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Author Notes:

Correspondence should be addressed to Mandy L. Ford; mandy.ford@emory.edu.

Maggie L. Diller and Mandy L. Ford contributed to literature review, drafting of paper, and paper revision. Keith A. Delman, Ragini R. Kudchadkar, and David H. Lawson contributed to paper revision.

The authors declare no competing interests, financial or otherwise.


Research Funding:

This work was supported by the Kennedy Seed Grant, the Winship Skin Cancer and Melanoma Fund, and funding through the Emory Transplant Center GM104323.

Additional support was provided by an anonymous donor to establish the Surgical Oncology/Medical Research Fellow Fund within the Division of Surgical Oncology in the Emory School of Medicine Department of Surgery.


  • Science & Technology
  • Life Sciences & Biomedicine
  • Cell Biology
  • Immunology
  • T(H)17 CELLS
  • MTOR

Balancing Inflammation: The Link between Th17 and Regulatory T Cells


Journal Title:

Mediators of Inflammation


Volume 2016


, Pages 6309219-6309219

Type of Work:

Article | Final Publisher PDF


CD4+ T cell compartments in mouse and man are composed of multiple distinct subsets each possessing unique phenotypic and functional characteristics. IL-17-producing CD4+ T cells (Th17 cells) represent a distinct subset of the CD4+ T cell lineage. Recent evidence suggests that Th17 cells carry out effector functions similar to cytotoxic CD8+ T cells and play an important role in the clearance of extracellular pathogens and fungi. Th17 cell differentiation and function are closely related to the development and function of regulatory T cells (T R E G). The balance between these two cell populations is essential for immune homeostasis and dysregulation of this balance has been implicated in a variety of inflammatory conditions including autoimmunity, allograft rejection, and tumorigenesis. Emerging evidence reports a significant amount of plasticity between the Th17 and regulatory T cell compartments, and the mechanisms by which these cells communicate and influence each other are just beginning to be understood. In this review, we highlight recent findings detailing the mechanisms driving Th17 and T R E G plasticity and discuss the biologic consequences of their unique relationship.

Copyright information:

© 2016 Maggie L. Diller et al.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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