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Chronic alcohol consumption in mice increases the proportion of peripheral memory T cells by homeostatic proliferation.

Zhang H, Meadows GG

Department of Pharmaceutical Sciences, College of Pharmacy, Washington State University, Box 646713, 334 Wegner Hall on Stadium Way, Pullman, WA 99164-6713. meadows@wsu.edu.

This study examined the mechanism underlying the increase of peripheral memory phenotype T cells that occurs during chronic alcohol consumption in mice. Female C57BL/6 mice were given 20% (w/v) alcohol in the drinking water for 2 weeks to 6 months. Chronic alcohol consumption significantly induced peripheral T cell lymphopenia; up-regulated expression of CD44 on T cells and increased the percentage of CD4(+)CD44(int/hi) and CD8(+)CD44(int/hi) Ly6C(+) T cells; up-regulated the expression of CD43 on CD8(+) T cells; increased the percentage of interferon-gamma-producing T cells; decreased the percentage of CD8(+)CD28(+) T cells; and down-regulated the expression of CD28 on CD4(+) T cells. Expression of CD25 and CD69 on peripheral CD8(+) T cells was not affected and inconsistently expressed on CD4(+) T cells. Neither cell type showed altered expression of CD137 or CD153. Alcohol withdrawal did not abrogate the increase in CD8(+)Ly6C(+)cells induced by alcohol consumption. In vivo bromodeoxyuridine incorporation experiments demonstrated that chronic alcohol consumption decreases naïve T cells that are presumed to have emigrated from the thymus and increases proliferation of memory T cells, but accelerates peripheral T cell turnover. Together these results indicate that chronic alcohol consumption results in T cell lymphopenia, which in turn induces T cell homeostatic proliferation that increases the proportion of peripheral memory T cells relative to naïve T cells.

Published 1 November 2005 in J Leukoc Biol, 78(5): 1070-80.
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