The Intrahepatic Expression and Distribution of BTLA and its Ligand HVEM in patients with HBV-related acute-on-chronic liver failureReportar como inadecuado




The Intrahepatic Expression and Distribution of BTLA and its Ligand HVEM in patients with HBV-related acute-on-chronic liver failure - Descarga este documento en PDF. Documentación en PDF para descargar gratis. Disponible también para leer online.

Diagnostic Pathology

, 7:142

First Online: 15 October 2012Received: 28 September 2012Accepted: 11 October 2012

Abstract

ObjectiveIt has been demonstrated that signals from the inhibitory receptor B and T lymphocyte attenuator BTLA are involved in regulating the pathogenesis of infectious diseases. However, the expression and anatomical distribution of BTLA and its ligand, the herpes virus entry mediator HVEM, have not yet been determined in cases of HBV-related acute-on-chronic liver failure HBV-ACLF patients.

MethodsIn this study, the expression of BTLA and HVEM in liver tissues from HBV-ACLF, chronic hepatitis B CHB patients and healthy individuals was analyzed by immunohistochemistry.

ResultsThe results of this analysis demonstrated that both molecules were observed in the HBV-ACLF samples and that their expression was chiefly in the infiltrating inflammatory cells and the damaged bile ducts. However, they were absent in liver sections from CHB patients and healthy controls. Immunofluorescence double-staining indicated that BTLA was found on CK-18 epithelial cells, CD31 endothelial cells, CD68 macrophages, CD56 NK cells, CD16 monocytes, CD3 , CD8 T cells, and Foxp3 regulatory T cells Treg. By contrast, HVEM expression was restricted to CK18 epithelial cells and CD68 macrophages. Moreover, the expression of several members of the B7 superfamily, including PD-L1, PD-L2, B7-H3 and B7-H4, was also detected in these liver tissues, and these proteins were co-expressed with HVEM. Interestingly, the expression of fibrinogen-like protein 2 FGL2, a virus-induced procoagulant molecule, was also found in liver sections from HBV-ACLF, this molecule also co-expresses with BTLA and HVEM.

ConclusionsThese results suggest that BTLA-HVEM signaling is likely to affect the pathogenesis of HBV-ACLF, a clear understanding of the functional roles of these proteins should further elucidate the disease process.

Virtual slidesThe virtual slides for this article can be found here:http:-www.diagnosticpathology.diagnomx.eu-vs-8080806838149123

KeywordsBTLA HBV-ACLF HVEM Immunohistochemistry B7 superfamily Electronic supplementary materialThe online version of this article doi:10.1186-1746-1596-7-142 contains supplementary material, which is available to authorized users.

Huan Xu, Dayan Cao contributed equally to this work.

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Autor: Huan Xu - Dayan Cao - Guoning Guo - Zhihua Ruan - Yuzhang Wu - Yongwen Chen

Fuente: https://link.springer.com/







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