Intrahepatic lymphocyte subpopulations and HLA class I antigen expression by hepatocytes in chronic hepatitis C.
The lymphocyte subpopulations in the peripheral blood and liver were studied in 17 patients with chronic active hepatitis type C (CAH C) by immunoenzymatic and immunofluorescence techniques, using mono-specific T cell antibodies and other reagents. The peripheral blood subsets showed no significant differences between the patients with CAH C and normal controls. In the liver, CD8-positive cells were predominant over CD4- and Leu 7-positive cells. Leu 7-, CD4-, and CD11-positive lymphocytes were all few in number. HLA class I antigen was expressed diffusely on the cell surfaces of the hepatocytes. Serum levels of soluble interleukin 2 receptor (sIL2R) in the CAH C patients were significantly higher than in normal controls (p less than 0.01). In CAH C, sIL2R levels were higher during exacerbations than during remissions (p less than 0.01). These results suggest that cytotoxic T cells (CD8- positive, CD4-negative, and CD11-negative) may play an important role in the pathogenesis of hepatocyte injury in patients with CAH C.
Onji
M
M
Third Department of Internal Medicine, Ehime University School of Medicine, Japan.
Kikuchi
T
T
Kumon
I
I
Masumoto
T
T
Nadano
S
S
Kajino
K
K
Horiike
N
N
Ohta
Y
Y
D000911:Antibodies, Monoclonal; D000943:Antigens, Differentiation / Q000378:metabolism; D016516:CD4-CD8 Ratio; D018959:CD57 Antigens; D006526:Hepatitis C / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D006521:Hepatitis, Chronic / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015395:Histocompatibility Antigens Class I / Q000032:analysis*; D006801:Humans; D008099:Liver / Q000276:immunology* / Q000378:metabolism / Q000473:pathology; D015375:Receptors, Interleukin-2 / Q000378:metabolism; D016176:T-Lymphocyte Subsets / Q000378:metabolism*
D000911:Antibodies, Monoclonal; D000943:Antigens, Differentiation; D018959:CD57 Antigens; D015395:Histocompatibility Antigens Class I; D015375:Receptors, Interleukin-2