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Generation of Human Monocyte-derived Dendritic Cells from Whole Blood
Published on: December 24, 2016
Dendritic cells and measles virus infection
S Schneider-Schaulies1, I M Klagge, V ter Meulen
1Institute for Virology and Immunobiology, University of Würzburg, Versbacher Str. 7, 97078 Würzburg, Germany.
Abstract:
Measles is a major cause of childhood mortality in developing countries which is mainly attributed to the ability of measles virus (MV) to suppress general immune responses. Paradoxically, virus-specific immunity is efficiently induced, which leads to viral clearance from the host and confers long-lasting protection against reinfection. As sensitisers of pathogen encounter and instructors of the adaptive immune response, dendritic cells (DCs) may play a decisive role in the induction and quality of the MV-specific immune activation. The ability of MV wild-type strains in particular to infect DCs in vitro is dearly established, and the receptor binding haemagglutinin protein of these viruses essentially determines this particular tropism. DC maturation as induced early after MV infection is likely to be of crucial importance for the induction of MV-specific immunity. DCs may, however, be instrumental in MV-induced immunosuppression. (1) T cell depletion could be brought about by DC-T cell fusion or TRAIL-mediated induction of apoptosis. (2) Inhibition of stimulated IL-12 production from MV-infected DCs might affect T cell responses in qualitative terms in favouring Th2 and suppressing Th1 responses. (3) The viral glycoprotein complex expressed at high levels on infected DCs late in infection is able to directly inhibit T cell proliferation by surface contact-dependent negative signalling. This most likely accounts for the failure of infected DC cultures to stimulate allogeneic and inhibit mitogen-stimulated T cell proliferation in vitro and the pronounced proliferative unresponsiveness of T cell ex vivo to polyclonal and antigen-specific stimulation which is a central finding of MV-induced immunosuppression.
Insights
Measles virus (MV) infects dendritic cells (DCs), crucial for immune response. While MV induces protective immunity, it also suppresses immune function through mechanisms involving DCs, impacting T cell responses and causing immunosuppression.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Measles virus (MV) causes significant childhood mortality, primarily due to its immunosuppressive capabilities.
- Despite general immune suppression, MV efficiently induces virus-specific immunity, leading to viral clearance and long-term protection.
- Dendritic cells (DCs) are key in initiating adaptive immunity and may influence measles-specific immune responses.
Purpose of the Study:
- To investigate the role of dendritic cells (DCs) in measles virus (MV)-induced immune modulation.
- To elucidate the mechanisms by which MV-infected DCs contribute to both protective immunity and immunosuppression.
Main Methods:
- In vitro studies examining MV wild-type strain tropism for DCs.
- Analysis of DC maturation following MV infection.
- Investigation of mechanisms of T cell suppression by MV-infected DCs, including DC-T cell fusion, TRAIL-mediated apoptosis, IL-12 inhibition, and viral glycoprotein-mediated signaling.
Main Results:
- MV wild-type strains efficiently infect DCs, with the hemagglutinin protein determining tropism.
- Early DC maturation post-MV infection is critical for inducing MV-specific immunity.
- MV-infected DCs contribute to immunosuppression through T cell depletion, skewing T cell responses (e.g., inhibiting Th1 via reduced IL-12), and direct inhibition of T cell proliferation via viral glycoproteins.
Conclusions:
- Dendritic cells play a dual role in measles virus infection, facilitating protective immunity while also mediating viral-induced immunosuppression.
- MV-infected DCs employ multiple strategies to impair T cell responses, contributing to the pathology of measles.
- Understanding these DC-mediated mechanisms is crucial for developing effective measles immunotherapies and vaccines.
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