IMR Press / FBL / Volume 9 / Issue 6 / DOI: 10.2741/1467

Frontiers in Bioscience-Landmark (FBL) is published by IMR Press from Volume 26 Issue 5 (2021). Previous articles were published by another publisher on a subscription basis, and they are hosted by IMR Press on as a courtesy and upon agreement with Frontiers in Bioscience.

Mechanisms of alcohol liver damage: aldehydes, scavenger receptors, and autoimmunity
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1 University of Nebraska Medical Center, Department of Internal Medicine, 988090 Nebraska Medical Center, Omaha, NE 68198-8090
2 Veterans Administration Alcohol Research Center, Omaha Veterans Administration Medical Center, 4101 Woolworth Avenue, Omaha, NE 68105
3 UT Southwestern, Department of Pathology, 5323 Harry Hines Blvd, Dallas, TX 75390-9072
4 University of Nebraska Medical Center, Department of Pathology and Microbiology, 986495 Nebraska Medical Center, Omaha, NE 68198-6495
Front. Biosci. (Landmark Ed) 2004, 9(6), 3145–3155;
Published: 1 September 2004

While most of the investigations into the causative events in the development of alcoholic liver disease (ALD) have been focused on multiple factors, increasing interest has centered around the possible role of immune mechanisms in the pathogenesis and perpetuation of ALD. This is because many of the clinical features of ALD suggest that immune effector mechanisms may be contributing to liver tissue damage, as evidenced by the detection of circulating autoantibodies, and the presence of CD4+ and CD8+ lymphoid cells in the livers of patients with ALD. One mechanism that has been associated with the development of autoimmune responses is the modification (haptenation or adduction) of liver proteins with aldehydes or other products of oxidative stress. This is because it has been shown that these adducted proteins can induce specific immune responses, to the adduct, the adduct plus protein (conformational antigens), as well as the unmodified parts of the protein. More importantly, it is possible to demonstrate that adducted self-proteins can induce reactivity to the normal self-protein and thereby induce autoimmune responses. Therefore, it is the purpose of this manuscript to outline the mechanism(s) by which these modified self proteins can induce autoimmune reactivity, and thus play a role in the development and/or progression of ALD.

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