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Ectromelia-encoded virulence factor C15 specifically inhibits antigen presentation to CD4+ T cells post peptide
Katherine S Forsyth1, Nathan H Roy1, Elise Peauroi1
1Department of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Plos Pathogens
|August 4, 2020
Summary
Ectromelia virus protein C15 selectively inhibits CD4+ T cell activation by disrupting antigen presentation and T cell synapse formation. This orthopoxvirus strategy impacts viral control by targeting crucial immune cells.
Area of Science:
- Virology
- Immunology
- Molecular Biology
Background:
- Smallpox and monkeypox are significant public health threats caused by orthopoxviruses.
- Orthopoxvirus virulence is associated with immunomodulatory B22 family proteins, absent in attenuated strains.
Purpose of the Study:
- To investigate the role of ectromelia virus C15 protein in immune evasion.
- To elucidate the mechanism by which C15 affects T cell activation.
Main Methods:
- Assessed C15's effect on CD4+ and CD8+ T cell activation using peptide and superantigen stimuli.
- Utilized imaging studies and lipid raft disruption assays to analyze T cell synapse formation.
- Investigated antigen presentation pathways and surface protein expression.
Main Results:
- C15 selectively inhibited CD4+ T cell activation, not CD8+ T cell activation.
- Inhibition occurred via interference with antigen presentation, not surface molecule downregulation.
- C15 disrupted CD4+ T cell synapse formation and lipid rafts.
- Antigenic stimulus shifted to uninfected antigen-presenting cells.
Conclusions:
- The ectromelia virus C15 protein is essential for targeted CD4+ T cell inhibition.
- C15 interferes with antigen presentation and T cell synapse formation, aiding viral immune evasion.
- Understanding this mechanism highlights CD4+ T cells' critical role in orthopoxvirus control.
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