Microbiota in T-cell homeostasis and inflammatory diseases

Abstract

The etiology of disease pathogenesis can be largely explained by genetic variations and several types of environmental factors. In genetically disease-susceptible individuals, subsequent environmental triggers may induce disease development. The human body is colonized by complex commensal microbes that have co-evolved with the host immune system. With the adaptation to modern lifestyles, its composition has changed depending on host genetics, changes in diet, overuse of antibiotics against infection and elimination of natural enemies through the strengthening of sanitation. In particular, commensal microbiota is necessary in the development, induction and function of T cells to maintain host immune homeostasis. Alterations in the compositional diversity and abundance levels of microbiota, known as dysbiosis, can trigger several types of autoimmune and inflammatory diseases through the imbalance of T-cell subpopulations, such as Th1, Th2, Th17 and Treg cells. Recently, emerging evidence has identified that dysbiosis is involved in the progression of rheumatoid arthritis, type 1 and 2 diabetic mellitus, and asthma, together with dysregulated T-cell subpopulations. In this review, we will focus on understanding the complicated microbiota-T-cell axis between homeostatic and pathogenic conditions and elucidate important insights for the development of novel targets for disease therapy.

Short-Term Amoxicillin-Induced Perturbation of the Gut Microbiota Promotes Acute Intestinal Immune Regulation in Brown Norway Rats

“…Multiple studies have revealed that bacterial stimulation is important for mucosal T cell responses and in particular important for balancing the ratio between Tregs and effector T (Lee and Kim, 2017). In the current study, a consortium consisting of Escherichia/Shigella, Klebsiella (Gammaproteobacteria), Bifidobacterium, and four genera belonging to Firmicutes, for which the relative abundance in the small intestine were higher in the amoxicillin group than in controls, positively correlated with the fraction of small intestinal Tregs.…”

Epithelial-microbial diplomacy: escalating border tensions drive inflammation in inflammatory bowel disease

“…In addition to their digestive function, bacteria within the gut are also important for maturation of the immune system and can modulate the immune response by both promoting certain functions and triggering anti-inflammatory responses. [9][10][11][12] The composition of the microbiota is fluid as alterations in diet and the presence of non-infectious disease have been shown to shift certain subpopulations within the gut microbiota. 13,14 These resulting communities can also induce phenotypic traits when administered to gnotobiotic mice.…”

Notch Signaling Promotes Development of Allergic Rhinitis by Suppressing Foxp3 Expression and Treg Cell Differentiation

“…Traditionally, allergic diseases were considered to be mainly caused by an imbalance of functional CD4+ T-cell subpopulations, including an imbalance of Th1/Th2 immune responses, allergic inflammation characterized by Th2-mediated hyperactivity, and inhibition of Th1 responses [1]. Recently, other T-cell subsets (e.g., Th17/Treg cells) have also been confirmed to be involved in the immunomodulation of allergic diseases [2]. Among these populations, Treg cells have been widely studied in light of their important role in inhibiting the migration and differentiation of other effector and inflammatory cells [3].…”