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Updated: Jul 16, 2026
Imaging the Human Immunological Synapse
Published on: December 26, 2019
Immune synapses formed with measles virus-infected dendritic cells are unstable and fail to sustain T cell activation
Yoanna Shishkova1, Harry Harms, Georg Krohne
1University of Würzburg, Institute for Virology and Immunobiology, Versbacher Street 7, D-97078 Würzburg, Germany.
Insights
Measles virus (MV)-infected dendritic cells (DCs) can initiate T cell interactions but fail to sustain them, leading to immunosuppression. MV glycoproteins on DCs destabilize immune synapses, inhibiting T cell activation.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Dendritic cells (DCs) are crucial for immune responses, and viral infections, like measles virus (MV), often induce immunosuppression by impairing DC function.
- The precise cellular mechanisms by which MV-infected DCs suppress T cell responses remain incompletely understood.
Purpose of the Study:
- To elucidate the cellular mechanisms underlying measles virus-induced immunosuppression mediated by dendritic cells.
- To investigate the role of MV-infected DCs in T cell activation and immune synapse formation.
Main Methods:
- Comparative analysis of MV-infected DCs versus lipopolysaccharide (LPS)-matured DCs.
- Assessment of DC migratory phenotype, motility, and integrin activation.
- Characterization of DC-T cell interfaces, including immune synapse organization, CD3 clustering, and MHC class II recruitment.
- Evaluation of T cell conjugation stability and activation.
- Utilizing recombinant MV encoding VSV G protein to assess the role of MV glycoproteins.
Main Results:
- MV-infected DCs exhibited subtle differences from LPS-matured DCs in migration and motility.
- The organization of MV-DC/T cell interfaces resembled functional immune synapses.
- However, the majority of MV-DC/T cell conjugates were unstable, leading to abortive T cell activation.
- Surface expression of MV glycoproteins on DCs was found to contribute to immune synapse destabilization and T cell inhibition.
Conclusions:
- MV-infected DCs can initiate T cell interactions but are impaired in sustaining stable conjugates and robust T cell activation.
- MV glycoproteins expressed on the DC surface play a direct role in destabilizing immune synapses, contributing to viral immunosuppression.
- Targeting MV glycoprotein interactions could be a strategy to restore T cell function during measles infection.
Abstract:
Interaction with dendritic cells (DCs) is considered as central to immunosuppression induced by viruses, including measles virus (MV). Commonly, viral infection of DCs abrogates their ability to promote T cell expansion, yet underlying mechanisms at a cellular level are undefined. We found that MV-infected DCs only subtly differed from LPS-matured with regard to integrin activation, acquisition of a migratory phenotype and motility. Similarly, the organization of MV-DC/T cell interfaces was consistent with that of functional immune synapses with regard to CD3 clustering and MHC class II surface recruitment. The majority of MV-DC/T cell conjugates was, however, unstable and only promoted abortive T cell activation. Thus, MV-infected DCs retain activities required for initiating, but not sustaining T cell conjugation and activation. This is partially rescued if surface expression of the MV glycoproteins on DCs is abolished by infection with a recombinant MV encoding VSV G protein instead, indicating that these contribute directly to synapse destabilization and thereby act as effectors of T cell inhibition.
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