Role of the IL-23/IL-17 Pathway in Rheumatic Diseases: An Overview.

Claudia Schinocca,Giulia Grasso,Francesco Ciccia,Lidia La Barbera,Serena Fasano,Giuliana Guggino,Chiara Rizzo

doi:10.3389/fimmu.2021.637829

Claudia Schinocca, Giulia Grasso + Show 5 more

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https://doi.org/10.3389/fimmu.2021.637829

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Abstract

Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12). IL-23 is mainly produced by macrophages and dendritic cells, in response to exogenous or endogenous signals, and drives the differentiation and activation of T helper 17 (Th17) cells with subsequent production of IL-17A, IL-17F, IL-6, IL-22, and tumor necrosis factor α (TNF-α). Although IL-23 plays a pivotal role in the protective immune response to bacterial and fungal infections, its dysregulation has been shown to exacerbate chronic immune-mediated inflammation. Well-established experimental data support the concept that IL-23/IL-17 axis activation contributes to the development of several inflammatory diseases, such as PsA, Psoriasis, Psoriatic Arthritis; AS, Ankylosing Spondylitis; IBD, Inflammatory Bowel Disease; RA, Rheumatoid Arthritis; SS, Sjogren Syndrome; MS, Multiple Sclerosis. As a result, emerging clinical studies have focused on the blockade of this pathogenic axis as a promising therapeutic target in several autoimmune disorders; nevertheless, a greater understanding of its contribution still requires further investigation. This review aims to elucidate the most recent studies and literature data on the pathogenetic role of IL-23 and Th17 cells in inflammatory rheumatic diseases.

Highlights

Claudia Schinocca 1, Chiara Rizzo 1, Serena Fasano 2, Giulia Grasso 1, Lidia La Barbera 1, Francesco Ciccia 2 and Giuliana Guggino 1*
Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12)
Well-established experimental data support the concept that IL-23/IL-17 axis activation contributes to the development of several inflammatory diseases, such as Psoriatic arthritis (PsA), Psoriasis, Psoriatic Arthritis; AS, Ankylosing Spondylitis; IBD, Inflammatory Bowel Disease; RA, Rheumatoid Arthritis; s Syndrome (SS), Sjogren Syndrome; MS, Multiple Sclerosis

Summary

Introduction

Claudia Schinocca 1, Chiara Rizzo 1, Serena Fasano 2, Giulia Grasso 1, Lidia La Barbera 1, Francesco Ciccia 2 and Giuliana Guggino 1*. Interleukin-23 (IL-23) is a pro-inflammatory cytokine composed of two subunits, IL-23A (p19) and IL-12/23B (p40), the latter shared with Interleukin-12 (IL-12). Well-established experimental data support the concept that IL-23/IL-17 axis activation contributes to the development of several inflammatory diseases, such as PsA, Psoriasis, Psoriatic Arthritis; AS, Ankylosing Spondylitis; IBD, Inflammatory Bowel Disease; RA, Rheumatoid Arthritis; SS, Sjogren Syndrome; MS, Multiple Sclerosis. This review aims to elucidate the most recent studies and literature data on the pathogenetic role of IL-23 and Th17 cells in inflammatory rheumatic diseases. Interleukin-23 (IL-23) is a member of the IL-12 cytokine family composed of the IL-23p19 subunit and the IL-12/23p40 subunit, the latter shared with IL-12, encoded by genes located on chromosomes 12q13.2 and 11q1.3, respectively [1,2,3]

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