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首页> 外文期刊>Annual Review of Immunology >Translating Immunology into Therapeutic Concepts for Inflammatory Bowel Disease
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Translating Immunology into Therapeutic Concepts for Inflammatory Bowel Disease

机译：将免疫学转化为炎症性肠病的治疗概念

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Inflammatory bowel disease (IBD) defines a spectrum of complex disorders. Understanding how environmental risk factors, alterations of the intestinal microbiota, and polygenetic and epigenetic susceptibility impact on immune pathways is key for developing targeted therapies. Mechanistic understanding of polygenic IBD is complemented by Mendelian disorders that present with IBD, pharmacological interventions that cause colitis, autoimmunity, and multiple animal models. Collectively, this multifactorial pathogenesis supports a concept of immune checkpoints that control microbial-host interactions in the gut by modulating innate and adaptive immunity, as well as epithelial and mesenchymal cell responses. In addition to classical immunosuppressive strategies, we discuss how resetting the microbiota and restoring innate immune responses, in particular autophagy and epithelial barrier function, might be key for maintaining remission or preventing IBD. Targeting checkpoints in genetically stratified subgroups of patients with Mendelian disorder-associated IBD increasingly directs treatment strategies as part of personalized medicine.
机译：炎症性肠病（IBD）定义了一种复杂疾病的光谱。了解环境风险因素，肠道微生物瘤的改变以及对免疫途径的多遗传性和表观遗传敏感性的影响是开发靶向疗法的关键。对多基因IBD的机械理解是由IBD，药理学干预患者引起结肠炎，自身免疫和多种动物模型的药理学干预措施。统称，这种多因素病机会通过调节先天和适应性免疫以及上皮和间充质细胞应答，支持免疫检查点的概念，其控制肠道中的微生物宿主相互作用，以及上皮和间充质细胞应答。除了经典免疫抑制策略之外，我们讨论了如何重置微生物群和恢复先天免疫应答，特别是自噬和上皮屏障功能，可能是维持缓解或预防IBD的关键。针对孟德尔障碍相关IBD患者的遗传分层亚组的检查点越来越引导治疗策略作为个性化医学的一部分。

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