T-cell activation after chronic ethanol ingestion in mice

Abstract

Chronic excessive consumption of ethanol causes immunodeficiency in human beings and in mice. Immunologic changes have been described in both species, including T-cell and innate immune system cell activation, among others. The features of chronic ethanol-induced activation have similarities in the two species, including an increased effector subset in both CD4 + and CD8 + T cells. There are also features of activation observed in the splenic macrophages of mice consuming ethanol chronically, including increased up-regulation of CD80 and CD86. Because these molecules are involved in T-cell–antigen-presenting cell interactions in vivo, it is of interest to ask whether these and other pathways of interaction are important in the T-cell activation and cytokine skewing described in chronic ethanol abuse. Preliminary findings from comparisons of wild-type, CD40 ligand knock-out, and CD28 knock-out C57BL/6 mice strongly support the suggestion of a critical role for T-cell–antigen-presenting cell interactions in the immune alterations observed in chronic ethanol abuse.