BTLA (B and T lymphocyte attenuator, CD272) is a type I transmembrane glycoprotein with four extracellular cysteine-rich domains. It is an inhibitory molecule structurally and functionally similar to cytotoxic T lymphocyte antigen-4 (CTLA-4) and programmed death-1 (PD-1). These molecules belong to the immunoglobulin superfamily that binds B7 family members. Different from CTLA-4 and PD-1 binding with the B7 family members, BTLA interacts with herpes virus entry mediator (HVEM) which belongs to TNFR family. BTLA/HVEM interaction was the first demonstration of crosstalk between these two family members. BTLA/HVEM interaction negatively modulates T cell activation. HVEM induces BTLA tyrosine phosphorylation and inhibits T-cell proliferation. There is accumulating evidence suggesting that BTLA/HVEM signaling also plays an important role in autoimmunity and infection at mucosal surfaces. The BTLA/HVEM interaction does not prevent the simultaneous binding of other HVEM ligands such as LIGHT or Lymphotoxin-alpha. BTLA is expressed on T cells, B cells, macrophages, dendritic cells, and natural killer cells. Constitutive expression level of BTLA on resting T cells are very low, but increase after the activation of T cells. BTLA is highly expressed on resting B cells.
Size
10 μg
Concentration
n/a
Applications
BA
Other Names
CD272, B- and T-lymphocyte attenuator, B- and T-lymphocyte-associated protein