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CD8 + T细胞及其细胞因子在银屑病发病机制中的作用

The Role of CD8+ T-Cells and their Cytokines in the Pathogenesis of Psoriasis.

作者信息

Volarić Iva, Vičić Marijana, Prpić-Massari Larisa

机构信息

Professor Larisa Prpić-Massari, MD, PhD, Department of Dermatovenerology , Clinical Hospital Center Rijeka, University of Rijeka, Krešimirova 42, 51000 Rijeka; Croatia.

出版信息

Acta Dermatovenerol Croat. 2019 Sep;27(3):159-162.

PMID:31542059
Abstract

The important role of CD8+ T-cells in the pathogenesis of psoriasis is well-determined. However, besides type 1 cytokines that were formerly known, it was recently found that these cells secrete type 17 and type 22 cytokines. The majority of IL-17A+CD8+ T-cells in the blood belong to a subset of innate T-cells named mucosa-associated invariant T-cells (MAIT). However, the majority of IL-17A+CD8+ T-cells in psoriatic epidermis are conventional T-cells and are up-regulated in psoriasis. In contrast to Th17 cells that secrete only IL-17, Tc17 cells secrete IFN-ϒ, TNF-α, CCL20, IL-22, and granzyme B as well. The key cytokine is IL-17A, which promotes keratinocyte hyperproliferation and stimulates them to produce other proinflammatory cytokines. These activities initiate and propagate the inflammation and architectural changes in the skin that clinically manifest as psoriatic lesions. However, a relatively novel cell subtype named Tc22 has been discovered in psoriasis that could secrete IL-22 in the absence of IL-17 and IFN-gamma. IL-22 stimulates proliferation and de-differentiation of keratinocytes, subsequently leading to epidermal acanthosis. As the understanding of the pathogenesis of psoriasis increases, the new selective therapies may offer an optimal balance between increased clinical benefit and reduced risk of side-effects.

摘要

CD8 + T细胞在银屑病发病机制中的重要作用已得到充分确定。然而,除了以前已知的1型细胞因子外,最近发现这些细胞还分泌17型和22型细胞因子。血液中大多数IL-17A + CD8 + T细胞属于一种名为黏膜相关恒定T细胞(MAIT)的天然T细胞亚群。然而,银屑病表皮中大多数IL-17A + CD8 + T细胞是传统T细胞,且在银屑病中上调。与仅分泌IL-17的Th17细胞不同,Tc17细胞还分泌IFN-γ、TNF-α、CCL20、IL-22和颗粒酶B。关键细胞因子是IL-17A,它促进角质形成细胞过度增殖,并刺激它们产生其他促炎细胞因子。这些活动引发并传播皮肤中的炎症和结构变化,临床上表现为银屑病皮损。然而,在银屑病中发现了一种相对新颖的细胞亚型Tc22,它可以在不分泌IL-17和IFN-γ的情况下分泌IL-22。IL-22刺激角质形成细胞增殖和去分化,随后导致表皮棘皮症。随着对银屑病发病机制的认识不断增加,新的选择性疗法可能会在提高临床疗效和降低副作用风险之间实现最佳平衡。

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