Insights & Perspectives
Immune tolerance: Are regulatory T cell subsets needed to explain suppression of autoimmunity?
Version of Record online: 15 MAR 2012
Copyright © 2012 WILEY Periodicals, Inc.
Volume 34, Issue 7, pages 569–575, July 2012
How to Cite
Tian, L., Humblet-Baron, S. and Liston, A. (2012), Immune tolerance: Are regulatory T cell subsets needed to explain suppression of autoimmunity?. Bioessays, 34: 569–575. doi: 10.1002/bies.201100180
- Issue online: 14 JUN 2012
- Version of Record online: 15 MAR 2012
- regulatory T cells
The potential for self-reactive T cells to cause autoimmune disease is held in check by Foxp3+ regulatory T cells (Tregs), essential mediators of peripheral immunological tolerance. Tregs have the capacity to suppress multiple branches of the immune system, tightly controlling the different subsets of effector T cells across multiple different tissue environments. Recent genetic experiments have found mutations that disrupt specific Treg: effector T cell relationships, leading to the possibility that subsets of Tregs are required to suppress each subset of effector T cells. Here we review the environmental factors and mechanisms that allow Tregs to suppress specific subsets of effector T cells, and find that a parsimonious explanation of the genetic data can be made without invoking Treg subsets. Instead, Tregs show a functional and chemotactic plasticity based on microenvironmental influences that allows the common pool of cells to suppress multiple distinct immune responses.