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Nitric oxide in infectious and autoimmune diseases
1Department of Immunology, University of Glasgow, UK.
Ciba Foundation Symposium
|January 1, 1995
Summary
Nitric oxide (NO) regulates immune responses and is sensitive to microorganisms. T helper cell cytokines balance NO production, preventing over-expansion of T helper 1 cells linked to immunopathologies.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Nitric oxide (NO) plays a dual role in biological functions, mediating antimicrobial activity and contributing to immunopathologies.
- Macrophages activated by gamma-interferon (IFN-γ) and lipopolysaccharide produce NO, affecting various microorganisms.
- NO involvement is noted in conditions like diabetes, rheumatoid arthritis, and multiple sclerosis, highlighting the need for tight regulatory control.
Purpose of the Study:
- To elucidate the regulatory mechanisms of nitric oxide (NO) synthesis.
- To investigate the role of T helper 1 (Th1) and T helper 2 (Th2) cell cytokines in NO regulation.
- To explore NO's function as a self-regulatory molecule in immune responses.
Main Methods:
- Analysis of cytokine-mediated regulation of inducible NO synthase (iNOS) expression.
- Investigation of the effects of T helper 1 (IFN-γ) and T helper 2 (interleukin-4) cytokines on iNOS induction.
- Assessment of NO production by Th1 cells and its impact on Th1 cell proliferation.
Main Results:
- IFN-γ, produced by Th1 cells, is a potent inducer of iNOS.
- Interleukin-4, produced by Th2 cells, inhibits iNOS induction at the transcriptional level.
- High concentrations of NO can inhibit the proliferation of Th1 cells.
Conclusions:
- NO synthesis is tightly regulated by opposing cytokines from Th1 and Th2 cells.
- NO acts as a mediator in Th1/Th2 cell interactions.
- NO functions as a self-regulatory molecule, preventing Th1 cell over-expansion and associated immunopathologies.