Ippoliti G, Lucioni M, Leonardi G, Paulli M. Immunomodulation with rabbit anti-thymocyte globulin in solid organ transplantation. World J Transplant 2015; 5(4): 261-266 [PMID: 26722653 DOI: 10.5500/wjt.v5.i4.261]
Corresponding Author of This Article
Giovanbattista Ippoliti, MD, Internal Medicine, Policlinico di Monza, Via Amati 111, 20900 Monza, Italy. g-ippoliti@libero.it
Research Domain of This Article
Transplantation
Article-Type of This Article
Minireviews
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Transplant. Dec 24, 2015; 5(4): 261-266 Published online Dec 24, 2015. doi: 10.5500/wjt.v5.i4.261
Immunomodulation with rabbit anti-thymocyte globulin in solid organ transplantation
Giovanbattista Ippoliti, Marco Lucioni, Giuseppe Leonardi, Marco Paulli
Giovanbattista Ippoliti, Internal Medicine, Policlinico di Monza, 20900 Monza, Italy
Giovanbattista Ippoliti, Division of Cardiac Surgery, University of Pavia School of Medicine, Foundation “IRCCS San Matteo” Hospital, 27100 Pavia, Italy
Marco Lucioni, Marco Paulli, Anatomic Pathology, Foundation IRCCS Policlinico San Matteo, University of Pavia, 27100 Pavia, Italy
Giuseppe Leonardi, Advanced Heart Failure Unit, AO Universitaria “Policlinico-V.Emanuele”, 95123 Catania, Italy
Author contributions: All authors contributed to the paper.
Conflict-of-interest statement: There are no relevant conflicts to declare.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Giovanbattista Ippoliti, MD, Internal Medicine, Policlinico di Monza, Via Amati 111, 20900 Monza, Italy. g-ippoliti@libero.it
Telephone: +39-38-223510 Fax: +39-38-2049371
Received: June 26, 2015 Peer-review started: June 29, 2015 First decision: July 28, 2015 Revised: September 24, 2015 Accepted: October 12, 2015 Article in press: October 13, 2015 Published online: December 24, 2015 Processing time: 180 Days and 4.1 Hours
Abstract
Rabbit anti-thymocyte globulin’s manifold mechanisms of action may be attribuited to its polyclonal nature. Its T-cell depleting effect on lymphoid cells is well established: Occurring in the blood and secondary lymphoid tissues, depletion proceeds through complement-dependent lysis, opsonization and apoptotic pathways. Clinical studies have shown that rabbit anti-thymocyte globulin’s immunomodulatory effect extends beyond the initial T-cell depletion and up to the period during which lymphocyte populations begin to recover. The drug is able to mediate immunomodulation and graft tolerance by functionally inactivating cell surface receptors involved in antigen recognition, leukocyte trafficking and leukocyte endothelium adhesion. The complex and prolonged immunomodulation induced by this drug contributes to its efficacy in solid organ transplantation, mainly by reducing the incidence of acute graft rejection.
Core tip: The effect of rabbit anti-thymocyte globulin on peripheral lymphocytes is believed to be cytolitic and hence to deplete, to opsonize and to apoptose T cells. Recent studies have shown that rabbit anti-thymocyte globulin also exerts an immunomodulatory effect on various components of immune response, such as adhesion molecules, dendritic cells and Foxp3+ Tregs.
