Killer cell immunoglobulin-like receptor genotype and killer cell immunoglobulin-like receptor–human leukocyte antigen C ligand compatibility affect the severity of hepatitis C virus recurrence after liver transplantation

✍ Scribed by Alejandro Espadas de Arias; Simone Elizabeth Haworth; Luca Saverio Belli; Patrizia Burra; Giovambattista Pinzello; Marcello Vangeli; Ernesto Minola; Maria Guido; Patrizia Boccagni; Tullia Maria De Feo; Rosanna Torelli; Massimo Cardillo; Mario Scalamogna; Francesca Poli

• Publisher: John Wiley and Sons
• Year: 2009
• Tongue: English
• Weight: 156 KB
• Volume: 15
• Category: Article
• ISSN: 1527-6465
• DOI: 10.1002/lt.21673

✦ Synopsis

In 20% to 30% of infected individuals, hepatitis C virus (HCV) can cause cirrhosis and hepatocellular carcinoma, for which liver transplantation is the best treatment available. HCV re-infection is universal, and hepatitis disease recurrence occurs in most cases with a 30% probability of progression to graft cirrhosis at 5 years post-transplant. The immunological response to HCV involves natural killer (NK) cells and killer cell immunoglobulin-like receptors (KIRs), which specifically recognize human leukocyte antigen (HLA) class I antigens present on target cells. The effector functions of NK cells are influenced by inhibitory KIR interaction with self-HLA class I ligands, with HLA-C being the most predominant. This study examines the roles of KIR genotypes and their HLA ligands in both HCV disease recurrence and its progression. A total of 151 patients were included in the cohort, and their clinical details were recorded. Liver biopsies were used to define the absence/presence of recurrent hepatitis, the degree of fibrosis, and the progression to cirrhosis over a 10-year period. Mismatching of KIR-HLA-C ligands between donor-recipient pairs was associated with the recurrence of hepatitis (P ϭ 0.008). The presence of KIR2DL3 in the recipient correlated with progression to liver fibrosis (P ϭ 0.04). The mismatching of HLA-KIR ligands favored the progression of the recurrent hepatitis to fibrosis only in the presence of KIR2DL3 (P ϭ 0.04). These preliminary results indicate that the KIR genotype and KIR-HLA-C ligand compatibility play roles in the recurrence and progression of hepatitis C disease in liver transplant recipients.