Pathogenic advances in rheumatoid arthritis: a review

Rheumatoid arthritis (RA) affects approximately one percent of people worldwide. It falls within the category of an inflammatory immune-mediated illness where the primary tissue location is the joint. Environmental and genetic factors combine to cause RA. The exact onset of the disease is unknown, a...

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Main Authors: Abdullah, Muhammad Nazrul Hakim, Md Tohid, Siti Farah, Keong, Yong Yoke, Nordin, Nurul Syuhada
Format: Article
Language:English
Published: Universiti Kuala Lumpur 2024
Online Access:http://psasir.upm.edu.my/id/eprint/120361/
http://psasir.upm.edu.my/id/eprint/120361/1/120361.pdf
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author Abdullah, Muhammad Nazrul Hakim
Md Tohid, Siti Farah
Keong, Yong Yoke
Nordin, Nurul Syuhada
author_facet Abdullah, Muhammad Nazrul Hakim
Md Tohid, Siti Farah
Keong, Yong Yoke
Nordin, Nurul Syuhada
author_sort Abdullah, Muhammad Nazrul Hakim
building UPM Institutional Repository
collection Online Access
description Rheumatoid arthritis (RA) affects approximately one percent of people worldwide. It falls within the category of an inflammatory immune-mediated illness where the primary tissue location is the joint. Environmental and genetic factors combine to cause RA. The exact onset of the disease is unknown, as is the appropriate time at which to diagnose it as RA. In RA, the synovial membrane and surrounding tissues are attacked by the immune system. The pathophysiology of RA still raises three unanswered problems. First, how the environment or heredity drives the immune system. Secondly, how it persisted in causing inflammation in the surrounding joint, and thirdly, how inflammation results in damage to bones. There are various number of cells associated in the progression of RA disease. Proinflammatory cytokines are mostly produced by macrophages, which can also serve as antigen-presenting cells. In joints, the fibroblast-like synoviocytes (FLS) interact with cells of the innate host immune system and activate B and T cells causing an increase in chemokines and cytokines production such as TNF-α, IL-1, and IL-6 thus allowing a feedback loop to occur. B cells, T cells, and macrophages will all play a part in these extra encounters. Matrix metalloproteinases (MMPs), prostaglandins (PGs), and inflammatory cytokines were also produced in varying quantities by the activated fibroblast-like synoviocytes within the synovial membrane. The accumulation of chemokines and nitric oxide (NO) also contributes to inflammation and tissue catabolism. MMPs enter the synovial fibroblast (SF) directly as a result of the positive feedback loop, which can lead to the degeneration of bone and cartilage. We herein summarized the key pathogenic advances informing these issues with the basics of rheumatoid arthritis and its mediators, together with the cell signalling pathways involved.
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spelling upm-1203612025-10-01T01:25:13Z http://psasir.upm.edu.my/id/eprint/120361/ Pathogenic advances in rheumatoid arthritis: a review Abdullah, Muhammad Nazrul Hakim Md Tohid, Siti Farah Keong, Yong Yoke Nordin, Nurul Syuhada Rheumatoid arthritis (RA) affects approximately one percent of people worldwide. It falls within the category of an inflammatory immune-mediated illness where the primary tissue location is the joint. Environmental and genetic factors combine to cause RA. The exact onset of the disease is unknown, as is the appropriate time at which to diagnose it as RA. In RA, the synovial membrane and surrounding tissues are attacked by the immune system. The pathophysiology of RA still raises three unanswered problems. First, how the environment or heredity drives the immune system. Secondly, how it persisted in causing inflammation in the surrounding joint, and thirdly, how inflammation results in damage to bones. There are various number of cells associated in the progression of RA disease. Proinflammatory cytokines are mostly produced by macrophages, which can also serve as antigen-presenting cells. In joints, the fibroblast-like synoviocytes (FLS) interact with cells of the innate host immune system and activate B and T cells causing an increase in chemokines and cytokines production such as TNF-α, IL-1, and IL-6 thus allowing a feedback loop to occur. B cells, T cells, and macrophages will all play a part in these extra encounters. Matrix metalloproteinases (MMPs), prostaglandins (PGs), and inflammatory cytokines were also produced in varying quantities by the activated fibroblast-like synoviocytes within the synovial membrane. The accumulation of chemokines and nitric oxide (NO) also contributes to inflammation and tissue catabolism. MMPs enter the synovial fibroblast (SF) directly as a result of the positive feedback loop, which can lead to the degeneration of bone and cartilage. We herein summarized the key pathogenic advances informing these issues with the basics of rheumatoid arthritis and its mediators, together with the cell signalling pathways involved. Universiti Kuala Lumpur 2024 Article PeerReviewed text en http://psasir.upm.edu.my/id/eprint/120361/1/120361.pdf Abdullah, Muhammad Nazrul Hakim and Md Tohid, Siti Farah and Keong, Yong Yoke and Nordin, Nurul Syuhada (2024) Pathogenic advances in rheumatoid arthritis: a review. Asian Journal of Medicine and Health Sciences, 7 (2). pp. 1-20. ISSN 2637-0603 https://ejournal.unikl.edu.my/index.php/ajmhs/article/view/226 10.70672/f6wjrh07
spellingShingle Abdullah, Muhammad Nazrul Hakim
Md Tohid, Siti Farah
Keong, Yong Yoke
Nordin, Nurul Syuhada
Pathogenic advances in rheumatoid arthritis: a review
title Pathogenic advances in rheumatoid arthritis: a review
title_full Pathogenic advances in rheumatoid arthritis: a review
title_fullStr Pathogenic advances in rheumatoid arthritis: a review
title_full_unstemmed Pathogenic advances in rheumatoid arthritis: a review
title_short Pathogenic advances in rheumatoid arthritis: a review
title_sort pathogenic advances in rheumatoid arthritis: a review
url http://psasir.upm.edu.my/id/eprint/120361/
http://psasir.upm.edu.my/id/eprint/120361/
http://psasir.upm.edu.my/id/eprint/120361/
http://psasir.upm.edu.my/id/eprint/120361/1/120361.pdf