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Synovial fluid mononuclear cells exhibit a spontaneous HLA-DR driven proliferative response
1Rheumatology Unit, United Medical School, Guy's Hospital, London.
Clinical and Experimental Immunology
|October 1, 1987
Summary
The spontaneous proliferation of synovial fluid mononuclear cells (SFMC) in inflammatory joint diseases is a T cell response. This process is driven by HLA-DR and IL-2, similar to the autologous mixed lymphocyte reaction (AMLR).
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Synovial fluid mononuclear cells (SFMC) spontaneously proliferate in vitro.
- This proliferation is observed in patients with rheumatoid arthritis (RA) and seronegative spondyloarthropathies (SN).
- The underlying mechanism of SFMC proliferation is not fully understood.
Purpose of the Study:
- To test the hypothesis that SFMC proliferation is analogous to the autologous mixed lymphocyte reaction (AMLR).
- To investigate the role of T cells, HLA-DR, and interleukin-2 (IL-2) in SFMC spontaneous proliferation.
- To explore the implications for antigen-presenting cell/T cell interactions in inflammatory joint diseases.
Main Methods:
- Studied the effects of cyclosporin A, anti-HLA-DR antibody, and recombinant IL-2 (rIL-2) on SFMC proliferation.
- Utilized SFMC from patients with RA and various SN.
- Analyzed the impact of these agents on spontaneous SFMC proliferation in vitro.
Main Results:
- SFMC proliferation is a T cell-mediated response.
- Cyclosporin A and anti-HLA-DR antibody inhibited SFMC proliferation.
- rIL-2 enhanced SFMC proliferation, an effect blocked by anti-HLA-DR antibody.
- These findings indicate an HLA-DR driven, IL-2 dependent mechanism analogous to AMLR.
Conclusions:
- Spontaneous SFMC proliferation in inflammatory joint diseases is partly an HLA-DR driven, IL-2 dependent event.
- This phenomenon resembles the autologous mixed lymphocyte reaction (AMLR).
- Supports the role of antigen-presenting cell/T cell interactions in the synovial membrane in RA and related conditions.