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Cell-mediated immunity to mycobacteria: a double-sided sword?
S H Kaufmann1, I E Flesch, M E Munk
1Department of Medical Microbiology and Immunology, University of Ulm, Federal Republic of Germany.
Rheumatology International
|January 1, 1989
Summary
Mycobacteria infect macrophages, triggering T cell responses for acquired resistance. However, T cells targeting shared heat shock protein epitopes may cause autoimmune reactions.
Area of Science:
- Immunology
- Microbiology
- Pathogenesis
Background:
- Mycobacteria are intracellular pathogens that replicate within macrophages.
- Acquired resistance involves specific helper T lymphocytes activating antimycobacterial capacities in macrophages.
- Cytolytic T lymphocytes and T cells targeting mycobacterial heat shock proteins (HSPs) are implicated in antimycobacterial immunity.
Purpose of the Study:
- To explore the role of T cells specific for mycobacterial heat shock proteins in the immune response to mycobacteria.
- To investigate the potential for autoimmune reactions due to cross-reactivity between mycobacterial and self-heat shock proteins.
Main Methods:
- Analysis of T cell responses to mycobacterial antigens.
- Investigation of T cell cross-reactivity between microbial and mammalian heat shock proteins.
- Assessment of potential autoimmune consequences of T cell activation.
Main Results:
- T cells directed against mycobacterial heat shock proteins are involved in the antimycobacterial immune response.
- Heat shock proteins are highly conserved, allowing for cross-reactivity between microbial and mammalian molecules at the T cell level.
- Shared epitopes between mycobacterial and self-heat shock proteins can lead to T cell activation against host tissues.
Conclusions:
- T cell responses to mycobacterial heat shock proteins contribute to acquired resistance against mycobacterial infections.
- Cross-reactivity between mycobacterial and self-heat shock proteins poses a risk for initiating autoimmune reactions.
- Understanding this cross-reactivity is crucial for managing mycobacterial infections and preventing associated autoimmunity.