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World J Immunol. Jul 27, 2017; 7(2): 24-31
Published online Jul 27, 2017. doi: 10.5411/wji.v7.i2.24
Role of interleukin-1-family cytokines on effector CD4 T cell differentiation
Thaiz Rivera Vargas, François Martin, Lionel Apetoh
Thaiz Rivera Vargas, François Martin, Lionel Apetoh, INSERM, U1231, 21000 Dijon, France
Thaiz Rivera Vargas, François Martin, Lionel Apetoh, Faculté de Médecine, Université de Bourgogne, 21000 Dijon, France
Lionel Apetoh, Centre Georges François Leclerc, 21000 Dijon, France
Author contributions: All the authors contributed to this paper.
Supported by Fondation de France (to Apetoh L and Rivera Vargas T); the Association pour la recherche sur le cancer (to Apetoh L); the Institut Mérieux (to Apetoh L); the Conseil Régional de Bourgogne (to Apetoh L); the FEDER, the Agence Nationale de la Recherche, No. ANR-13-JSV3-0001 (to Apetoh L) and No. ANR-11-LABX-0021; the ARSEP (to Apetoh L); the Ligue Régionale contre le cancer Comité Grand-Est (to Apetoh L); and the European Commission (Marie Curie Fellowship PCIG10-GA-2011-303719); Apetoh L has received funding from the European Research Council (ERC) under the European Union’s Horizon 2020 research and innovation programme (grant agreement No. 677251).
Conflict-of-interest statement: The authors declare that no conflict of interest exists.
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: Dr. Lionel Apetoh, INSERM, U1231, 7 Bd Jeanne d’Arc, 21000 Dijon, France. lionel.apetoh@inserm.fr
Telephone: +33-3-80393371 Fax: +33-3-80393434
Received: December 29, 2016
Peer-review started: December 31, 2016
First decision: February 16, 2017
Revised: March 30, 2017
Accepted: April 16, 2017
Article in press: April 17, 2017
Published online: July 27, 2017
Abstract

The ability of CD4 T cells to differentiate into various effector or regulatory T cell subsets explains the successful adaptation of immune responses to different types of infectious pathogens. Immune responses in the context of cancer are also shaped by CD4 T cells, which can directly affect cancer prognosis in patients. While the proinflammatory mediator interleukin (IL)-1β was initially shown to enhance Th2 cell responses, recent findings support a predominant role of two other members of the IL-1 family, IL-18 and IL-33, on the production of Th1 and Th2-derived cytokines. In addition, IL-1β was found to profoundly affect the biology of two recently identified CD4 T cell subsets, Th17 and Th9 cells. IL-1β is critical for Th17 cell differentiation and it enhances the production of IL-9 and IL-21 by Th9 cells, thus increasing their anticancer properties. We will here review the mechanisms accounting for the ability of IL-1 cytokines to affect the differentiation of CD4 effector T cells with a focus on Th17 and Th9 cells. The physiopathological relevance of IL-1-driven effects on CD4 T cells will also be discussed.

Keywords: Inflammation, Innate immunity, Adaptive immunity, CD4, Th17, Th9, Interleukin-1, Inflammatory diseases, Cancer

Core tip: While the proinflammatory activities of interleukin (IL)-1 have been studied since the late 1970s, the ability of IL-1 family members to affect CD4 T cell differentiation, one key process in shaping adaptive immune responses, has only been characterized recently. Specifically, IL-1 family members can endow CD4 T cells with proinflammatory abilities. In this mini-review, the physiopathological relevance of CD4 T cell-driven activation in the presence of IL-1 family members will be discussed.