Related Experiment Videos
T cell fibronectin and mycobacterial adversarial strategy
1New York Medical College, Department of Experimental Pathology, Valhalla 10595.
International Journal of Clinical & Laboratory Research
|January 1, 1993
Summary
T cells produce unique fibronectin crucial for inflammatory responses. Mycobacterial antigen 85 proteins inactivate this fibronectin, potentially causing tuberculin anergy in tuberculosis patients.
Area of Science:
- Immunology
- Cell Biology
- Microbiology
Background:
- T cells synthesize a unique cellular fibronectin upon antigenic stimulation.
- This T cell fibronectin plays a role in initiating delayed hypersensitivity inflammatory reactions in vivo.
- Mycobacterial secretory proteins, specifically the antigen 85 complex, are known to bind fibronectin.
Purpose of the Study:
- To investigate the interaction between T cell fibronectin and the mycobacterial antigen 85 complex.
- To elucidate the role of this interaction in the context of delayed hypersensitivity and tuberculin anergy.
Main Methods:
- Analysis of fibronectin synthesis and secretion by sensitized T cells.
- Assessment of the effect of mycobacterial antigen 85 complex on T cell fibronectin function.
- Evaluation of the impact on delayed hypersensitivity reactions in vivo.
Main Results:
- Sensitized T cells produce a distinct cellular fibronectin in response to antigen.
- The fibronectin-binding antigen 85 complex from mycobacteria inactivates T cell fibronectin.
- This inactivation diminishes the expression of anti-mycobacterial delayed hypersensitivity.
Conclusions:
- T cell fibronectin and antigen 85 interaction offers a potential mechanism for tuberculin anergy.
- This finding provides new insights into the immunopathology of tuberculosis.
- Understanding this interaction could inform therapeutic strategies for tuberculosis.