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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >TNFalpha genotype influences development of IgA-ASCA antibodies in Crohn's disease patients with CARD15 wild type.
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TNFalpha genotype influences development of IgA-ASCA antibodies in Crohn's disease patients with CARD15 wild type.

机译：TNFα基因型影响患有CARD15野生型克罗恩病患者的IgA-ASCA抗体的发育。

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摘要

A typical feature of Crohn's disease (CD) patients is the development of antibodies against self- (PAB) or exogenous (ASCA) antigens, a process in which mucosal cytokine expression pattern might be involved. On the other hand, mutations in CARD15, a genetic risk factor for CD, alter cytokine production in response to bacterial infection. In the present study, we evaluated the role of functionally relevant IL-10 and TNFalpha gene polymorphisms in the synthesis of these antibodies and their relationship with CARD15 mutations. In CARD15 wild type patients, high TNFalpha producer genotypes protect against IgA-ASCA development, whereas an inverse association was observed in autoantibody synthesis (PAB). These associations were not observed in patients with CARD15 mutations, probably due to the lack of TNFalpha release as a consequence of the failure of CARD15 protein to recognize the peptidoglycan. Thus, we proposed a CARD15-TNFalpha circuit that might play a role in mucosal immune surveillance.
机译：克罗恩氏病（CD）患者的典型特征是针对自身（PAB）或外源（ASCA）抗原的抗体的发展，这一过程可能涉及粘膜细胞因子表达模式。另一方面，CD的遗传危险因素CARD15中的突变会改变细胞因子的产生，以响应细菌感染。在本研究中，我们评估了功能相关的IL-10和TNFalpha基因多态性在这些抗体的合成中的作用以及它们与CARD15突变的关系。在CARD15野生型患者中，高TNFalpha生产者基因型可防止IgA-ASCA的发展，而在自身抗体合成（PAB）中观察到反向关联。在CARD15突变的患者中未观察到这些关联，这可能是由于CARD15蛋白无法识别肽聚糖导致TNFalpha释放不足所致。因此，我们提出了可能在粘膜免疫监视中起作用的CARD15-TNFalpha电路。

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