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- W4313386002 abstract "Abstract Innate and adaptive lymphocytes respond to and manipulate their microenvironment through diverse cellular communication pathways including tumor necrosis factor (TNF) network signaling. A frequent target of cancers and viruses is the TNF receptor herpesvirus entry mediator (HVEM, TNFRSF14) and its ligand-receptor network because of the central role of this signaling system in maintaining immune homeostasis, and in regulating inflammatory responses. Notably, the biophysical basis for altered agonistic activity by pathogen and tumor-associated receptor variants remains unclear. Here we show that HVEM mutations associated with human follicular and diffuse large B cell lymphoma uniformly disrupt binding to CD160, while subsets of mutations retain binding to B and T lymphocyte attenuator (BTLA) and LIGHT (TNFSF14). We show that while HVEM activation of the inhibitory receptor BTLA is restricted by the expression of CD160 in lymphocytes, selectivity for BTLA by mutated HVEM or a viral paralog results in unhindered inhibition of ERK signaling and activation of IL-2 transcription. Together, the acquisition of ligand selectivity for BTLA by tumors and viruses illustrates a common mechanism of immune modulation utilized by intracellular pathogens to thwart inflammatory signaling." @default.
- W4313386002 created "2023-01-06" @default.
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- W4313386002 date "2015-05-01" @default.
- W4313386002 modified "2023-09-28" @default.
- W4313386002 title "Lymphoma-associated mutant Herpesvirus entry mediator selects for B and T lymphocyte attenuator inhibitory signaling (TUM9P.1009)" @default.
- W4313386002 doi "https://doi.org/10.4049/jimmunol.194.supp.210.11" @default.
- W4313386002 hasPublicationYear "2015" @default.
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