Biological and clinical significance of T helper 17 cell plasticity. Issue 4 (14th October 2019)

• Record Type: Journal Article
• Authors: Mazzoni, Alessio; Maggi, Laura; Liotta, Francesco; Cosmi, Lorenzo; Annunziato, Francesco
• Is Part Of: Immunology. Volume 158:Issue 4(2019)
• Page Start: 287
• Page End: 295
• Publication Date: 2019-10-14
• Subjects: inflammation -- T helper 1 -- T helper 17; Immunology -- Periodicals
• DOI: 10.1111/imm.13124
• Languages: English
• ISSNs: 0019-2805

Abstract

Abstract: Mature T helper (Th) effector cells originate following antigen recognition by naive T precursors. The maturation process is accompanied by the acquisition of specific effector functions that distinguish at least three different T helper subsets: Th1, Th2 and Th17. In general, maturation of somatic cells is accompanied by terminal differentiation. However, accumulating evidence shows that effector T cells retain a certain degree of plasticity. This is especially true for Th17 cells, which have been shown to converge towards other phenotypes in response to specific microenvironmental pressure. In this review we will discuss the experimental evidence that supports the hypothesis of Th17 plasticity, with particular emphasis on the generation of Th17‐derived 'non‐classic' Th1 cells, and the molecular networks that control it. Moreover, we will consider why Th17 plasticity is important for host protection, but also why it can have pathogenic functions during chronic inflammation. Regarding the last point, we will discuss a possible role for biological drugs in the control of Th17 plasticity and disease course. Abstract : This review covers the basic aspects of Th17 cell development and plasticity with particular focus on the underlying molecular networks. A section is dedicated to recent data defining the role of Th17 plasticity as a defense shield against invading pathogens, but also as a possible pathogenic mechanism in the establishment and maintenance of chronic inflammation. Finally, the review offers a translational point of view highlighting how biological drugs can be used to interfere in vivo with Th17 plasticity.