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Induction of membrane ceramides: a novel strategy to interfere with T lymphocyte cytoskeletal reorganisation in viral immunosuppression.DC-SIGN mediated sphingomyelinase-activation and ceramide generation is essential for enhancement of viral uptake in dendritic cellsRegulation of gene expression in lymphocytes and antigen-presenting cells by measles virus: consequences for immunomodulation.Accumulation of splice variants and transcripts in response to PI3K inhibition in T cells.Neutral sphingomyelinase in physiological and measles virus induced T cell suppression.Measles virus-induced immunosuppression: from effectors to mechanisms.Cytoskeletal dynamics: concepts in measles virus replication and immunomodulation.Membrane dynamics and interactions in measles virus dendritic cell infections.The role of sphingomyelin breakdown in measles virus immunmodulation.Human endogenous retrovirus envelope proteins target dendritic cells to suppress T-cell activation.Inhibition of Acid Sphingomyelinase Allows for Selective Targeting of CD4+ Conventional versus Foxp3+ Regulatory T Cells.Hemagglutinin protein of wild-type measles virus activates toll-like receptor 2 signaling.Measles virus interacts with and alters signal transduction in T-cell lipid raftsThe Activity of the Neutral Sphingomyelinase Is Important in T Cell Recruitment and Directional Migration.Immune synapses formed with measles virus-infected dendritic cells are unstable and fail to sustain T cell activation.Measles virus induces expression of SIP110, a constitutively membrane clustered lipid phosphatase, which inhibits T cell proliferation.Neutral sphingomyelinase 2 is a key factor for PorB-dependent invasion of Neisseria gonorrhoeae.The PI3K pathway acting on alternative HIV-1 pre-mRNA splicing.Measles virus transmission from dendritic cells to T cells: formation of synapse-like interfaces concentrating viral and cellular components.Measles virus modulates dendritic cell/T-cell communication at the level of plexinA1/neuropilin-1 recruitment and activity.Measles virus contact with T cells impedes cytoskeletal remodeling associated with spreading, polarization, and CD3 clustering.The neutral sphingomyelinase 2 in T cell receptor signaling and polarity.Preculture of PBMCs at high cell density increases sensitivity of T-cell responses, revealing cytokine release by CD28 superagonist TGN1412.The Neutral Sphingomyelinase 2 Is Required to Polarize and Sustain T Cell Receptor Signaling.
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name
Elita Avota
@en
type
label
Elita Avota
@en
prefLabel
Elita Avota
@en