CLE21 Antibody

Molecular Structure and Function of CLEC-2 Antibodies

CLEC-2 (C-type lectin domain family 1 member B) is a ~32 kDa type II transmembrane glycoprotein expressed on platelets, megakaryocytes, and myeloid cells. Its extracellular domain contains a single carbohydrate recognition domain (CRD), while the cytoplasmic region includes a YXXL hemITAM motif critical for signaling . Antibodies targeting CLEC-2 are designed to modulate its interactions with ligands like podoplanin or snake venom proteins (e.g., rhodocytin), influencing platelet activation, thrombosis, and immune responses .

Data synthesized from .

Target-Specific Antibodies and Their Mechanisms

Several monoclonal antibodies (mAbs) have been developed to study CLEC-2 function:

AYP1 and HEL1 Antibodies

• AYP1:

  • Epitope: Distinct from HEL1; blocks podoplanin-induced platelet aggregation .

  • Fab fragments: Do not inhibit platelet aggregation, suggesting full-length IgG is required for dimerization-driven activation .

  • Immunodepletion: Depletes CLEC-2 from human platelets for ~11 days post-injection .

• HEL1:

  • Epitope: Non-overlapping with AYP1; induces platelet aggregation via CLEC-2 dimerization .

  • Fab Fragments: Fail to block aggregation, confirming activation requires intact IgG .

BD OptiBuild™ BV421 Mouse Anti-Human CLEC-2

• Conjugate: BD Horizon™ BV421 dye (Ex: 407 nm, Em: 421 nm), enabling detection via Pacific Blue™ filters .

• Brightness: 10x brighter than Pacific Blue™ conjugates, enhancing flow cytometry sensitivity .

• Applications: Flow cytometry, immunoprecipitation, and research on platelet activation .

Platelet Activation and Thrombosis

• Podoplanin-Binding Studies: Antibodies like AYP1 and HEL1 disrupt podoplanin-CLEC-2 interactions, inhibiting platelet aggregation and thrombus formation .

• Snake Venom Proteins: CLEC-2 antibodies neutralize rhodocytin-induced platelet activation, validating CLEC-2 as a therapeutic target .

Immunodepletion and Functional Studies

• Human CLEC-2 Knock-In (KI) Models: Antibodies (AYP1/HEL1) deplete CLEC-2 from platelets, reducing aggregation responses to collagen or ADP .

• Cross-Reactivity: No significant differences in platelet function between human CLEC-2 KI and wild-type mice, supporting translational relevance .

Antibody-Dependent Cellular Cytotoxicity (ADCC)

• Mechanism: CLEC-2 antibodies may recruit immune effector cells (e.g., NK cells) via Fcγ receptors, promoting target cell lysis .

• Therapeutic Potential: Targeting CLEC-2 in cancer (e.g., metastatic tumors expressing podoplanin) or infectious diseases (e.g., HIV-1 entry) .