Immune response and inflammatory pathway of ulcerative colitis

Immune response and inflammatory pathway of ulcerative colitis
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DOI:
10.1515/jbcpp-2018-0036
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发表时间:
2019-01-01
影响因子:
--
通讯作者:
Jarukamjorn, Kanokwan
Jarukamjorn, Kanokwan
中科院分区:
其他
文献类型:
--
作者:
Tatiya-aphiradee, Nitima;Chatuphonprasert, Waranya;Jarukamjorn, Kanokwan

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溃疡性结肠炎(UC)是一种特发性复发性炎性疾病。虽然UC的病因尚不清楚,但其特征可能是肠黏膜炎症,从直肠开始,可能累及整个结肠。UC的免疫反应和炎症途径表明,组织损伤是由细胞和细胞因子的动态复合物驱动的。各种类型的细胞,包括抗原呈递细胞(树突状细胞和巨噬细胞)、T辅助细胞、调节性T细胞和自然杀伤T细胞,通过调节、抑制和维持炎症在UC的发病过程中起着至关重要的作用。此外,细胞因子网络因其信号功能而成为细胞通讯不可或缺的重要组成部分。促炎因子[肿瘤坏死因子-a、白细胞介素(IL)-1、IL-6、IL-9、IL-13、IL-33]在上调中起显著作用,抗炎因子(转化生长因子- β、IL-10、IL-37)在下调中起显著作用。UC的发病机制包括与肠道多个组成部分相关的免疫炎症途径,包括上皮屏障、共生菌群、抗原识别、免疫反应失调、白细胞募集和遗传因素。了解UC的免疫炎症途径可能会导致特定治疗和/或更有效的新治疗的发展。
Ulcerative colitis (UC) is an idiopathic relapsing inflammatory disease. Although the etiology of UC remains unclear, it could be characterized by inflammation of the intestinal mucosa, starting from the rectum and potentially involving the entire colon. The immune response and inflammatory pathway of UC have shown that tissue damage is driven by dynamic and complexes of cells and cytokines. Various types of cells, including antigen-presenting cells (dendritic cells and macrophages), T helper cells, regulatory T cells, and natural killer T cells, play a crucial role in UC pathogenesis by regulation, suppression, and maintenance of inflammation. Moreover, cytokine networks become an important part due to their signaling function, which is indispensable for cell communication. Pro-inflammatory cytokines [tumor necrosis factor-a, interleukin (IL)-1, IL-6, IL-9, IL-13, and IL-33] play significant roles in upregulation, while anti-inflammatory cytokines (transforming growth factor-beta, IL-10, and IL-37) play significant roles in downregulation of disease progression. The pathogenesis of UC consists of immuno-inflammatory pathways related to the multiple components of the intestine, including the epithelial barrier, commensal microflora, antigen recognition, dysregulation of immunological responses, leukocyte recruitment, and genetic factors. The understanding of immuno-inflammatory pathways of UC might lead to the development of a specific therapy and/or a novel treatment that could be more efficient.