Activation of Synovial Fluid T Lymphocytes by 60-Kd Heat-Shock Proteins in Patients with Inflammatory synovitis
Version of Record online: 9 DEC 2005
Copyright © 1992 American College of Rheumatology
Arthritis & Rheumatism
Volume 35, Issue 1, pages 43–48, January 1992
How to Cite
Pope, R. M., Lovis, R. M. and Gupta, R. S. (1992), Activation of Synovial Fluid T Lymphocytes by 60-Kd Heat-Shock Proteins in Patients with Inflammatory synovitis. Arthritis & Rheumatism, 35: 43–48. doi: 10.1002/art.1780350107
- Issue online: 9 DEC 2005
- Version of Record online: 9 DEC 2005
- Manuscript Accepted: 30 JUL 1991
- Manuscript Received: 17 MAY 1991
- VA Research Service
- Illinois Chapter of the Arthritis Foundation
- Northwestern University Multipurpose Arthritis Center. Grant Number: AR-30692
Objective. Synovial fluid lymphocytes from patients with rheumatoid arthritis and with other forms of inflammatory synovitis demonstrate enhanced proliferative responses to Mycobacterium tuberculosis antigens, in particular, the 65-kd heat-shock protein. There is a high degree of homology between the human and the mycobacterial 60-kd family of heat-shock proteins. These studies were performed to determine if the enhanced response to the mycobacterial 65-kd heat-shock protein was due to cross-reactivity of an immune response generated against the human homolog.
Methods. These studies were performed by in vitro culture of isolated synovial fluid mononuclear cells with crude and purified antigens.
Results. The synovial fluid lymphocytes of a majority of patients with rheumatoid arthritis recognized the mycobacterial 65-kd heat-shock protein, as evidenced by T cell proliferation. In contrast, only 18% of all samples tested responded to a highly purified recombinant human 60-kd heat-shock protein. With only one exception, proliferative responses to the mycobacterial antigen were stronger than those to the human homolog. The proliferative responses generated against mycobacterial 65-kd heat-shock proteins from different sources were highly correlated.
Conclusion. The findings suggest that the enhanced proliferative response to the mycobacterial 65-kd heat-shock protein noted in most patients with rheumatoid arthritis and other forms of inflammatory synovitis is not due to cross-reactivity of an immune response directed against the human heat-shock protein.