Mini Review ARTICLE
The effect of TNF-α on Regulatory T Cell Function in Graft versus Host Disease
- 1Medicine, University of Perugia, Italy
FoxP3+ regulatory T cells (Tregs) are a subset of CD4+ T cells that can suppress proliferation and effector functions of T cells, B cells, NK cells, and antigen-presenting cells. Treg deficiency causes dramatic immunologic disease in both animal models and humans. As they are capable to suppress the function and the proliferation of conventional CD4+ and CD8+ T cells, Treg-based cell therapies are under evaluation for the treatment of various autoimmune diseases and are currently employed to prevent graft versus host disease (GvHD) in clinical trials of hematopoietic stem cell transplantation. Even though tumor necrosis factor-α (TNF-α) is well known for its pro-inflammatory role, recent studies show that it promotes Treg activation and suppressive function. In the present review, we discuss the role of TNF-α in Treg function and the possible implications on the actual treatments for immune-mediated diseases, with a particular attention to GvHD.
Keywords: TNF-α, regulatory T cells, TNFR2, Immune Regulation, tolerance, Hematopoietic Stem Cell Transplantation, graft versus host disease
Received: 29 Nov 2017;
Accepted: 08 Feb 2018.
Edited by:Xin Chen, University of Macau, China
Reviewed by:Lianjun Zhang, University of Lausanne, Switzerland
Baojun Zhang, Duke University, United States
Copyright: © 2018 Mancusi, Piccinelli, Velardi and Pierini. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: MD, PhD. Antonio Pierini, University of Perugia, Medicine, Perugia, Italy, email@example.com