Intestinal Immunomodulatory Cells (T Lymphocytes): A Bridge between Gut Microbiota and Diabetes

Abstract

Diabetes mellitus (DM) is one of the most familiar chronic diseases threatening human health. Recent studies have shown that the development of diabetes is closely related to an imbalance of the gut microbiota. Accordingly, there is increasing interest in how changes in the gut microbiota affect diabetes and its underlying mechanisms. Immunomodulatory cells play important roles in maintaining the normal functioning of the human immune system and in maintaining homeostasis. Intestinal immunomodulatory cells (IICs) are located in the intestinal mucosa and are regarded as an intermediary by which the gut microbiota affects physiological and pathological properties. Diabetes can be regulated by IICs, which act as a bridge linking the gut microbiota and DM. Understanding this bridge role of IICs may clarify the mechanisms by which the gut microbiota contributes to DM. Based on recent research, we summarize this process, thereby providing a basis for further studies of diabetes and other similar immune-related diseases.

Figure 1

Blue indicates the gut microbiota, purple indicates T lymphocytes, and green indicates different targets of diabetes. Red lines represent inhibitory action. Solid black lines represent a positive effect (promotion). PSA: polysaccharide A; ASF: altered Schaedler flora; SCFA: short-chain fatty acids; SFB: segmented filamentous bacteria; APCS: antigen-presenting cells; TLR: Toll-like receptor; TH0, 1, 2, and 17 cells: T helper 0, 1, 2, and 17 cells; Treg: regulatory T cell; SAA: serum amyloid A; MAPK: mitogen-activated protein kinase; JNK: c-Jun N-terminal kinase; ERK: extracellular signal-regulated kinase; NF-κB: nuclear factor kappa B; STAT4 and 6: signal transducer and activator of transcription 4 and 6; MHC: major histocompatibility complex; eNOS: endothelial nitric oxide synthase; VEGFR2: vascular endothelial growth factor receptor 2; Jak: Janus kinase; Tyk: tyrosine kinase; CREB: cAMP-response element binding protein; CRTC2: CREB-regulated transcription coactivator 2.