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Updated: Jun 7, 2026
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Chemiluminescence-based Assays for Detection of Nitric Oxide and its Derivatives from Autoxidation and Nitrosated Compounds
Published on: February 16, 2022
Lymphocyte development requires S-nitrosoglutathione reductase
Zhiyong Yang1, Zhi-En Wang, Paschalis-Thomas Doulias
1Department of Microbiology and Immunology, University of California San Francisco, San Francisco, CA 94143, USA.
Journal of Immunology (Baltimore, Md. : 1950)
|October 29, 2010
Summary
S-nitrosoglutathione reductase (GSNOR) is vital for immune system development. GSNOR deficiency in mice impairs lymphocyte development by increasing S-nitrosylation and apoptosis, highlighting its protective role.
Area of Science:
- Immunology
- Molecular Biology
- Biochemistry
Background:
- Nitric oxide (NO) is crucial for immune function.
- The specific role of NO in immune system development remains unclear.
- S-nitrosoglutathione reductase (GSNOR) regulates protein S-nitrosylation.
Purpose of the Study:
- To investigate the role of GSNOR in lymphocyte development.
- To elucidate the mechanisms by which GSNOR influences immune system maturation.
Main Methods:
- Genetic deletion of GSNOR in mice.
- Analysis of lymphocyte populations (T and B cells) in periphery and thymus.
- Assessment of protein S-nitrosylation and apoptosis.
- Genetic deletion of inducible NO synthase (iNOS) to assess NO dependency.
Main Results:
- GSNOR deficiency led to a significant reduction in peripheral T and B lymphocytes.
- GSNOR-deficient thymocytes exhibited increased protein S-nitrosylation and apoptosis, with fewer CD4 single-positive cells.
- Lymphopenia, increased S-nitrosylation, and apoptosis in GSNOR-deficient mice were ameliorated by iNOS deletion.
- GSNOR's protective effect on lymphocyte development was intrinsic to hematopoietic cells.
Conclusions:
- GSNOR plays a critical physiological role in immune system development.
- GSNOR likely protects lymphocyte development by regulating protein S-nitrosylation and apoptosis.
- The findings highlight GSNOR as a key regulator in adaptive immunity initiation.
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