Anti-Human CD22 Antibody Pair

Product Description: CD22 molecule (CD22), also known as SIGLEC-2, is a regulatory molecule that plays a crucial role in preventing the overactivation of the immune system and the development of autoimmune diseases. It is a transmembrane protein found on the surface of mature B cells and to a lesser extent on some immature B cells. CD22 functions as an inhibitory receptor for B cell receptor (BCR) signaling by binding to sialic acid-containing ligands, which leads to the inhibition of BCR signaling through the association with SHP-1, a protein tyrosine phosphatase. The molecule consists of seven immunoglobulin domains in its extracellular part and a 141-amino acid cytoplasmic tail. The glycosylation of CD22 is essential for its surface expression and epitope recognition by monoclonal antibodies. CD22 is involved in B cell trafficking to Peyer's patches in mice and has been shown to restore homeostatic microglial phagocytosis in aging brains when blocked. Protein Function: Most highly expressed siglec (sialic acid-binding immunoglobulin-like lectin) on B-cells that plays a role in various aspects of B-cell biology including differentiation, antigen presentation, and trafficking to bone marrow (PubMed:34330755, PubMed:8627166). Binds to alpha 2,6-linked sialic acid residues of surface molecules such as CD22 itself, CD45 and IgM in a cis configuration. Can also bind to ligands on other cells as an adhesion molecule in a trans configuration (PubMed:20172905). Acts as an inhibitory coreceptor on the surface of B-cells and inhibits B-cell receptor induced signaling, characterized by inhibition of the calcium mobilization and cellular activation. Mechanistically, the immunoreceptor tyrosine-based inhibitory motif domain is phosphorylated by the Src kinase LYN, which in turn leads to the recruitment of the protein tyrosine phosphatase 1/PTPN6, leading to the negative regulation of BCR signaling (PubMed:8627166). If this negative signaling from is of sufficient strength, apoptosis of the B-cell can be induced (PubMed:20516366) [The Uniprot Consortium]