Th17 cell pathogenicity and plasticity in rheumatoid arthritis

Yang, Pei; Qian, Feiya; Zhang, Ming-Fei; Ao-ao, Xu; Wang, Xiang; Jiang, Baoping; Zhou, Lingling

doi:10.1002/jlb.4ru0619-197r

Cited by 117 publications

(86 citation statements)

References 101 publications

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“…Several other autoimmune diseases affecting many persons have relatively common pathogenesis driven by Th1 and Th17 cells, namely psoriasis, PsA, and rheumatoid arthritis (RA). 44,45 These specific cytokine networks also exist in inflammatory bowel diseases and multiple sclerosis, although they are adapted to mucosal and brain inflammation, respectively. 46,47 The expanding number of biologics used to improve these autoimmune diseases confirms the major role of cytokines in autoimmunity.…”

Section: Cytokines Involved In Autoimmunitymentioning

confidence: 99%

The evaluation of cytokines to help establish diagnosis and guide treatment of autoinflammatory and autoimmune diseases

Nézondet

Poubelle

Pelletier

2020

Journal of Leukocyte Biology

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Our knowledge of the role of cytokines in pathologic conditions has increased considerably with the emergence of molecular and genetic studies, particularly in the case of autoinflammatory monogenic diseases. Many rare disorders, considered orphan until recently, are directly related to abnormal gene regulation, and the treatment with biologic agents (biologics) targeting cytokine receptors, intracellular signaling or specific cytokines improve the symptoms of an increasing number of chronic inflammatory diseases. As it is currently impossible to systematically conduct genetic studies for all patients with autoinflammatory and autoimmune diseases, the evaluation of cytokines can be seen as a simple, less time consuming, and less expensive alternative. This approach could be especially useful when the diagnosis of syndromes of diseases of unknown etiology remains problematic. The evaluation of cytokines could also help avoid the current trial-and-error approach, which has the disadvantages of exposing patients to ineffective drugs with possible unnecessary side effects and permanent organ damages. In this review, we discuss the various possibilities, as well as the limitations of evaluating the cytokine profiles of patients suffering from autoinflammatory and autoimmune diseases, with methods such as direct detection of cytokines in the plasma/serum or following ex vivo stimulation of PBMCs leading to the production of their cytokine secretome. The patients' secretome, combined with biomarkers ranging from genetic and epigenetic analyses to immunologic biomarkers, may help not only the diagnosis but also guide the choice of biologics for more efficient and rapid treatments.

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Section: Cytokines Involved In Autoimmunitymentioning

confidence: 99%

The evaluation of cytokines to help establish diagnosis and guide treatment of autoinflammatory and autoimmune diseases

Nézondet

Poubelle

Pelletier

2020

Journal of Leukocyte Biology

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“…IL-17A is an early promoter of T-cell-induced inflammatory response, which can be amplified by promoting the release of pre-inflammatory cytokines (16). IL-17A serves a crucial role in the inflammatory reaction, tissue damage and immunological defense (17)(18)(19). A previous study revealed that IL-17A may be involved in H9c2 cell development (20).…”

Section: Introductionmentioning

confidence: 99%

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

et al. 2020

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Accumulating evidence has indicated that microRNAs (miRNAs/miRs) regulate the occurrence and development of various diseases, including diabetes, osteoporosis and cardiovascular conditions. However, the role of miRNAs in acute myocardial infarction (AMI) is not completely understood. The present study aimed to evaluate the therapeutic efficacy and mechanisms underlying the effects of miR-126-5p on H9c2 cell proliferation and apoptosis by targeting interleukin (IL)-17A. A total of 40 patients with AMI and 40 healthy volunteers were recruited in the present study and the expression levels of serum miR-126-5p and IL-17A were determined. Following confirmation that IL-17A was a target of miR-126-5p via a dual-luciferase reporter assay, H9c2 cells were exposed to hypoxic conditions. H9c2 cell viability and apoptosis were subsequently assessed. Additionally, the protein expression levels of apoptosis-associated proteins were detected following transfection. Compared with healthy individuals, miR-126-5p expression was significantly decreased in the serum samples of patients with AMI, whereas IL-17A, the target of miR-126-5p, was significantly increased. Following hypoxic treatment, miR-126-5p overexpression enhanced H9c2 cell viability compared with the NC group, which was subsequently reversed following co-transfection with pcDNA3.1-IL-17A. Additionally, the results indicated that hypoxia-induced H9c2 cell apoptosis was significantly reduced following transfection with miR-126-5p mimics via the PI3K/AKT signaling pathway compared with the NC group. The present study indicated that miR-126-5p may serve as a novel miRNA that regulates H9c2 cell viability and apoptosis by targeting IL-17A under hypoxic conditions. Therefore, miR-126-5p may serve as a crucial biomarker for the diagnosis of AMI.

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“…1) (Lee et al 2009;Wang et al 2014;Krausgruber et al 2016). Conversion of Th17 cells into this highly pathogenic phenotype has been suggested to contribute to the development of chronic inflammatory and autoimmune diseases (Ueno et al 2018;Yang et al 2019).…”

Section: Homeostatic Th17 Cells and Pathogenic Th17 Cellsmentioning

confidence: 99%

Calcium Signaling in T Cells and Chronic Inflammatory Disorders of the Oral Cavity

et al. 2021

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Acute immune responses to microbial insults in the oral cavity often progress to chronic inflammatory diseases such as periodontitis and apical periodontitis. Chronic oral inflammation causes destruction of the periodontium, potentially leading to loss of the dentition. Previous investigations have demonstrated that the composition of oral immune cells, rather than the overall extent of cellular infiltration, determines the pathological development of chronic inflammation. The role of T lymphocyte populations, including Th1, Th2, Th17, and Treg cells, has been extensively described. Studies now propose pathogenic Th17 cells as a distinct subset, uniquely classifiable from traditional Th17 populations. In situ differentiation of pathogenic Th17 cells has been verified as a source of destructive inflammation, which critically drives pathogenesis in chronic inflammatory diseases such as diabetes, rheumatoid arthritis, and inflammatory bowel disease. Pathogenic Th17 cells resemble a Th1 penotype and produce not only interleukin 17 (IL-17) but also γ-interferon (IFN-γ) and granulocyte-macrophage colony-stimulating factor (GM-CSF). The proinflammatory cytokine-specific mechanisms known to induce IL-17 expression in Th17 cells are well characterized; however, differentiation mechanisms that lead to pathogenic Th17 cells are less understood. Recently, Ca2+ signaling through Ca2+ release-activated Ca2+ channels (CRAC) in T cells has been uncovered as a major signaling axis involved in the regulation of T-cell-mediated chronic inflammation. In particular, pathogenic Th17 cell–mediated immunological diseases appear to be effectively targeted via such Ca2+ signaling pathways. Pathogenic plasticity of Th17 cells has been extensively illustrated in autoimmune and chronic inflammatory diseases. Although their specific causal relationship to oral infection-induced chronic inflammatory diseases is not fully established, pathogenic Th17 cells may be involved in the underlining mechanism. This review highlights the current understanding of T-cell phenotype regulation, calcium signaling pathways in this event, and the potential role of pathogenic Th17 cells in chronic inflammatory disorders of the oral cavity.

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Th17 cell pathogenicity and plasticity in rheumatoid arthritis

Cited by 117 publications

References 101 publications

The evaluation of cytokines to help establish diagnosis and guide treatment of autoinflammatory and autoimmune diseases

The evaluation of cytokines to help establish diagnosis and guide treatment of autoinflammatory and autoimmune diseases

miR‑126‑5p regulates H9c2 cell proliferation and apoptosis under hypoxic conditions by targeting IL‑17A

Calcium Signaling in T Cells and Chronic Inflammatory Disorders of the Oral Cavity

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