Imbalance Between Soluble and Membrane-Bound CD100 Regulates Monocytes Activity in Hepatitis B Virus-Associated Acute-on-Chronic Liver Failure
| Autor: | Ye Liu, Xue Li, Dong-Na Zhang, Ying Gao, Feng-Yu Xi, Yu Li, Guang-Ze Zhu |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Hepatitis B virus CD14 T cell Immunology CD8-Positive T-Lymphocytes medicine.disease_cause Monocytes 03 medical and health sciences Hepatitis B Chronic 0302 clinical medicine Immune system Interferon Virology medicine Humans business.industry Acute-On-Chronic Liver Failure Granzyme B 030104 developmental biology medicine.anatomical_structure Molecular Medicine 030211 gastroenterology & hepatology Tumor necrosis factor alpha business CD8 medicine.drug |
| Zdroj: | Viral Immunology. 34:273-283 |
| ISSN: | 1557-8976 0882-8245 |
| Popis: | CD100 is an important immune semaphorin that is a secreted and membrane bound protein involved in infectious diseases. However, CD100 expression profile and the regulation to innate immune system in hepatitis B virus (HBV)-associated acute-on-chronic liver failure (ACLF) was not previously reported. The aim of this study was to investigate CD100 level and modulatory function of CD100 to CD14+ monocytes in HBV-ACLF patients. Plasma-soluble CD100 (sCD100) level and membrane-bound CD100 (mCD100) expression on peripheral CD14+ monocytes was analyzed in HBV-ACLF patients. CD14+ monocytes-induced cytotoxicity and CD14+ monocytes-mediated T cell activation in response to CD100 stimulation was also assessed in direct and indirect contact coculture culture systems. HBV-ACLF patients had lower plasma sCD100 and higher mCD100 level on CD14+ monocytes compared with asymptomatic HBV carriers, chronic hepatitis B patients, and controls. CD14+ monocytes from HBV-ACLF patients induced limited target Huh7.5 cell death and secreted less interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and granzyme B in both direct and indirect contact coculture systems compared with controls. Recombinant sCD100 not only enhanced CD14+ monocytes-mediated Huh7.5 cell death and granzyme B secretion, but it also elevated CD14+ monocytes-induced IFN-γ/interleukin-17 production by CD4+ T cells as well as IFN-γ/TNF-α secretion by CD8+ T cells in HBV-ACLF patients. The current data indicated that severe inflammation induced sCD100/mCD100 imbalance to inactivate CD14+ monocytes response, which might be beneficial for the survival of HBV-ACLF patients. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|