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Lymphocyte extracellular matrix interactions. Induction of interferon by connective tissue components
W Ofosu-Appiah1, R J Warrington, K Morgan
1Department of Internal Medicine, University of Manitoba, Winnipeg, Canada.
Scandinavian Journal of Immunology
|May 1, 1989
Summary
Rheumatoid arthritis (RA) patients' T-cells respond to connective tissue components (CTC). These cells produce interferon (IFN) when stimulated by CTC, especially with fibronectin, indicating a potential immune response pathway in RA.
Area of Science:
- Immunology
- Rheumatology
- Cell Biology
Background:
- Rheumatoid arthritis (RA) involves immune system dysregulation.
- The role of T-cell responses to extracellular matrix components in RA pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the reactivity of interleukin 2 (IL-2)-responsive T cells from RA patients and healthy donors to connective tissue components (CTC).
- To determine if these T cells produce interferon (IFN) upon stimulation with CTC and fibronectin.
Main Methods:
- Limiting dilution analysis of lymphocytes from synovial fluid (SF) and peripheral blood (PB) of RA patients and PB of normal donors.
- Assessing T-cell clone reactivity to native/denatured type I/II collagen and proteoglycan.
- Measuring interferon-gamma (IFN-γ) production in response to CTC and fibronectin.
Main Results:
- All T-cell clones from both RA patients and normal donors produced IFN in the presence of CTC.
- A synergistic effect was observed between CTC and fibronectin, enhancing IFN-γ production.
- Fibronectin alone did not induce IFN-γ production.
Conclusions:
- IL-2-responsive T cells can be activated by connective tissue components to produce IFN-γ.
- This interaction suggests a potential mechanism for immune activation in RA involving T cells and extracellular matrix.
- The findings highlight a novel pathway for T-cell activation in the context of RA.