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B and T lymphocyte associated
Protein BTLA PDB 2aw2.png
PDB rendering based on 2aw2.
Available structures
PDB Ortholog search: PDBe, RCSB
Symbols BTLA ; BTLA1; CD272
External IDs OMIM607925 MGI2658978 HomoloGene52233 GeneCards: BTLA Gene
Species Human Mouse
Entrez 151888 208154
Ensembl ENSG00000186265 ENSMUSG00000052013
UniProt Q7Z6A9 Q7TSA3
RefSeq (mRNA) NM_001085357 NM_001037719
RefSeq (protein) NP_001078826 NP_001032808
Location (UCSC) Chr 3:
112.46 – 112.5 Mb
Chr 16:
45.22 – 45.25 Mb
PubMed search [1] [2]

B- and T-lymphocyte attenuator is a protein that in humans is encoded by the BTLA gene.[1][2] BTLA has also been designated as CD272 (cluster of differentiation 272).


BTLA expression is induced during activation of T cells, and BTLA remains expressed on Th1 cells but not Th2 cells. Like PD1 and CTLA4, BTLA interacts with a B7 homolog, B7H4.[2] However, unlike PD-1 and CTLA-4, BTLA displays T-Cell inhibition via interaction with tumor necrosis family receptors (TNF-R), not just the B7 family of cell surface receptors. BTLA is a ligand for tumour necrosis factor (receptor) superfamily, member 14 (TNFRSF14), also known as herpes virus entry mediator (HVEM). BTLA-HVEM complexes negatively regulate T-cell immune responses.

Clinical significance[edit]

BTLA activation inhibits the function of human CD8+ cancer-specific T cells.[3]


  1. ^ Watanabe N, Gavrieli M, Sedy JR, Yang J, Fallarino F, Loftin SK, Hurchla MA, Zimmerman N, Sim J, Zang X, Murphy TL, Russell JH, Allison JP, Murphy KM (Jun 2003). "BTLA is a lymphocyte inhibitory receptor with similarities to CTLA-4 and PD-1". Nat Immunol 4 (7): 670–9. doi:10.1038/ni944. PMID 12796776. 
  2. ^ a b "Entrez Gene: BTLA B and T lymphocyte associated". 
  3. ^ Derré L, Rivals J-P, Jandus C, Pastor S, Rimoldi D, Romero P, Michielin O, Olive D, Speiser DE (2009). "BTLA mediates inhibition of human tumor-specific CD8+ T cells that can be partially reversed by vaccination". J Clin Invest 120 (1): 157–67. doi:10.1172/JCI40070. PMC 2799219. PMID 20038811. Lay summaryGenetic Engineering & Biotechnology News. 

Further reading[edit]

External links[edit]

This article incorporates text from the United States National Library of Medicine, which is in the public domain.