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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2021
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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) |
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rheumatoid arthritis heterogeneity pathophysiology interaction genetics mechanism Immunologic diseases. Allergy RC581-607 |
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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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