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CD100 up-regulation induced by interferon-α on B cells is related to hepatitis C virus infection
Yu He1, Yonghong Guo1, Yun Zhou1
1Department of Infectious Diseases and Center of liver Diseases, Tangdu Hospital, the Fourth Military Medical University, Xi'an, Shaanxi, People's Republic of China.
Insights
Chronic hepatitis C virus (HCV) infection activates B cells, increasing CD100 expression. Interferon-alpha/ribavirin therapy normalizes B cell activation and CD100 levels, aiding HCV clearance.
Area of Science:
- Immunology
- Virology
Background:
- CD100 (Sema4D) regulates immune cell responses.
- Its role in B cell immunity during chronic hepatitis C virus (HCV) infection is not well understood.
Purpose of the Study:
- To investigate CD100 expression on B cells in chronic HCV patients.
- To assess changes in CD100 and B cell activation markers before and after antiviral therapy.
Main Methods:
- Longitudinal study of 20 chronic HCV patients.
- Flow cytometry analysis of B cell markers (CD100, CD72, CD69, CD86).
- Assessment before and after pegylated interferon-alpha (Peg-IFN-α) and ribavirin (RBV) treatment.
Main Results:
- Increased frequency of CD5+ B cells and elevated CD100, CD69, CD86 expression in HCV patients.
- These markers normalized in patients with sustained virological response.
- IFN-α treatment further upregulated CD100, inversely correlating with HCV-RNA decline.
Conclusions:
- B cells exhibit an activated phenotype in chronic HCV infection.
- IFN-α therapy helps restore B cell homeostasis.
- Upregulated CD100 expression may contribute to HCV clearance.
Objectives:
CD100, also known as Sema4D, is a member of the semaphorin family and has important regulatory functions that promote immune cell activation and responses. The role of CD100 expression on B cells in immune regulation during chronic hepatitis C virus (HCV) infection remains unclear.
Materials And Methods:
We longitudinally investigated the altered expression of CD100, its receptor CD72, and other activation markers CD69 and CD86 on B cells in 20 chronic HCV-infected patients before and after treatment with pegylated interferon-alpha (Peg-IFN-α) and ribavirin (RBV) by flow cytometry.
Results:
The frequency of CD5+ B cells as well as the expression levels of CD100, CD69 and CD86 was significantly increased in chronic HCV patients and returned to normal in patients with sustained virological response after discontinuation of IFN-α/RBV therapy. Upon IFN-α treatment, CD100 expression on B cells and the two subsets was further up-regulated in patients who achieved early virological response, and this was confirmed by in vitro experiments. Moreover, the increased CD100 expression via IFN-α was inversely correlated with the decline of the HCV-RNA titer during early-phase treatment.
Conclusions:
Peripheral B cells show an activated phenotype during chronic HCV infection. Moreover, IFN-α therapy facilitates the reversion of disrupted B cell homeostasis, and up-regulated expression of CD100 may be indirectly related to HCV clearance.
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