Western blot shows lysates of human peripheral blood mononuclear cells (PBMC). PVDF membrane was probed with 2 µg/mL of Mouse Anti-Human CD1d Monoclonal Antibody (Catalog # MAB6979) followed by HRP-conjugated Anti-Mouse IgG Secondary Antibody (Catalog # HAF007). A specific band was detected for CD1d at approximately 52 kDa (as indicated). This experiment was conducted under reducing conditions and using Immunoblot Buffer Group 1.
Preparation and Storage
Sterile PBS to a final concentration of 0.5 mg/mL.
Reconstitution Buffer Available
The product is shipped at ambient temperature. Upon receipt, store it immediately at the temperature recommended below. *Small pack size (SP) is shipped with polar packs. Upon receipt, store it immediately at -20 to -70 °C
Stability & Storage
Use a manual defrost freezer and avoid repeated freeze-thaw cycles.
12 months from date of receipt, -20 to -70 °C as supplied.
1 month, 2 to 8 °C under sterile conditions after reconstitution.
6 months, -20 to -70 °C under sterile conditions after reconstitution.
CD1d is a 48 kDa transmembrane glycoprotein in the CD1 family of glycolipid antigen-presenting MHC-like molecules. Mature human CD1d consists of a 282 amino acid (aa) extracellular domain (ECD) with one Ig-like domain, a 21 aa transmembrane segment, and a 13 aa cytoplasmic tail. Within aa 19-300 (the ECD), human CD1d shares 65% and 68% aa sequence identity with mouse and rat CD1d, respectively. Complexes of CD1d with beta 2-microglobulin and endogenous glycolipids are constitutively expressed on antigen presenting cells, cortical thymocytes, liver sinusoidal endothelial cells, Kupffer cells, and hepatocytes (1). CD1d-presented glycolipids are recognized by canonical NKT cells that utilize an invariant mouse Va14-Ja18 chain in their T cell receptor (Va24-Ja18 in human) (2, 3). The interaction with glycolipid-loaded CD1d is critical for NKT cell development and induces their rapid secretion of both Th1 and Th2 type cytokines (3-6). In humans, infection with HSV-1 suppresses NKT cell activation by blocking the intracellular cycling of CD1d in antigen presenting cells (7).
Bendelac, A. et al. (2007) Annu. Rev. Immunol. 25:297.
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