There is a close relation between T helper (Th) 1 cells and nitric oxide in disease. Thus it is possible that a reciprocal regulatory mechanism exists between them. This paper briefly describes the experimental studies which have helped elucidate the mechanism by which nitric oxide selectively enhances Th 1 cell proliferation and the potential effect of nitric oxide on regulatory T (Treg) cells. On the basis of the results the authors propose that nitric oxide represents an additional signal for the induction of T cell subset response, contributing to the increasingly complex network of immune regulation essential for health and disease.
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- Ag, antigen
- cGMP, 3′,5′-cyclic guanosine monophosphate
- IL-12R, interleukin-12 receptor
- iNOS, inducible nitric oxide synthase
- NOC-18, 2,2′-(hydroxynitrosohydrazino)bis-ethamine
- ODQ, 1-H-oxodiazolo-(1,2,4)-(4,3-a) guinoxaline-1-one
- sGC, soluble guanylyl cyclase
- TCR, T cell receptor
- Th, helper T cell
- Tc, cytotoxic T cell
- Tp, T cells precursor
- Treg, regulatory T cell
This work was supported by the Wellcome Trust, Medical Research Council, UK, Arthritis Research Campaign, UK, the Chief Scientist’s Office, Scotland, and the European Union. WN was supported by the Committee of Scientific Research of Poland (grants 4PO 5BO 1319 and 2PO 5BO 8527).
Competing interests: none declared
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