Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications

Rheumatoid arthritis is an autoimmune disease that exhibits significant clinical heterogeneity. There are various treatments for rheumatoid arthritis, including disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and inflammatory cytokine...

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Autores principales: Jianan Zhao, Shicheng Guo, Steven J. Schrodi, Dongyi He
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Lenguaje:EN
Publicado: Frontiers Media S.A. 2021
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spelling oai:doaj.org-article:1d9be0209f0246b68da5a479a432aaf92021-12-01T02:33:18ZMolecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications1664-322410.3389/fimmu.2021.790122https://doaj.org/article/1d9be0209f0246b68da5a479a432aaf92021-11-01T00:00:00Zhttps://www.frontiersin.org/articles/10.3389/fimmu.2021.790122/fullhttps://doaj.org/toc/1664-3224Rheumatoid arthritis is an autoimmune disease that exhibits significant clinical heterogeneity. There are various treatments for rheumatoid arthritis, including disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and inflammatory cytokine inhibitors (ICI), typically associated with differentiated clinical effects and characteristics. Personalized responsiveness is observed to the standard treatment due to the pathophysiological heterogeneity in rheumatoid arthritis, resulting in an overall poor prognosis. Understanding the role of individual variation in cellular and molecular mechanisms related to rheumatoid arthritis will considerably improve clinical care and patient outcomes. In this review, we discuss the source of pathophysiological heterogeneity derived from genetic, molecular, and cellular heterogeneity and their possible impact on precision medicine and personalized treatment of rheumatoid arthritis. We provide emphasized description of the heterogeneity derived from mast cells, monocyte cell, macrophage fibroblast-like synoviocytes and, interactions within immune cells and with inflammatory cytokines, as well as the potential as a new therapeutic target to develop a novel treatment approach. Finally, we summarize the latest clinical trials of treatment options for rheumatoid arthritis and provide a suggestive framework for implementing preclinical and clinical experimental results into clinical practice.Jianan ZhaoJianan ZhaoShicheng GuoShicheng GuoSteven J. SchrodiSteven J. SchrodiDongyi HeDongyi HeDongyi HeFrontiers Media S.A.articlerheumatoid arthritisheterogeneitypathophysiologyinteractiongeneticsmechanismImmunologic diseases. AllergyRC581-607ENFrontiers in Immunology, Vol 12 (2021)
institution DOAJ
collection DOAJ
language EN
topic rheumatoid arthritis
heterogeneity
pathophysiology
interaction
genetics
mechanism
Immunologic diseases. Allergy
RC581-607
spellingShingle rheumatoid arthritis
heterogeneity
pathophysiology
interaction
genetics
mechanism
Immunologic diseases. Allergy
RC581-607
Jianan Zhao
Jianan Zhao
Shicheng Guo
Shicheng Guo
Steven J. Schrodi
Steven J. Schrodi
Dongyi He
Dongyi He
Dongyi He
Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
description Rheumatoid arthritis is an autoimmune disease that exhibits significant clinical heterogeneity. There are various treatments for rheumatoid arthritis, including disease-modifying anti-rheumatic drugs (DMARDs), glucocorticoids, non-steroidal anti-inflammatory drugs (NSAIDs), and inflammatory cytokine inhibitors (ICI), typically associated with differentiated clinical effects and characteristics. Personalized responsiveness is observed to the standard treatment due to the pathophysiological heterogeneity in rheumatoid arthritis, resulting in an overall poor prognosis. Understanding the role of individual variation in cellular and molecular mechanisms related to rheumatoid arthritis will considerably improve clinical care and patient outcomes. In this review, we discuss the source of pathophysiological heterogeneity derived from genetic, molecular, and cellular heterogeneity and their possible impact on precision medicine and personalized treatment of rheumatoid arthritis. We provide emphasized description of the heterogeneity derived from mast cells, monocyte cell, macrophage fibroblast-like synoviocytes and, interactions within immune cells and with inflammatory cytokines, as well as the potential as a new therapeutic target to develop a novel treatment approach. Finally, we summarize the latest clinical trials of treatment options for rheumatoid arthritis and provide a suggestive framework for implementing preclinical and clinical experimental results into clinical practice.
format article
author Jianan Zhao
Jianan Zhao
Shicheng Guo
Shicheng Guo
Steven J. Schrodi
Steven J. Schrodi
Dongyi He
Dongyi He
Dongyi He
author_facet Jianan Zhao
Jianan Zhao
Shicheng Guo
Shicheng Guo
Steven J. Schrodi
Steven J. Schrodi
Dongyi He
Dongyi He
Dongyi He
author_sort Jianan Zhao
title Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
title_short Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
title_full Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
title_fullStr Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
title_full_unstemmed Molecular and Cellular Heterogeneity in Rheumatoid Arthritis: Mechanisms and Clinical Implications
title_sort molecular and cellular heterogeneity in rheumatoid arthritis: mechanisms and clinical implications
publisher Frontiers Media S.A.
publishDate 2021
url https://doaj.org/article/1d9be0209f0246b68da5a479a432aaf9
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