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

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.

Pubmed ID: 15568026

Authors

  • Sedy JR
  • Gavrieli M
  • Potter KG
  • Hurchla MA
  • Lindsley RC
  • Hildner K
  • Scheu S
  • Pfeffer K
  • Ware CF
  • Murphy TL
  • Murphy KM

Journal

Nature immunology

Publication Data

January 21, 2005

Associated Grants

  • Agency: NIA NIH HHS, Id: AG00252
  • Agency: NIAID NIH HHS, Id: AI33068
  • Agency: NIAID NIH HHS, Id: AI48073
  • Agency: NCI NIH HHS, Id: CA69381
  • Agency: NIAID NIH HHS, Id: P01 AI31238
  • Agency: NHLBI NIH HHS, Id: P50 HL54619

Mesh Terms

  • Animals
  • Cell Line
  • Humans
  • Ligands
  • Lymphocyte Activation
  • Mice
  • Mice, Inbred BALB C
  • Receptors, Immunologic
  • Receptors, Tumor Necrosis Factor
  • Receptors, Tumor Necrosis Factor, Member 14
  • Receptors, Virus
  • Recombinant Fusion Proteins