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Published on: December 10, 2013
CD14 Is Involved in the Interferon Response of Human Macrophages to Rubella Virus Infection
Erik Schilling1, Lukas Pfeiffer2, Sunna Hauschildt3,4
1Institute of Clinical Immunology, Medical Faculty, Leipzig University, Johannisallee 30, 04103 Leipzig, Germany.
Abstract:
Macrophages (MΦ) as specialized immune cells are involved in rubella virus (RuV) pathogenesis and enable the study of its interaction with the innate immune system. A similar replication kinetics of RuV in the two human MΦ types, the pro-inflammatory M1-like (or GM-MΦ) and anti-inflammatory M2-like (M-MΦ), was especially in M-MΦ accompanied by a reduction in the expression of the innate immune receptor CD14. Similar to RuV infection, exogenous interferon (IFN) β induced a loss of glycolytic reserve in M-MΦ, but in contrast to RuV no noticeable influence on CD14 expression was detected. We next tested the contribution of CD14 to the generation of cytokines/chemokines during RuV infection of M-MΦ through the application of anti-CD14 blocking antibodies. Blockage of CD14 prior to RuV infection enhanced generation of virus progeny. In agreement with this observation, the expression of IFNs was significantly reduced in comparison to the isotype control. Additionally, the expression of TNF-α was slightly reduced, whereas the chemokine CXCL10 was not altered. In conclusion, the observed downmodulation of CD14 during RuV infection of M-MΦ appears to contribute to virus-host-adaptation through a reduction of the IFN response.
Insights
Rubella virus (RuV) infection reduces CD14 expression in M2 macrophages, impacting the innate immune response. Blocking CD14 enhances RuV replication and lowers interferon production, suggesting a role in virus adaptation.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Macrophages (MΦ) are key immune cells involved in rubella virus (RuV) pathogenesis.
- Understanding RuV interaction with the innate immune system is crucial.
Purpose of the Study:
- To investigate the role of CD14 in MΦ during RuV infection.
- To elucidate the impact of CD14 modulation on innate immune responses to RuV.
Main Methods:
- Comparing RuV replication kinetics in M1-like (GM-MΦ) and M2-like (M-MΦ) macrophages.
- Assessing CD14 expression changes post-RuV infection and exogenous interferon-beta (IFN-β) treatment.
- Utilizing anti-CD14 blocking antibodies to study CD14's contribution to cytokine/chemokine generation during RuV infection.
Main Results:
- RuV infection, particularly in M-MΦ, reduced CD14 expression.
- Exogenous IFN-β mimicked RuV's effect on glycolytic reserve but not CD14 expression.
- Blocking CD14 enhanced RuV progeny generation and significantly reduced IFN expression.
Conclusions:
- Downmodulation of CD14 during RuV infection of M-MΦ contributes to virus-host adaptation.
- Reduced CD14 expression is linked to a diminished IFN response, facilitating viral persistence.
