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T-cell activation after chronic ethanol ingestion in mice
Journal article   Peer reviewed

T-cell activation after chronic ethanol ingestion in mice

Robert T Cook, Xiaoyan Zhu, Ruth A Coleman, Zuhair K Ballas, Thomas J Waldschmidt, Nancy B Ray, Douglas R LaBrecque and Brian L Cook
Alcohol (Fayetteville, N.Y.), Vol.33(3), pp.175-181
2004
DOI: 10.1016/j.alcohol.2004.06.007
PMID: 15596085

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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.
T cells Alcohol T-cell–APC interactions

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