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
Processing time: 209 Days and 22.3 Hours
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.
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.