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J Leukoc Biol. 2020 Mar 23. doi: 10.1002/JLB.1MR0120-196R. [Epub ahead of print]

Mechanisms of TREG cell adaptation to inflammation.

Alvarez F1,2,3, Al-Aubodah TA1,2,3, Yang YH2,3,4, Piccirillo CA1,2,3,4.

Author information

1
Department of Microbiology and Immunology, McGill University, Montréal, Québec, Canada.
2
Program in Infectious Diseases and Immunology in Global Health, Centre for Translational Biology, Research Institute of the McGill University Health Centre, Montréal, Québec, Canada.
3
Centre of Excellence in Translational Immunology (CETI), Montréal, Québec, Canada.
4
Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Québec, Canada.

Abstract

Inflammation is an important defense mechanism. In this complex and dynamic process, drastic changes in the tissue micro-environment play key roles in dictating the nature of the evolving immune response. However, uncontrolled inflammation is detrimental, leading to unwanted cellular damage, loss of physiological functions, and even death. As such, the immune system possesses tools to limit inflammation while ensuring rapid and effective clearance of the inflammatory trigger. Foxp3+ regulatory T (TREG ) cells, a potently immunosuppressive CD4+ T cell subset, play a crucial role in immune tolerance by controlling the extent of the response to self and non-self Ags, all-the-while promoting a quick return to immune homeostasis. TREG cells adapt to changes in the local micro-environment enabling them to migrate, proliferate, survive, differentiate, and tailor their suppressive ability at inflamed sites. Several inflammation-associated factors can impact TREG cell functional adaptation in situ including locally released alarmins, oxygen availability, tissue acidity and osmolarity and nutrient availability. Here, we review some of these key signals and pathways that control the adaptation of TREG cell function in inflammatory settings.

KEYWORDS:

Foxp3; alarmins; differentiation; functional adaptation; inflammation; metabolic

PMID:
32202345
DOI:
10.1002/JLB.1MR0120-196R

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