Crohn's disease (CD) and ulcerative colitis (UC) are chronic inflammatory disorders of the gastrointestinal tract that share clinical and pathological characteristics. The most accredited hypothesis is that both CD and UC result from a deregulated mucosal immune response to normal constituents of the gut microflora. Evidence, however, indicates that the main pathological processes in these two diseases are distinct. In CD, the tissue-damaging inflammatory reaction is driven by activated type 1 helper T-cell (Th1), whereas a humoral response predominates in UC. Consistently, a marked accumulation of macrophages making interleukin (IL)-12, the major Th1-inducing factor, is seen in CD but not in UC mucosa. Preliminary studies also indicate that administration of a monoclonal antibody blocking the IL-12/p40 subunit can be useful to induce and maintain clinical remission in CD patients. Notably, the recently described IL-23 shares the p40 subunit with IL-12, raising the possibility that the clinical benefit of the anti-IL-12/p40 antibody in CD may also be due to the neutralization of IL-23 activity. This review summarizes the current information on the expression and functional role of IL-12 and IL-12-associated signaling pathways both in patients with CD and experimental models of colitis, thus emphasizing major differences between IL-12 and IL-23 activity on the development of intestinal inflammation.

译文

:克罗恩病(CD)和溃疡性结肠炎(UC)是胃肠道的慢性炎性疾病,具有临床和病理学特征。最公认的假设是CD和UC均来自对肠道菌群正常成分的粘膜免疫反应失控。然而,证据表明这两种疾病的主要病理过程是不同的。在CD中,组织破坏性炎症反应是由激活的1型辅助性T细胞(Th1)驱动的,而体液反应在UC中占主导地位。一致地,在CD中可见大量的巨噬细胞积聚,使白介素(IL)-12(主要的Th1诱导因子)在CD中可见,而在UC粘膜中则未见。初步研究还表明,给予阻断IL-12 / p40亚基的单克隆抗体可用于诱导和维持CD患者的临床缓解。值得注意的是,最近描述的IL-23与IL-12共有p40亚基,从而增加了抗IL-12 / p40抗体在CD中的临床益处也可能是由于IL-23活性的中和所引起的可能性。这篇综述总结了关于CD患者和结肠炎实验模型中IL-12和IL-12相关信号通路的表达和功能作用的最新信息,从而强调了IL-12和IL-23活性在结肠炎患者中的主要差异。肠道炎症的发展。

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