[Mechanisms of suppression of regulatory T-cells (Treg)].

Juan Manuel Guzmán Flores, Diana Patricia Portales‐Pérez

PubMed · 2014 · 24 citations · 58 references

Concepts

TL;DR

The immune system discriminates self from non‑self, with regulatory T‑cells (Tregs) suppressing immune responses to maintain homeostasis, yet their characterization is hampered by a lack of exclusive markers and their mechanisms—cytokine secretion, cell death, microenvironment modulation, and surface receptor signaling—are linked to obesity and type 2 diabetes through inflammation. This review surveys proposed Treg markers, recent mechanistic insights, and their influence on obesity and type 2 diabetes. We examine how Tregs employ cytokine production, cell‑death induction, microenvironment modulation, and surface receptor interactions to regulate immunity.

Abstract

An important feature of immunology is understanding how the immune system is able to discriminate between self and non-self. Regulatory T-cells (Treg) actively inhibit immune responses involved in the pathological and physiological responses, and, in consequence, contribute to the maintenance of homeostasis. The characterization of these regulatory T-cells has been controversial due to the lack of exclusive markers for their identification and isolation. The mechanisms that regulatory T-cells use to function are: cytokines, death cells, modullation of the microenvironment, and surface receptors. The immune system and Treg cells have been related to obesity and type 2 diabetes mellitus through the inflammatory process. In this work, we review the proposed markers for Treg cells, recent data on the mechanism used for the main function of Treg cells, immune regulation, and we conclude with the impact of these cells on obesity and type 2 diabetes mellitus.

References

58