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Heat-shock proteins and autoimmunity in humans
1Department of Immunohematology and Bloodbank, University Hospital, Leiden, The Netherlands.
Springer Seminars in Immunopathology
|January 1, 1991
Summary
Heat shock proteins (HSPs) and T cells are implicated in autoimmune diseases like reactive arthritis (ReA) and rheumatoid arthritis (RA). While HSP65 is recognized in ReA, its specific role in RA pathogenesis remains unclear.
Area of Science:
- Immunology
- Autoimmunity
- Microbiology
Background:
- T cells and antibodies against heat shock proteins (HSPs) are found in both healthy individuals and patients.
- HSP65-reactive T cells are implicated in animal models of autoimmune diseases, including autoimmune arthritis (AA) and insulin-dependent diabetes mellitus (IDDM).
Purpose of the Study:
- To investigate the role of heat shock proteins (HSPs), particularly HSP65, in the pathogenesis of human autoimmune joint diseases, reactive arthritis (ReA) and rheumatoid arthritis (RA).
Main Methods:
- Review of experimental findings regarding the involvement of mycobacterial antigens, especially HSP65, in the etiology of RA.
- Analysis of T cell recognition of HSP65 and other mycobacterial antigens in synovial fluid of ReA and RA patients.
Main Results:
- In ReA, direct stimulation of joint T cells by infectious agents' antigens precedes inflammation, with HSP65 being a recognized antigen.
- In RA, while mycobacteria are suggested, clear data implicating infection in initiation is lacking.
- T cells recognizing HSP65 and other mycobacterial antigens are present in RA joints, but no specific antigen is definitively linked to pathogenesis.
Conclusions:
- HSP65 may play a role in ReA pathogenesis as it's recognized by synovial T cells.
- The specific involvement of particular (myco)bacterial antigens, including HSP65, in the pathogenesis of RA is not clearly indicated, despite their presence in affected joints.