Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract (GI tract). Despite extensive research, its exact pathogenesis remains elusive. However, multiple factors are thought to be involved in the onset and progression of IBD. Aside from genetic risk factors, microbial dysbiosis, environmental cues, defects in the epithelial barrier, as well as a dysregulated intestinal immune response, are critical players driving a vicious cycle, which ultimately results in chronic disease. An orchestrated interaction between the intestinal microbiota and the immune response, especially TH17 cells, is critical for maintaining and re-establishing intestinal homeostasis. Nonetheless, a misguided interaction contributes to the pathogenesis of IBD. Indeed, depending on the microenvironment, intestinal TH17 cells possess dual properties. Either they act to control the inflammatory response, or they acquire pro-inflammatory features promoting the development of intestinal pathology. This context-dependent phenotype of TH17 cells has recently been associated with the microbiota composition, which shapes the inflammatory milieu of the gut. To establish precision immunomodulation as a therapeutic strategy for patients with IBD, it is critical to understand how intestinal microorganisms are involved in actively directing the dichotomous nature of TH17 cells and their cytokine products.
Neuendorff et al. (Thu,) studied this question.