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Commentary 10.1172/JCI126517

Foxp3+ T lymphocytes: immune regulators within the lung allograft

Elizabeth A. Lendermon and John F. McDyer

Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Address correspondence to: John F. McDyer, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, NW 628, Pittsburgh, Pennsylvania 15213, USA. Phone: 412.624.8915; Email: mcdyerjf@upmc.edu.

Find articles by Lendermon, E. in: JCI | PubMed | Google Scholar

Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Address correspondence to: John F. McDyer, Division of Pulmonary, Allergy, and Critical Care Medicine, University of Pittsburgh School of Medicine, 3459 Fifth Avenue, NW 628, Pittsburgh, Pennsylvania 15213, USA. Phone: 412.624.8915; Email: mcdyerjf@upmc.edu.

Find articles by McDyer, J. in: JCI | PubMed | Google Scholar |

First published December 18, 2018 - More info

Published in Volume 129, Issue 2 on February 1, 2019
J Clin Invest. 2019;129(2):494–495. https://doi.org/10.1172/JCI126517.
Copyright © 2019, American Society for Clinical Investigation
First published December 18, 2018 - Version history

Antibody-mediated rejection (AMR) has emerged as an important cause of lung graft failure. In the current issue of the JCI, a study by Li et al. identifies a critical role of Foxp3+ T cells residing within lung allografts in the regulation of AMR. This study not only provides new insights into the nature of lung allografts as a primary site where T and B cell priming and immune regulation can occur, but also introduces the mouse orthotopic lung transplant as a model for studying the immunobiology of AMR. Because AMR can be so difficult to effectively treat in lung transplant recipients, the development of an animal model is a major advance in understanding the immunopathogenesis of AMR.

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