Year: 2013
Type: article
Abstract: Defining the molecular interactions required to program activated CD8 T cells to survive and become memory cells may allow us to understand how to augment anti-viral immunity. HVEM (herpes virus entry mediator) is a member of the tumor necrosis factor receptor (TNFR) family that interacts with ligands in the TNF family, LIGHT and Lymphotoxin-α, and in the Ig family, B and T lymphocyte attenuator (BTLA) and CD160. The Ig family members initiate inhibitory signaling when engaged with HVEM, but may also activate survival gene expression. Using a model of vaccinia virus infection, we made the unexpected finding that deficiency in HVEM or BTLA profoundly impaired effector CD8 T cell survival and development of protective immune memory. Mixed adoptive transfer experiments indicated that BTLA expressed in CD8α+ dendritic cells functions as a trans-activating ligand that delivers positive co-signals through HVEM expressed in T cells. Our data demonstrate a critical role of HVEM-BTLA bidirectional cosignaling system in antiviral defenses by driving the differentiation of memory CD8 T cells.
Source: PLoS ONE
Language: English
Topic: T-cell and B-cell Immunology
Subfield: Immunology
Field: Immunology and Microbiology
Domain: Life Sciences
Open Access status: gold
Estimated APC paid: $2,382
Awards: Anti Herpesvirus Signaling by LTab and LIGHT, G1453815790, G1657500643, TNFR Members in T Cell Immunity to Vaccinia, G218382676, G3353305694, TNFR Members in T Cell Immunity to Vaccinia, G3682158250, G3844218122, G3993626653, G4005856830, G4126962603, Lymphotoxin alpha Beta and LIGHT cytokine systems, G7445370438, G7841112980, LYMPHOTOXIN AB AND LIGHT CYTOKINE SYSTEMS, G9000045684, G9000097582, G9000181232, G9000185027
OpenAlex ID: W2031764503