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Genes and immunopathology

机译：基因和免疫病理学

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Chronic intestinal inflammation might result from persistent infection or from a defect in down-regulating an immunological response to the normal antigenic load within the intestine. Since it is now cleat that there is a genetic component for IBD, especially Crohn's disease, it is conceivable that mutations in genes involved in microbiological defence, in antigen presentation, immunoregulation, or in epithelial barrier function might underlie disease pathogenesis, especially if the mutations led to loss of function. For Crohn's disease, mutations in the N0D2 gene, located on chromosome 16, are present in about 40% of patients with ileal disease. The resulting NOD2 protein fails to bind to muramyl dipep-tide, a component of peptidoglycan, and hence there is a failure to activate NFkB. It is not clear how this renders patients susceptible to Crohn's disease, but the recent observations that NOD2 is expressed, not only in monocytes, but also in Paneth cells, and that there is failure to synthesize defensins 5 and 6 from Paneth cells in patients with N0D2 mutations, may suggest a major defect in microbiological defence in these patients.
机译：慢性肠炎可能由持续感染或从下调肠内正常抗原载荷的免疫响应的缺陷导致缺陷。由于现在是IBD的遗传组分，特别是克罗恩病，可以想到，参与微生物防御，抗原呈递，免疫调节或上皮阻隔功能中的基因的突变可能是疾病发病机制，特别是如果突变导致失去功能。对于克罗恩病，位于染色体16的N0D2基因中的突变，以约40％的髂骨疾病患者存在。所得的NoD2蛋白不能与蛋白倍潮，肽聚糖的组分无结合，因此存在启动NFKB的不存在。目前尚不清楚这一促使患者易患克罗恩病的患者，但最近的观察结果不仅表达了nod2，而且在碱细胞中，还没有合成患者的Paneth细胞中的Defensins 5和6。 N0D2突变可能表明这些患者的微生物防御中的重大缺陷。

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