Alcohol Consumption Alters Antigen-Specific Th1 Responses: Mechanisms of Deficit and Repair

Authors


  • Presented at the Alcohol-Induced Immunopathology Symposium, New Orleans, LA, October 17–18, 1997.

  • This study was supported in part by Grants AA08275 and AA10058 from the National Institute on Alcohol Abuse and Alcoholism.

Reprint requests: Carl Waltenbaugh, Ph.D., Department of Microbiology-Immunology, Northwestern University Medical School, 303 East Chicago Avenue, Chicago, IL 60611-3073.

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.

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