నైరూప్య

Inflammatory bowel disease's immunopathology.

Frank Willing

The immune system, the environment, and susceptibility genes interact in a complicated series of ways that lead to inflammatory bowel disease (IBD). 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. Intestinal epithelial cells, innate lymphoid cells, cells of the innate and adaptive (T-cells and B-cells) immune systems, and their secreted mediators are some of the mucosal immune system components that are implicated in the pathogenesis of IBD. The activation of the innate immune system may be mediated by increased toll-like receptor activity and results from either a mucosal vulnerability or a failure in the sampling of gut luminal antigen, presumably through the process of autophagy. 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 disru pt gut homeostasis and cause IBD.