Alcohol consumption alters antigen-specific Th1 responses: Mechanisms of deficit and repair

Carl Waltenbaugh*, Kristine Vasquez, Jeffrey D. Peterson

*Corresponding author for this work

Research output: Contribution to journalArticle

44 Scopus citations

Abstract

Among the physiological effects associated with excessive alcohol consumption are alterations in immune function. Alcohol impairs T-helper 1 lymphocyte (Th1) regulated, cell-mediated immune responses. Antibody responses, regulated by T-helper 2 lymphocyte (Th2), are either unimpaired or enhanced. Antigen presenting cells are central to the development of both Th1 and Th2 regulated immune responses. We used both T-cell receptor transgenic and conventionally immunized mice to demonstrate that ethanol consumption directly affects antigen presenting cells that, in turn, determines whether Th1 or Th2 response patterns predominate. Ethanol consumption inhibits Th1- associated interleukin-12 and interferon-γ cytokine production and delayed- type hypersensitivity. Administration of exogenous recombinant interleukin- 12 both restores interferon-γ levels and delayed-type hypersensitivity responses in ethanol-consuming mice.

Original languageEnglish (US)
Pages (from-to)220S-223S
JournalAlcoholism: Clinical and Experimental Research
Volume22
Issue number5 SUPPL.
StatePublished - Aug 1 1998

Keywords

  • Alcohol
  • Cell Mediated Immunity
  • Glutathione
  • Mouse Recombinant Interleukin-12

ASJC Scopus subject areas

  • Medicine (miscellaneous)
  • Toxicology
  • Psychiatry and Mental health

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