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Multifaceted Role of Th17 Cells in Psoriatic Disease
Published in Siba P. Raychaudhuri, Smriti K. Raychaudhuri, Debasis Bagchi, Psoriasis and Psoriatic Arthritis, 2017
In 2005, the discovery of CD3+/CD4+ Th17 cells changed the paradigm for understanding autoinflammatory disease processes [7,8]. Th17 cells are a distinct form of CD4+ T cells that by either induction or activation can produce a completely distinct cytokine repertoire. These cells respond to the interleukin 1 receptor 1 (IL-1R1) and interleukin 23 receptor (IL-23R) signaling pathways. It has been postulated that transforming growth factor β (TGFβ), IL-1, IL-6, and IL-23 induce retinoic acid orphan receptors (RORγt and RORα), which result in the upregulation of IL-23R and eventual differentiation of naïve CD4+ T cells into Th17 cells. This has been eloquently summarized in a model for the development of Th17 cells, consisting of three overlapping steps: differentiation, amplification, and stabilization [9]. In particular, TGFβ and IL-6 induce differentiation, IL-21 expressed by developing Th17 cells mediates amplification, and IL-23 expands and stabilizes previously differentiated Th17 cells (also summarized in Table 6.1) [9].
Genetics
Published in M. Alan Menter, Caitriona Ryan, Psoriasis, 2017
Of a handful of genes that are known to harbor a predisposing coding alteration, the interleukin 23 receptor (IL23R) was the first to be described.44 The predisposing polymorphism is a p.R381Q change and the R risk allele is very common in both cases and controls. The same polymorphism is associated with a number of other autoimmune diseases including multiple sclerosis,45 CD, and ankylosing spondylitis.3
Associations between IL-23R gene polymorphisms and the susceptibility of rheumatoid arthritis: a meta-analysis
Published in Artificial Cells, Nanomedicine, and Biotechnology, 2019
Qinghua Zou, Yi Zhao, Yong Wang, Yongfei Fang, Yi Liu
Interleukin 23 receptor (IL-23R) is produced by antigen-presenting cells (like macrophages and dendritic cells) with the actions of certain infections [11]. It plays a key role not only in inflammatory diseases but also in innate immunity and adaptive immunity [12,13]. In addition, IL-23R also dramatically affects the process of cell transformation from CD4+T to Th17, which increases the number of Th17 cells and maintains their activity, thus inducing the generation of proinflammatory cytokine IL-17 [14]. In accordance with relevant experimental models, Th17 lymphocyte subsets which secrete IL-17 may cause the damages in various positions, involving bones, cartilages, joints, brains, lungs, hearts and intestinal tracts [15]. In addition, researches also demonstrate that the variants in IL-23R gene increase the susceptibilities of AIDs in patients with inflammatory bowel disease, psoriasis or multiple sclerosis [16,17]. Sato et al. suggested that IL-23R/IL-17 axis played a vital role not only in the growth stage of autoimmune arthritis but also in osteoclasia stage, indicating that IL-23R may correlate with the susceptibility of RA [18].
Association between Genetic Polymorphisms of Inflammatory Response Genes and Acute Pancreatitis
Published in Immunological Investigations, 2019
Antonio Rodriguez-Nicolas, Pilar Jiménez, F. David Carmona, Javier Martín, Ana M. Matas Cobos, Francisco Ruiz-Cabello, Eduardo Redondo-Cerezo
A control group of 1517 healthy individuals were used for the study of interleukin-23 receptor (IL23R) rs11209026, TNF rs1800629, receptor-interacting serine/threonine-protein kinase 2 (RIPK2) rs42490, nucleotide-binding oligomerization domain-containing protein 2 (NOD2) rs9302752 and monocyte chemoattractant protein-1 (MCP1) rs1024611. These individuals had served as controls in a previous study (Mayes et al., 2014). An additional group of 390 additional healthy volunteer blood donors from the Granada area was used as controls for the study of nuclear factor kappa B subunit 1 (NFKB1) rs28362491, also known as the -94 ATTG insertion/deletion NFKB1 promoter polymorphism. Written consent was obtained from all participants.
Complex role of IL-23R polymorphisms on ankylosing spondylitis: a meta-analysis
Published in Expert Review of Clinical Immunology, 2018
Linqing Zhong, Wei Wang, Hongmei Song
Ankylosing spondylitis (AS) is a kind of inflammatory arthritis predominantly involving the axial skeleton. Its main clinical features are chronic back pain and progressive stiffness of the spine. Even though undergoing positive treatments, many AS patients end up in severe disability, thus greatly affecting their work and impairing quality of life [1,2]. Such poor outcome, as well as the high prevalence and the heavy economic burden make it urgent to find out the pathogenesis of AS [3,4]. However, up to now, we know little about the pathogenesis of AS. Genetic background is believed to be the predominant factor facilitating the onset of AS [5]. A growing number of studies explored the association of interleukin-23 receptor gene (IL-23R) with AS, but there was no consensus reached. Interleukin 23 receptor, encoded by the IL-23R, is a specific subunit of the complex IL-23R/IL12Rβ1, which mediates the signaling of the IL-23. Once binding to IL-23R/IL12Rβ1 complex, IL-23 translates signals downstream through the IL-23/IL-17 axis [6], activating Th17 cells and type 3 innate lymphoid cells (ILC3) and leading to the production of IL-23-related cytokines, such as IL-17 and IL-22 [7,8], which were perceived as involving the pathogenesis of AS. In fact, IL-23R was also found to be associated with spondyloarthritis-related diseases, such as psoriasis and inflammatory bowel disease [9,10]. Numerous studies have investigated the association between AS and IL-23R, but the conclusions are uncertain and controversial. Several meta-analysis articles were published evaluating the relationship between IL-23R polymorphisms and AS [11–16]. However, new and related studies have completed recently, providing new evidence which was not involved in previous meta-analysis. Besides, previous meta-analysis mainly incorporated Caucasian population while several studies of Asian origin were not included. What is more, our study analyzed 10 widely studied polymorphisms of IL-23R, whereas others discussed several of them. Therefore, to obtain a more comprehensive understanding of the association between IL-23R polymorphisms and AS, a new meta-analysis was performed including all the relevant studies.