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Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis

Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. These autoantibodies (anticitrullinated protein/peptide ant...

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Autores principales: Fang, Qinghua, Ou, Jiaxin, Nandakumar, Kutty Selva
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854956/
https://www.ncbi.nlm.nih.gov/pubmed/31772505
http://dx.doi.org/10.1155/2019/6363086
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author Fang, Qinghua
Ou, Jiaxin
Nandakumar, Kutty Selva
author_facet Fang, Qinghua
Ou, Jiaxin
Nandakumar, Kutty Selva
author_sort Fang, Qinghua
collection PubMed
description Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. Some of these antibodies are present in the patients' serum several years before the onset of clinical disease. Various genetic and environmental factors are associated with autoantibody production against different autoantigenic targets. Both the activating and inhibitory FcγRs and the activation of different complement cascades contribute to the downstream effector functions in the antibody-mediated disease pathology. Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed for early diagnosis of the clinical disease. Recently, a direct link was proposed between the presence of autoantibodies and bone erosion as well as in the induction of pain. In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and the significance of IgG-Fc glycosylation are discussed.
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spelling pubmed-68549562019-11-26 Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis Fang, Qinghua Ou, Jiaxin Nandakumar, Kutty Selva Mediators Inflamm Review Article Rheumatoid arthritis is a systemic, polygenic, and multifactorial syndrome characterized by erosive polyarthritis, damage to joint architecture, and presence of autoantibodies against several self-structures in the serum and synovial fluid. These autoantibodies (anticitrullinated protein/peptide antibodies (ACPAs), rheumatoid factors (RF), anticollagen type II antibodies, antiglucose-6 phosphate isomerase antibodies, anticarbamylated protein antibodies, and antiacetylated protein antibodies) have different characteristics, diagnostic/prognostic value, and pathological significance in RA patients. Some of these antibodies are present in the patients' serum several years before the onset of clinical disease. Various genetic and environmental factors are associated with autoantibody production against different autoantigenic targets. Both the activating and inhibitory FcγRs and the activation of different complement cascades contribute to the downstream effector functions in the antibody-mediated disease pathology. Interplay between several molecules (cytokines, chemokines, proteases, and inflammatory mediators) culminates in causing damage to the articular cartilage and bones. In addition, autoantibodies are proven to be useful disease markers for RA, and different diagnostic tools are being developed for early diagnosis of the clinical disease. Recently, a direct link was proposed between the presence of autoantibodies and bone erosion as well as in the induction of pain. In this review, the diagnostic value of autoantibodies, their synthesis and function as a mediator of joint inflammation, and the significance of IgG-Fc glycosylation are discussed. Hindawi 2019-10-27 /pmc/articles/PMC6854956/ /pubmed/31772505 http://dx.doi.org/10.1155/2019/6363086 Text en Copyright © 2019 Qinghua Fang et al. http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Fang, Qinghua
Ou, Jiaxin
Nandakumar, Kutty Selva
Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title_full Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title_fullStr Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title_full_unstemmed Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title_short Autoantibodies as Diagnostic Markers and Mediator of Joint Inflammation in Arthritis
title_sort autoantibodies as diagnostic markers and mediator of joint inflammation in arthritis
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6854956/
https://www.ncbi.nlm.nih.gov/pubmed/31772505
http://dx.doi.org/10.1155/2019/6363086
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