InVivoMAb anti-mouse BTLA (CD272)

CloneCatalog #Category
HMBT-6B2 BE0364InVivoMAb Antibodies
$150 - $3920 Login for Academic & Non-profit Pricing

About InVivoMAb anti-mouse BTLA (CD272)

The HMBT-6B2 monoclonal antibody reacts with mouse B- and T-lymphocyte attenuator (BTLA) also known as CD272. BTLA is an Ig superfamily member which is expressed on B cells, T cells, macrophages, dendritic cells, NK cells, and NKT cells. Like PD-1 and CTLA-4, BTLA interacts with a B7 homolog, B7-H4.  However, unlike PD-1 and CTLA-4, BTLA displays T cell inhibition via interaction with tumor necrosis family receptors, not just the B7 family of cell surface receptors. BTLA is a ligand for herpes virus entry mediator (HVEM). BTLA-HVEM complexes have been shown to negatively regulate T cell immune responses.

InVivoMAb anti-mouse BTLA (CD272) Specifications

Isotype Armenian Hamster IgG
Immunogen Mouse BTLA-Fc fusion protein
Reported Applications
  • in vivo BTLA blockade
  • Flow cytometry
Formulation
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives
Endotoxin
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
Purity
  • >95%
  • Determined by SDS-PAGE
Sterility 0.2 μM filtered
Production Purified from tissue culture supernatant in an animal free facility
Purification Protein G
RRID AB_2894782
Molecular Weight 150 kDa
Storage The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.

Application References

InVivoMAb anti-mouse BTLA (CD272)

  • Flow cytometry

Mathew, R., et al. (2014). "A negative feedback loop mediated by the Bcl6-cullin 3 complex limits Tfh cell differentiation." J Exp Med 211(6): 1137-1151. PubMed

Induction of Bcl6 (B cell lymphoma 6) is essential for T follicular helper (Tfh) cell differentiation of antigen-stimulated CD4(+) T cells. Intriguingly, we found that Bcl6 was also highly and transiently expressed during the CD4(+)CD8(+) (double positive [DP]) stage of T cell development, in association with the E3 ligase cullin 3 (Cul3), a novel binding partner of Bcl6 which ubiquitinates histone proteins. DP stage-specific deletion of the E3 ligase Cul3, or of Bcl6, induced the derepression of the Bcl6 target genes Batf (basic leucine zipper transcription factor, ATF-like) and Bcl6, in part through epigenetic modifications of CD4(+) single-positive thymocytes. Although they maintained an apparently normal phenotype after emigration, they expressed increased amounts of Batf and Bcl6 at basal state and produced explosive and prolonged Tfh responses upon subsequent antigen encounter. Ablation of Cul3 in mature CD4(+) splenocytes also resulted in dramatically exaggerated Tfh responses. Thus, although previous studies have emphasized the essential role of Bcl6 in inducing Tfh responses, our findings reveal that Bcl6-Cul3 complexes also provide essential negative feedback regulation during both thymocyte development and T cell activation to restrain excessive Tfh responses.

  • in vivo BTLA blockade

Ishida, W., et al. (2012). "B and T lymphocyte attenuator regulates the development of antigen-induced experimental conjunctivitis." Graefes Arch Clin Exp Ophthalmol 250(2): 289-295. PubMed

PURPOSE: To investigate the roles that B and T lymphocyte attenuator (BTLA) and herpesvirus entry mediator (HVEM) play in the development of antigen-induced experimental conjunctivitis (EC). METHODS: BALB/c mice were immunized with ragweed (RW) in alum. Ten days later, the mice were challenged with RW in eye drops. After 24 hours, the conjunctivas, blood and spleens were collected for histological analysis, measurement of serum immunoglobulin (Ig) levels, and both flow cytometric analysis and cytokine assays, respectively. The mice were injected intraperitoneally with anti-BTLA antibody, anti-HVEM antibody or control antibody during either induction phase or effector phase. RESULTS: Induction-phase treatment with anti-BTLA antibody but not anti-HVEM antibody significantly increased conjunctival eosinophil infiltration. Treatment with either antibody during the effector phase did not affect conjunctival eosinophil infiltration. Anti-BTLA antibody treatment during the induction phase reduced the B cell compartment and increased the CD11b-positive cell compartment in splenocytes. Additionally, anti-BTLA treatment upregulated IL-4 and IL-10 production of splenocytes stimulated by RW. CONCLUSIONS: BTLA regulated the development of EC possibly by downregulating Th2 cytokine production and adjusting the compartments of immunocompetent cells. The regulation of EC by BTLA may be mediated by BTLA ligands other than HVEM.