Abstrakt

Inflammation of the bowels: immunopathology

Michael Panwar

The immune system, the environment, and susceptibility genes interact in a complicated series of ways that lead to Inflammatory Bowel Disease (IBD). Viernes, fungus, and the host microbiome all contribute significantly to the onset of IBD, either directly by inducing inflammation or indirectly through changes in the immune system. Researchers can now quantify the diverse microbiome components, which will enable further advancements in the understanding of the genesis of IBD. IBD's pathogenesis has been linked to a number of mucosal immune system elements, including intestinal epithelial cells, innate lymphoid cells, cells of the innate and adaptive immune systems, and their secreted mediators. A mucosal vulnerability or a flaw in the sampling of gut luminal antigen results in the activation of the innate immune system, which may be mediated by increased toll-like receptor activity. Naive T-cells are subsequently mediated by the antigen-presenting cells to differentiate into effector T helper (Th) cells, such as Th1, Th2, and Th17, which disrupt gut homeostasis and cause IBD.