Ultra-LEAF™ Purified anti-human CD273 (B7-DC, PD-L2) Antibody, CD273, A20050B,BioLegend,947803

Host

Rat

Reactivity

Human

Application

Block - Quality tested

Platform ID

BAB614972931

BioLegend

Headquarters

8999 BioLegend Way San Diego, CA 92121 United States

Contact

Tel: 1-858-455-9588
Fax: +49 (4131) 7023913

Email:

Product Specifications
Scientific Background

Specifications

NameUltra-LEAF™ Purified anti-human CD273 (B7-DC, PD-L2) Antibody, CD273, A20050B
Cat. No.947803
HostRat
RRIDAB_2894535 (BioLegend Cat. No. 947803)AB_2894535 (BioLegend Cat. No. 947804)
IsotypeRat IgG2b, κ
ReactivityHuman
ApplicationBlock - Quality tested
ClonalityMonoclonal
Clone NumberA20050B
ConcentrationThe antibody is bottled at the concentration indicated on the vial, typically between 2 mg/mL and 3 mg/mL. Older lots may have also been bottled at 1 mg/mL. To obtain lot-specific concentration and expiration, please enter the lot number in ourCertificate of Analysisonline tool.
TargetCD273
ImmunogenRecombinant human PD-L2 (B7-DC, CD273)-Fc chimera
PurityThe Ultra-LEAF™ (Low Endotoxin, Azide-Free) antibody was purified by affinity chromatography.
Formulation0.2 µm filtered in phosphate-buffered solution, pH 7.2, containing no preservative.
StorageThe antibody solution should be stored undiluted between 2°C and 8°C. This Ultra-LEAF™ solution contains no preservative; handle under aseptic conditions.
Regulatory StatusResearch Use Only

Scientific Background

PD-L2 is a type I transmembrane protein of 273 amino acids, and it is a member of the B7 family. Human PD-L2 has 70% amino acid identity to its mouse orthologue. PD-L2 is the second ligand for PD-1, and its binding to PD-1 leads to the inhibition of T cell receptor–mediated lymphocyte proliferation and cytokine secretion. PD-L2/PD-1 interaction suppresses immune responses against autoantigens and tumors and plays an important role in the maintenance of peripheral immune tolerance. Antibody blocking of PD-L2 on dendritic cells results in enhanced T cell proliferation and cytokine production. Interaction of PD-1 by PD-L1-Ig or PD-L2-Ig fusion protein has an inhibitory effect on proliferation and cytokine production during anti-CD3-mediated stimulation. PD-L2 is expressed in biopsies from human asthmatics and lungs of aeroallergen-treated mice and its expression correlates with the asthma severity. In vivo blockade of PD-L2 reduces the severity of allergen-driven airway hyperresponsiveness (AHR).  Blockage of PD-L2 induces the IL-12 production by DC; IL-12 may limit the severity of allergen-induced AHR antagonizing IL-13. In addition, blockade of PD-1 does not have effect on AHR; therefore, PD-L2 controls asthma severity in a PD-1 independent manner. PD-L2 binds to a second receptor, RGMb (repulsive guidance molecule b) which is expressed in lung interstitial macrophages and alveolar epithelial cells and is a co-receptor for bone morphogenetic proteins BMP2/4. Blockade of the RGMb/PD-L2 interaction significantly impaired the development of respiratory tolerance since the initial T cell expansion is inhibited.

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