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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >FLIP and FasL expression by inflammatory cells vs thyrocytes can be predictive of chronic inflammation or resolution of autoimmune thyroiditis.
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FLIP and FasL expression by inflammatory cells vs thyrocytes can be predictive of chronic inflammation or resolution of autoimmune thyroiditis.

机译：炎性细胞与甲状腺细胞的FLIP和FasL表达可预测慢性炎症或自身免疫性甲状腺炎的消退。

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摘要

Spontaneous autoimmune thyroiditis (SAT) in NOD.H-2h4 mice is a model of chronic inflammation of the thyroid, while granulomatous experimental autoimmune thyroiditis (G-EAT) is a model with spontaneous resolution of inflammation. In chronic inflammation (SAT), Fas, FasL, and FLIP were upregulated and predominant in inflammatory cells. There were few apoptotic cells, and low expression of active caspase-8 and -3. In resolving G-EAT in CBA/J and NOD.H-2h4 mice, FasL and FLIP were predominantly expressed by thyrocytes. There were many apoptotic inflammatory cells, and increased expression of active caspase-8 and -3. Depletion of CD8+ T cells inhibited G-EAT resolution and resulted in chronic inflammation. FLIP was expressed predominantly by inflammatory cells, and apoptosis of inflammatory cells and expression of active caspase-3 was reduced as in chronic SAT. Thus, differences in expression of pro- or antiapoptotic molecules in SAT or G-EAT were apparently related to the acute vs chronic nature of the inflammatory response rather than the method of disease induction. Upregulation of FLIP by inflammatory cells may block Fas-mediated apoptosis, contributing to chronic inflammation, whereas increased FLIP expression by thyrocytes in resolving G-EAT may protect thyrocytes from apoptosis, and FasL expression by thyrocytes may induce apoptosis of inflammatory cells, contributing to resolution.
机译：NOD.H-2h4小鼠中的自发性自身免疫性甲状腺炎（SAT）是甲状腺慢性炎症的模型，而肉芽肿性实验性自身免疫性甲状腺炎（G-EAT）是炎症自发消退的模型。在慢性炎症（SAT）中，Fas，FasL和FLIP被上调并在炎症细胞中占主导地位。凋亡细胞少，并且活性caspase-8和-3的表达低。在解决CBA / J和NOD.H-2h4小鼠中的G-EAT问题中，FasL和FLIP主要由甲状腺细胞表达。有许多凋亡的炎性细胞，并且活跃的caspase-8和-3的表达增加。 CD8 + T细胞的耗竭抑制了G-EAT的分解，并导致了慢性炎症。 FLIP主要由炎性细胞表达，与慢性SAT相比，炎性细胞的凋亡和活性caspase-3的表达减少。因此，SAT或G-EAT中促凋亡或抗凋亡分子表达的差异显然与炎性反应的急性与慢性性质有关，而不是与疾病诱导方法有关。炎性细胞上调FLIP可能阻止Fas介导的凋亡，从而导致慢性炎症，而在解决G-EAT时，甲状腺细胞FLIP表达的增加可能保护甲状腺细胞免于凋亡，而甲状腺细胞FasL表达可能诱导炎性细胞凋亡，从而有助于消退。

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