表现由促炎性CD4阳性T辅助细胞产生,产生干扰素-γ(Th1)或白介素(IL)-17(Th17)。这些Th1和Th17细胞与真皮树突状细胞,巨噬细胞,肥大细胞和嗜中性粒细胞相互作用。它们共同导致炎症,主要涉及干扰素-γ,肿瘤坏死因子,IL-8,IL-12,IL-17,IL-19和IL-23。新疗法要么针对T细胞,肿瘤坏死因子和IL-12 / IL-23,要么将免疫反应转变为保护性的IL-4为主的Th2表型。

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