The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans

Claudia Colomba, Anna Aiello, Calogero Caruso, Giulia Accardi, Giuseppina Candore, Mattia Emanuela Ligotti, Janardan P. Pandey, Massimo Bilancia, Danilo Di Bona, Luigi Macchia, Giovanni Duro, Sergio Rizzo

Research output: Contribution to journalArticle

Abstract

Hepatitis B virus (HBV) infection causes a self-limiting disease in most individuals. However, < 10% of infected subjects develop a chronic disease. Genetic host variability of polymorphic genes at the interface of innate and acquired immunity, such as killer immunoglobulin-like receptors (KIR), their human leucocyte antigen (HLA) and IgG allotypes (GM), could explain this different clinical picture. We previously showed a protective role of the KIR2DL3 gene for the development of chronic hepatitis B (CHB), and a detrimental role of the KIR ligand groups, HLA-A-Bw4 and HLA-C2. We have expanded the previous analysis genotyping patients for GM23 and GM3/17 allotypes. The comparison of the patients with CHB with those who resolved HBV infection showed that the presence of GM17 allele virtually eliminated the risk of developing CHB (OR, 0·03; 95% CI, 0·004–0·16; P < 0·0001). In addition, the combination of GM17, KIR2DL3, HLA-A-Bw4 and HLA-C2 was highly sensitive to predict the outcome of HBV infection.
Original languageEnglish
Pages (from-to)178-182
Number of pages5
JournalImmunology
Publication statusPublished - 2020

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology

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