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首页> 外文期刊>Clinical immunology: The official journal of the Clinical Immunology Society >TNF alpha production to TLR2 ligands in active IBD patients.
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TNF alpha production to TLR2 ligands in active IBD patients.

机译：在活跃的IBD患者中，TNFα产生为TLR2配体。

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摘要

Strong evidence suggests that microbial components are involved in the etiopathology of inflammatory bowel diseases (IBD). Since pathogen-associated molecular patterns are recognized by TLRs, dysregulation of TLR-mediated microbial recognition could be taking place in IBD patients. An in vitro assay with different TLR agonists was used to reproduce the immunostimulation via TLR ligands. Elevated TNFalpha production was found in response to LTA and Zymosan in 48% of active Crohn's disease and ulcerative colitis patients when compared to inactive patients or controls. The expression of CD14 did not differ in active patients, whereas TLR2 was significantly upregulated on monocytes from 71% of those patients with high production of TNFalpha. The marked increase of TNFalpha response to TLR2 ligands correlated with a higher TLR2 expression in a group of IBD patients, suggesting that an abnormal mechanism may provide an excess of inflammatory mediators during the active phase of IBDs.
机译：有力的证据表明，微生物成分与炎症性肠病（IBD）的病因有关。由于TLR可以识别病原体相关的分子模式，因此IBD患者可能发生TLR介导的微生物识别失调。使用具有不同TLR激动剂的体外测定法可通过TLR配体重现免疫刺激。与不活动的患者或对照组相比，在活动的克罗恩病和溃疡性结肠炎患者中，有48％的患者对LTA和酵母聚糖产生了TNFα升高。在活跃患者中CD14的表达没有差异，而在高TNFα产生者中，有71％的患者单核细胞上TLR2明显上调。在一组IBD患者中，TNFα对TLR2配体的应答明显增加与较高的TLR2表达相关，这表明异常的机制可能在IBD的活性期提供过量的炎性介质。

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