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Post‐transplant reactivation of hepatitis C virus: lymphocyte infiltration and the expression of adhesion molecules and their ligands in liver allografts
Author(s) -
LIPSON KATRI,
LAPPALAINEN MAIJA,
HÖCKERSTEDT KRISTER,
LAUTENSCHLAGER IRMELI
Publication year - 2006
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2006.apm_130.x
Subject(s) - liver transplantation , hepatitis c virus , cd8 , antigen , infiltration (hvac) , cell adhesion molecule , immunology , lymphocyte function associated antigen 1 , medicine , lymphocyte , cd3 , virus , pathology , transplantation , intercellular adhesion molecule 1 , physics , thermodynamics
Hepatitis C virus (HCV) recurrence after liver transplantation has been associated with chronic rejection. Biopsies from 10 patients with post‐transplant HCV were examined for expression of adhesion molecules ICAM‐1, VCAM‐1, and ELAM‐1, number of lymphocytes positive for their ligands LFA‐1, VLA‐4, and SLeX, and activation markers MHC class II antigens and IL2‐R by immunohistochemistry. The phenotypes of the graft‐infiltrating lymphocytes were determined. Results were compared to those for patients with normal graft function or rejection. Five recipients with HCV reactivation and one with de novo HCV had a biopsy available showing induction of ICAM‐1 in sinusoidal endothelium (p<0.05) and hepatocytes (p<0.01), and Class II antigens in hepatocytes (p<0.01), compared to normal controls. Lymphocytes in the graft infiltrate expressed LFA‐1, VLA‐4, and Class II antigens, but IL2‐R was not significantly expressed. CD3+, CD4+, and CD8+ cells were observed. In our study, HCV recurrence was not associated with acute or chronic rejection, and the inflammation was due to the viral infection.