Archivio istituzionale della ricerca dell'Università degli Studi di Palermo
IRIS è il sistema di gestione integrata dei dati della ricerca (persone, pubblicazioni, progetti, attività) adottato dall’Università di Palermo, e ha lo scopo di raccogliere, conservare, documentare, e diffondere ad accesso aperto le informazioni relative alla produzione scientifica degli autori afferenti all’Ateneo.
EnglishHepatitis 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.
Di Bona, D., Pandey, J., Aiello, A., Bilancia, M., Candore, G., Caruso, C., et al. (2020). The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans. IMMUNOLOGY, 178-182 [10.1111/imm.13133].
| Data di pubblicazione: | 2020 | |
| Titolo: | The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans | |
| Autori: | ||
| Citazione: | Di Bona, D., Pandey, J., Aiello, A., Bilancia, M., Candore, G., Caruso, C., et al. (2020). The immunoglobulin γ marker 17 allotype and KIR/HLA genes prevent the development of chronic hepatitis B in humans. IMMUNOLOGY, 178-182 [10.1111/imm.13133]. | |
| Rivista: | ||
| Digital Object Identifier (DOI): | http://dx.doi.org/10.1111/imm.13133 | |
| 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. | |
| URL: | http://onlinelibrary.wiley.com/journal/10.1111/(ISSN)1365-2567 | |
| Settore Scientifico Disciplinare: | Settore MED/04 - Patologia Generale | |
| Appare nelle tipologie: | 1.01 Articolo in rivista |
File in questo prodotto:
| File | Descrizione | Tipologia | Licenza | |
|---|---|---|---|---|
| IMMUNOLOGY .pdf | ARTICOLO | Versione Editoriale | Administrator Richiedi una copia |
Copyright © 2021