TY - JOUR
T1 - Cell-mediated hepatic injury in alcoholic liver disease
AU - Chedid, Antonio
AU - Mendenhall, Charles L.
AU - Moritz, Thomas E.
AU - French, Samuel W.
AU - Chen, Thomas S.
AU - Morgan, Timothy R.
AU - Roselle, Gary A.
AU - Nemchausky, Bernard A.
AU - Tamburro, Carlo H.
AU - Schiff, Eugene R.
AU - McClain, Craig J.
AU - Marsano, Luis S.
AU - Allen, John I.
AU - Samanta, Arun
AU - Weesner, Robert E.
AU - Henderson, William G.
N1 - Funding Information:
Funded by the Cooperative Studies Program of the Department of Veterans Affairs Medical Research Service and by a grant (to AC.) from the National Institute of Alcohol Abuse and Alcoholism.
Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 1993/7
Y1 - 1993/7
N2 - Background: The mechanism responsible for the initiation and perpetuation of alcoholic liver disease (ALD) remains poorly understood. This investigation attempted to elucidate the role of cell-mediated immune phemonena in the pathogenesis of ethanol-induced liver injury. Methods: Frozen liver biopsy specimens from 144 patients with moderate to severe ALD were examined by the avidin-biotin immunoperoxidase technique for the expression of antigenic markers of T and B lymphocytes, natural killer cells, and class I and II MHC molecules in the tissue. Results: Expression of CDS by lymphocytes correlated significantly with regenerating nodules, intralobular inflammation, central sclerosis, and abnormalities of Kupffer cells. B cells were rarely present, and natural killer cells were absent. CD3+ lymphocytes expressed either CD4 or CD8 surface molecules. Enhanced class I MHC expression correlated significantly with portal inflammation, limiting plate erosion, vascular abnormalities, and hemosiderosis. Expression of class II MHC molecules correlated significantly with necrosis, bile stasis, and Mallory bodies. Conclusions: The distribution and persistence of CD4+ and CD84+ cells in actively advancing ALD, the enhanced MHC expression on hepatocytes, and their relationship to alcoholic hyalin and necrosis lend support to the hypothesis that a cytotoxic T lymphocytehepatocyte interaction plays a role, perhaps via lymphokine production, in the genesis or perpetuation of ALD.
AB - Background: The mechanism responsible for the initiation and perpetuation of alcoholic liver disease (ALD) remains poorly understood. This investigation attempted to elucidate the role of cell-mediated immune phemonena in the pathogenesis of ethanol-induced liver injury. Methods: Frozen liver biopsy specimens from 144 patients with moderate to severe ALD were examined by the avidin-biotin immunoperoxidase technique for the expression of antigenic markers of T and B lymphocytes, natural killer cells, and class I and II MHC molecules in the tissue. Results: Expression of CDS by lymphocytes correlated significantly with regenerating nodules, intralobular inflammation, central sclerosis, and abnormalities of Kupffer cells. B cells were rarely present, and natural killer cells were absent. CD3+ lymphocytes expressed either CD4 or CD8 surface molecules. Enhanced class I MHC expression correlated significantly with portal inflammation, limiting plate erosion, vascular abnormalities, and hemosiderosis. Expression of class II MHC molecules correlated significantly with necrosis, bile stasis, and Mallory bodies. Conclusions: The distribution and persistence of CD4+ and CD84+ cells in actively advancing ALD, the enhanced MHC expression on hepatocytes, and their relationship to alcoholic hyalin and necrosis lend support to the hypothesis that a cytotoxic T lymphocytehepatocyte interaction plays a role, perhaps via lymphokine production, in the genesis or perpetuation of ALD.
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U2 - 10.1016/0016-5085(93)90034-A
DO - 10.1016/0016-5085(93)90034-A
M3 - Article
C2 - 8514042
AN - SCOPUS:0027291549
VL - 105
SP - 254
EP - 266
JO - Gastroenterology
JF - Gastroenterology
SN - 0016-5085
IS - 1
ER -