Folwaczny Christian, Glas Jürgen, Török Helga-Paula
Poliklinik der Universität, Standort Innenstadt, Ludwig-Maximilians Universität, Munich, Germany.
Eur J Gastroenterol Hepatol. 2003 Jun;15(6):621-6. doi: 10.1097/00042737-200306000-00007.
Autoimmunity appears to be a key factor in Crohn's disease as it develops in a genetically susceptible host if the immunological tolerance towards bacterial antigens within the gastrointestinal tract is abrogated. The resulting excessive immunological activity leads to a chronic sometimes transmural inflammatory process within the bowel wall. However, several lines of evidence are compatible with an immunodeficiency preceding these processes: humoral or cellular immune defects can predispose to inflammatory bowel disease. An increased bacterial adherence at the intestinal mucosa, which is possibly attributable to impaired expression of defensins was observed in Crohn's disease. Furthermore, the 3020insC mutation of the NOD2/CARD15 gene which is associated with Crohn's disease results in impaired cytokine transcription. Lastly, therapeutic approaches such as the use of antibiotic therapy or granulocyte macrophage colony stimulating factor are in line with the concept of an immunodeficiency being a crucial element in Crohn's disease.
自身免疫似乎是克罗恩病的关键因素，因为在遗传易感宿主中，如果对胃肠道内细菌抗原的免疫耐受性被破坏，疾病就会发生。由此产生的过度免疫活性会导致肠壁内出现慢性、有时是透壁性的炎症过程。然而，有几条证据与这些过程之前存在免疫缺陷相符：体液或细胞免疫缺陷可能易患炎症性肠病。在克罗恩病中观察到肠道黏膜处细菌黏附增加，这可能归因于防御素表达受损。此外，与克罗恩病相关的NOD2/CARD15基因的3020insC突变会导致细胞因子转录受损。最后，诸如使用抗生素疗法或粒细胞巨噬细胞集落刺激因子等治疗方法符合免疫缺陷是克罗恩病关键因素这一概念。
