Restoration of ethanol-compromised T(h)1 responses by sodium orthovanadate

Alcohol consumption often diminishes antigen-specific cell-mediated immunity. In alcohol-consuming mice IFN-gamma and delayed-type hypersensitivity (DTH) responses are blunted, although antigen-specific T cell proliferation and IL-2 responses are largely unaffected, suggesting that alcohol different...

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Bibliographic Details
Published in:International immunology 2002-11, Vol.14 (11), p.1239-1245
Main Authors: Ostrovidov, Serge, Howard, Laurence M, Ikeda, Masato, Ikeda, Akiko, Waltenbaugh, Carl
Format: Article
Language:English
Subjects:
Adjuvants, Immunologic - pharmacology
Animals
Cell Division - drug effects
Cell Line
Ethanol - pharmacology
Female
Hypersensitivity - drug therapy
Hypersensitivity - immunology
In Vitro Techniques
Interferon-gamma - drug effects
Mice
Mice, Inbred BALB C
Protein Tyrosine Phosphatases - antagonists & inhibitors
Th1 Cells - drug effects
Th1 Cells - immunology
Vanadates - pharmacology
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Summary:Alcohol consumption often diminishes antigen-specific cell-mediated immunity. In alcohol-consuming mice IFN-gamma and delayed-type hypersensitivity (DTH) responses are blunted, although antigen-specific T cell proliferation and IL-2 responses are largely unaffected, suggesting that alcohol differentially affects signal transduction pathways. In the present report we explore the use of the phosphatase inhibitor, Na3 VO4 to restore IFN-gamma secretion in the presence of ethanol both in vivo and in vitro. We show that Na3 VO4 restores IFN-gamma in vitro and antigen-specific DTH in vivo to the levels seen in alcohol non-consuming mice. Our data support the contention that ethanol, by up-regulating phosphotyrosine phosphatase, diminishes the IFN-gamma signal transduction pathway.
ISSN:0953-8178
DOI:10.1093/intimm/dxf088