The Memory T Cell “Communication Web” in Context with Gastrointestinal Disorders—How Memory T Cells Affect Their Surroundings and How They Are Influenced by It

Abstract

Gut-related diseases like ulcerative colitis, Crohn’s disease, or colorectal cancer affect millions of people worldwide. It is an ongoing process finding causes leading to the development and manifestation of those disorders. This is highly relevant since understanding molecular processes and signalling pathways offers new opportunities in finding novel ways to interfere with and apply new pharmaceuticals. Memory T cells (mT cells) and their pro-inflammatory properties have been proven to play an important role in gastrointestinal diseases and are therefore increasingly spotlighted. This review focuses on mT cells and their subsets in the context of disease pathogenesis and maintenance. It illustrates the network of regulatory proteins and metabolites connecting mT cells with other cell types and tissue compartments. Furthermore, the crosstalk with various microbes will be a subject of discussion. Characterizing mT cell interactions will help to further elucidate the sophisticated molecular and cellular networking system in the intestine and may present new ideas for future research approaches to control gut-related diseases.

Ginsenoside Rg1 Alleviates Ulcerative Colitis in Obese Mice by Regulating the Gut Microbiota–Lipid Metabolism–Th1/Th2/Th17 Cells Axis

“…Particularly, pro-inflammatory cytokines like IFN-γ (Th1) and IL-17A (Th17) are secreted in significant quantities by effector T cells that are activated in response to antigen stimulation, and these cytokines exacerbate inflammation and damage in the colon. 61 However, a small fraction of these effector T cells differentiate into TCM cells, which persist in the body for a long time and play a critical role in maintaining remission and relapse in UC. Upon re-exposure to antigens, TCM cells rapidly migrate to the colon and differentiate into TEM cells, which also produce large amounts of IFN-γ and IL-17A, contributing to colonic inflammatory injury and exacerbating the clinical symptoms of UC.…”

“…Because T cells are essential to the onset and course of UC, their function in the immune system has been thoroughly investigated. Particularly, pro-inflammatory cytokines like IFN-γ (Th1) and IL-17A (Th17) are secreted in significant quantities by effector T cells that are activated in response to antigen stimulation, and these cytokines exacerbate inflammation and damage in the colon . However, a small fraction of these effector T cells differentiate into TCM cells, which persist in the body for a long time and play a critical role in maintaining remission and relapse in UC.…”

Transient gestational hypothyroxinemia accelerates and enhances ulcerative colitis-like disorder in the male offspring

“…Patients who suffer from UC present abdominal pain, diarrhea, the presence of blood in the feces, and psychological distress ( 30 ). T lymphocytes, such as Th17 and T reg lymphocytes, can contribute significantly to the pathogenesis of UC ( 32 ). In this study, UCLD was induced in the male HTX-offspring and the male Control-offspring by dextran sodium sulfate (DSS) administration for an acute period of 6 days ( 33 ).…”

Highly multiplexed spatial analysis identifies tissue-resident memory T cells as drivers of ulcerative and immune checkpoint inhibitor induced colitis

“…[14][15][16][17] Some reports indicate a relative decrease of colonic CD8 + TRM cells in ICI-colitis compared to ICI-treated patients without colitis, 14,16 possibly due to either an influx of circulating effector T cells, or transformation of resting TRM into inflammatory effectors with the loss of residency markers. CD8 + TRM cells are also considered proinflammatory actors in IBD, 18 although, similar to ICI-colitis, a relative decrease in CD8 + TRM cells in active IBD versus healthy control tissue has been found. 19,20 Interestingly, intra-epithelial CD8 + TRM cells have been shown to transcriptionally acquire an innate proinflammatory profile in inflammatory sites of Crohn's ileitis, 21 illustrating the relevance of epithelial-lamina propria localization in relation to cell function.…”