CELL-MEDIATED HEPATIC-INJURY IN ALCOHOLIC LIVER-DISEASE

被引:87
作者
CHEDID, A
MENDENHALL, CL
MORITZ, TE
FRENCH, SW
CHEN, TS
MORGAN, TR
ROSELLE, GA
NEMCHAUSKY, BA
TAMBURRO, CH
SCHIFF, ER
MCCLAIN, CJ
MARSANO, LS
ALLEN, JI
SAMANTA, A
WEESNER, RE
HENDERSON, WG
机构
[1] VET ADM MED CTR, LEXINGTON, KY 40511 USA
[2] VET ADM MED CTR, MINNEAPOLIS, MN 55417 USA
[3] VET ADM MED CTR, LONG BEACH, CA 90822 USA
[4] VET ADM MED CTR, CINCINNATI, OH 45220 USA
[5] VET ADM MED CTR, LOUISVILLE, KY 40202 USA
[6] UNIV CALIF LOS ANGELES, LOS ANGELES CTY HARBOR MED CTR, TORRANCE, CA 90509 USA
[7] VET ADM MED CTR, MIAMI, FL 33125 USA
[8] VET ADM MED CTR, E ORANGE, NJ 07019 USA
[9] EDWARD HINES VET ADM MED CTR, HINES, IL USA
关键词
D O I
10.1016/0016-5085(93)90034-A
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
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 CD3 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 CD8+ 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. © 1993.
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页码:254 / 266
页数:13
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