Citation

Pasala S, Barr T, Messaoudi I. Alcohol Res. 2015; 37(2): 185-197.

Affiliation

Division of Biomedical Sciences, School of Medicine, University of California, Riverside, Riverside, California.

Copyright

(Copyright © 2015, National Institute on Alcohol Abuse and Alcoholism (USA))

DOI

unavailable

PMID

26695744

PMCID

PMC4590616

Abstract

Alcohol exposure, and particularly chronic heavy drinking, affects all components of the adaptive immune system. Studies both in humans and in animal models determined that chronic alcohol abuse reduces the number of peripheral T cells, disrupts the balance between different T-cell types, influences T-cell activation, impairs T-cell functioning, and promotes T-cell apoptosis. Chronic alcohol exposure also seems to cause loss of peripheral B cells, while simultaneously inducing increased production of immunoglobulins. In particular, the levels of antibodies against liver-specific autoantigens are increased in patients with alcoholic liver disease and may promote alcohol-related liver damage. Finally, chronic alcohol exposure in utero interferes with normal T-cell and B-cell development, which may increase the risk of infections during both childhood and adulthood. Alcohol's impact on T cells and B cells increases the risk of infections (e.g., pneumonia, HIV infection, hepatitis C virus infection, and tuberculosis), impairs responses to vaccinations against such infections, exacerbates cancer risk, and interferes with delayed-type hypersensitivity. In contrast to these deleterious effects of heavy alcohol exposure, moderate alcohol consumption may have beneficial effects on the adaptive immune system, including improved responses to vaccination and infection. The molecular mechanisms underlying ethanol's impact on the adaptive immune system remain poorly understood.

Language: en