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Nitric oxide and redox mechanisms in the immune response

  1. Author:
    Wink, D. A.
    Hines, H. B.
    Cheng, R. Y. S.
    Switzer, C. H.
    Flores-Santana, W.
    Vitek, M. P.
    Ridnour, L. A.
    Colton, C. A.
  2. Author Address

    [Wink, DA; Cheng, RYS; Switzer, CH; Flores-Santana, W; Ridnour, LA] NCI, Radiat Biol Branch, NIH, Bethesda, MD 20892 USA [Hines, HB] USA, Integrated Toxicol Div, Med Res Inst Infect Dis, Frederick, MD USA [Vitek, MP; Colton, CA] Duke Univ, Med Ctr, Div Neurol, Durham, NC 27710 USA;Wink, DA (reprint author), NCI, Radiat Biol Branch, NIH, Bldg 10,Room B3-B35, Bethesda, MD 20892 USA;wink@mail.nih.gov glia01@aol.com
    1. Year: 2011
    2. Date: Jun
  1. Journal: Journal of Leukocyte Biology
    1. 89
    2. 6
    3. Pages: 873-891
  2. Type of Article: Review
  3. ISSN: 0741-5400
  1. Abstract:

    The role of redox molecules, such as NO and ROS, as key mediators of immunity has recently garnered renewed interest and appreciation. To regulate immune responses, these species trigger the eradication of pathogens on the one hand and modulate immunosuppression during tissue-restoration and wound-healing processes on the other. In the acidic environment of the phagosome, a variety of RNS and ROS is produced, thereby providing a cauldron of redox chemistry, which is the first line in fighting infection. Interestingly, fluctuations in the levels of these same reactive intermediates orchestrate other phases of the immune response. NO activates specific signal transduction pathways in tumor cells, endothelial cells, and monocytes in a concentration-dependent manner. As ROS can react directly with NO-forming RNS, NO bioavailability and therefore, NO response(s) are changed. The NO/ROS balance is also important during Th1 to Th2 transition. In this review, we discuss the chemistry of NO and ROS in the context of antipathogen activity and immune regulation and also discuss similarities and differences between murine and human production of these intermediates. J. Leukoc. Biol. 89: 873-891; 2011.

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External Sources

  1. DOI: 10.1189/jlb.1010550
  2. WOS: 000291108400008

Library Notes

  1. Fiscal Year: FY2010-2011
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