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Rheumatoid Arthritis - Musculoskeletal System
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Summary of rheumatoid arthritis including the mechanisms of action.
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Rheumatoid Arthritis Autoimmune disease primarily affecting synovial joints
Fatigue due to proinflammatory cytokines
Initiating event not fully understood but associated with both self
and microbial antigens such as the Epstein-Barr virus and heat
shock proteins (these are super antigens so don’t require
processing).
Self-antigens to the FC portion of IgG are called rheumatoid factors.
Imune response leads to pannus and synovitis.
Pannus is the formation of granulation tissue (fibrovascular tissue,
that forms as part of the wound healing process), in the rheumatoid
arthritis it is caused by synovial hyperplasia.
Furthermore the cartilage and underlying bone begin to
disintegrate.
The synovitis is responsible for the symptoms and the pannus is
responsible for the joint erosion (cartilage and bone).
Cells involved in pannus are: 2/3 fibroblasts and 1/3 macrophages.
Also contains B-cells, T-cells, dendritic cells, plasma cells and mast
cells.
Role of B-cells:
Production of autoantibodies:
Antibodies to the FC (rheumatoid factor) of the self-IgG molecule.
RF found in 70% of rheumatoid arthritis patients, not actually a
useful diagnostic.
Production of proinflamitory cytokines e.g. IL-6, TNF-α
Role of T-cells:
Based on a lecture delivered by Dr M Sharif at the university of Bristol 2015
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