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      B and T lymphocyte attenuator regulates T cell activation through interaction with herpesvirus entry mediator.

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          Abstract

          B and T lymphocyte attenuator (BTLA) provides an inhibitory signal to B and T cells. Previously, indirect observations suggested that B7x was a ligand for BTLA. Here we show that BTLA does not bind B7x; instead, we identify herpesvirus entry mediator (HVEM) as the unique BTLA ligand. BTLA bound the most membrane-distal cysteine-rich domain of HVEM, distinct from regions where the ligands LIGHT and lymphotoxin-alpha bound HVEM. HVEM induced BTLA tyrosine phosphorylation and association of the tyrosine phosphatase SHP-2 and repressed antigen-driven T cell proliferation, providing an example of reverse signaling to a non-tumor necrosis factor family ligand. The conservation of the BTLA-HVEM interaction between mouse and human suggests that this system is an important pathway regulating lymphocyte activation and/or homeostasis in the immune response.

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          Author and article information

          Journal
          Nat Immunol
          Nature immunology
          Springer Science and Business Media LLC
          1529-2908
          1529-2908
          Jan 2005
          : 6
          : 1
          Affiliations
          [1 ] Department of Pathology and Center for Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
          Article
          ni1144
          10.1038/ni1144
          15568026
          5d78fbee-9f47-49d7-99f8-5098104fd76f
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