CD8+ T 细胞及其细胞因子在牛皮癣发病机制中的作用。

Iva Volarić, Marijana Vičić, Larisa Prpić-Massari
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摘要

CD8+ T 细胞在银屑病发病机制中的重要作用已被充分确定。然而,除了以前已知的 1 型细胞因子外,最近还发现这些细胞能分泌 17 型和 22 型细胞因子。血液中的大多数 IL-17A+CD8+ T 细胞属于先天性 T 细胞亚群,被命名为粘膜相关不变性 T 细胞(MAIT)。然而,银屑病表皮中的大多数 IL-17A+CD8+ T 细胞是传统 T 细胞,在银屑病中上调。与只分泌 IL-17 的 Th17 细胞不同,Tc17 细胞也分泌 IFN-ϒ、TNF-α、CCL20、IL-22 和颗粒酶 B。关键的细胞因子是 IL-17A,它能促进角质形成细胞的过度增殖,并刺激它们产生其他促炎细胞因子。这些活动引发并加剧了皮肤的炎症和结构变化,临床上表现为银屑病皮损。然而,在银屑病中发现了一种名为 Tc22 的相对新颖的细胞亚型,它可以在没有 IL-17 和 IFN-gamma 的情况下分泌 IL-22。IL-22 可刺激角朊细胞增殖和去分化,进而导致表皮棘层增生。随着对银屑病发病机理认识的加深,新的选择性疗法可能会在增加临床疗效和降低副作用风险之间实现最佳平衡。
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The Role of CD8+ T-Cells and their Cytokines in the Pathogenesis of Psoriasis.

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.

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