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Nitric oxide and T helper cell immunity
1Department of Neurology, University of Southern California School of Medicine, Los Angeles 90033, USA. vanderve@hsc.usc.edu
International Immunopharmacology
|August 23, 2001
Summary
Nitric oxide (NO) generated by antigen-presenting cells suppresses T helper cell proliferation, indicating an immunosuppressive role in T-cell immunity. Superoxide may counteract this effect, potentially enhancing immune responses.
Area of Science:
- Immunology
- Cellular Biology
- Molecular Biology
Background:
- Nitric oxide (NO) is produced by antigen-presenting cells (APCs) during antigen presentation to T cells.
- The inducible nitric oxide synthase (iNOS) in APCs is activated by T-helper 1 (Th1) cell-derived interferon-gamma (IFN-gamma) and other T-cell factors.
- The role of NO in T-cell activation and T-cell-dependent immunity is complex and debated, particularly its immunosuppressive functions.
Purpose of the Study:
- To discuss the controversial role of nitric oxide (NO) in T helper (Th) cell activation and T-cell-dependent immunity.
- To emphasize the immunosuppressive effects of NO on T-cell proliferation and its regulatory role in the induction phase of T-cell-mediated immunity.
- To explore the interaction of NO with superoxide and its implications for T-cell regulation.
Main Methods:
- Review of existing literature and mouse models, including genetic deletion of iNOS in models of T-cell-mediated autoimmunity (e.g., experimental autoimmune encephalomyelitis).
- Analysis of the effects of NO on T-cell proliferation and cytokine production.
- Investigation into the role of NADPH oxidase as a source of superoxide that modulates NO activity.
Main Results:
- NO produced by APCs inhibits T-cell proliferation by blocking the G1/S transition, but does not inhibit T-cell cytokine production.
- Genetic deletion of iNOS exacerbates T-cell-mediated autoimmune diseases in mouse models, supporting an in vivo immunosuppressive role for NO.
- Interaction with superoxide diminishes the T-cell regulatory activity of NO, suggesting superoxide may counteract NO's immunosuppressive effects.
Conclusions:
- NO plays a significant regulatory role in the induction phase of T-cell-mediated immunity, primarily through immunosuppression of T-cell proliferation.
- Superoxide, potentially generated by NADPH oxidase, can counteract the immunosuppressive activity of NO, thereby enhancing T-cell-mediated immunity.
- Understanding the balance between NO and superoxide is crucial for comprehending the regulation of T-cell responses in health and disease.
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