关键词: Acquired immune system Immunopathology Inflammatory bowel disease Innate immune system Th22 lymphocytes

Mesh : Humans Animals Inflammatory Bowel Diseases / immunology T-Lymphocytes, Helper-Inducer / immunology Intestinal Mucosa / immunology microbiology

来  源:   DOI:10.1016/j.intimp.2024.112486

Abstract:
The two primary forms of inflammatory disorders of the small intestine andcolon that make up inflammatory bowel disease (IBD) are ulcerative colitis (UC) and Crohn\'s disease (CD). While ulcerative colitis primarily affects the colon and the rectum, CD affects the small and large intestines, as well as the esophagus,mouth, anus, andstomach. Although the etiology of IBD is not completely clear, and there are many unknowns about it, the development, progression, and recurrence of IBD are significantly influenced by the activity of immune system cells, particularly lymphocytes, given that the disease is primarily caused by the immune system stimulation and activation against gastrointestinal (GI) tract components due to the inflammation caused by environmental factors such as viral or bacterial infections, etc. in genetically predisposed individuals. Maintaining homeostasis and the integrity of the mucosal barrier are critical in stopping the development of IBD. Specific immune system cells and the quantity of secretory mucus and microbiome are vital in maintaining this stability. Th22 cells are helper T lymphocyte subtypes that are particularly important for maintaining the integrity and equilibrium of the mucosal barrier. This review discusses the most recent research on these cells\' biology, function, and evolution and their involvement in IBD.
摘要:
构成炎症性肠病(IBD)的小肠和结肠炎症性疾病的两种主要形式是溃疡性结肠炎(UC)和克罗恩病(CD)。虽然溃疡性结肠炎主要影响结肠和直肠,CD影响小肠和大肠,以及食道,嘴,肛门,和胃。虽然IBD的病因尚未完全明确,还有很多未知的东西,的发展,programming,IBD的复发受免疫系统细胞活性的显著影响,特别是淋巴细胞,鉴于该疾病主要是由免疫系统刺激和激活胃肠道(GI)成分引起的,由于环境因素如病毒或细菌感染引起的炎症,等。在有遗传倾向的个体中。维持稳态和粘膜屏障的完整性对于阻止IBD的发展至关重要。特定的免疫系统细胞以及分泌粘液和微生物组的数量对于维持这种稳定性至关重要。Th22细胞是辅助T淋巴细胞亚型,其对于维持粘膜屏障的完整性和平衡特别重要。这篇综述讨论了这些细胞生物学的最新研究,函数,和进化以及他们参与IBD。
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