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Published on: March 24, 2017
Mycobacterial proliferation in macrophages is prevented by incubation with lymphocytes activated in vitro with a
A Beschin1, L Brijs, P De Baetselier
1Microbiology and Genetics Unit, ICP, University of Louvain, Belgium.
Insights
Mycobacterium bovis bacillus Calmette Guérin antigen A60 activates T lymphocytes, producing interferon-gamma (IFN-gamma). This IFN-gamma then enhances macrophage activity, inhibiting intracellular mycobacterial growth.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Antigen A60 from Mycobacterium bovis bacillus Calmette Guérin (BCG) is known to induce immune responses.
- Understanding the specific mechanisms by which A60 modulates macrophage activity against intracellular pathogens is crucial.
Purpose of the Study:
- To investigate the role of antigen A60 in controlling intracellular proliferation of mycobacteria.
- To elucidate the T cell-derived cytokines involved in A60-mediated macrophage activation.
Main Methods:
- A murine macrophage model infected with Mycobacterium avium was used.
- Lymphocytes from A60-inoculated mice were stimulated in vitro with antigen A60.
- Analysis of lymphokine production (IL-2, IFN-gamma) and its effect on macrophage activation and mycobacterial proliferation.
Main Results:
- A60-specific T lymphocytes proliferated in vitro in response to antigen A60.
- Interleukin 2 (IL-2) and interferon-gamma (IFN-gamma) were identified as key lymphokines produced.
- Interferon-gamma (IFN-gamma) was found to be essential for macrophage activation and inhibition of intracellular mycobacterial growth.
Conclusions:
- Antigen A60 elicits a specific T lymphocyte response characterized by IFN-gamma production.
- IFN-gamma activates macrophages, leading to the suppression of intracellular mycobacterial proliferation.
- This study highlights a critical pathway for controlling mycobacterial infections involving antigen A60 and IFN-gamma.
Abstract:
Antigen A60 from Mycobacterium bovis bacillus Calmette Guérin was shown to trigger both humoral and cellular immune reactions. We explored the ability of A60 to block intracellular proliferation of phagocytosed mycobacteria with a model system involving peritoneal murine macrophages infected with Mycobacterium avium. Mixed lymphocytes from lymph nodes of mice inoculated with A60 hindered intracellular proliferation of this mycobacterium, owing to A60-specific cells, proliferation of which was induced in vitro in an antigen concentration-dependent manner. The lymphokines released by A60-stimulated T lymphocytes in vitro were identified as interleukin 2 (IL2) and interferon-gamma (IFN-gamma): their production showed a clear A60 dose dependence. When supernatants of such induced lymphocyte cultures were incubated with anti-IFN-gamma antibodies, macrophage activation was prevented, whereas anti-IL 2 immunoglobulin had little effect. Treatment of infected macrophages with recombinant IFN-gamma reduced intracellular proliferation of mycobacteria, while exogenous IL 2 and tumor necrosis factor were ineffective. Therefore, A60 elicits in vitro proliferation of T lymphocytes responding specifically to this antigen with production of IFN-gamma, which in turn activates macrophages and prevents multiplication of phagocytosed mycobacteria.
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