DATASHEET
Host:
Rabbit
Target Protein:
HLA-DPB1
Immunogen Range:
101-210/258
Clonality:
Polyclonal
Isotype:
IgG
Entrez Gene:
3115
Swiss Prot:
P04440
Source:
KLH conjugated synthetic peptide derived from human DPB1
Purification:
Purified by Protein A.
Storage Buffer:
0.01M TBS(pH7.4) with 1% BSA, 0.02% Proclin300 and 50% Glycerol.
Storage:
Shipped at 4°C. Store at -20°C for one year. Avoid repeated freeze/thaw cycles.
Background:
Binds peptides derived from antigens that access the endocytic route of antigen presenting cells (APC) and presents them on the cell surface for recognition by the CD4 T-cells. The peptide binding cleft accommodates peptides of 10-30 residues. The peptides presented by MHC class II molecules are generated mostly by degradation of proteins that access the endocytic route, where they are processed by lysosomal proteases and other hydrolases. Exogenous antigens that have been endocytosed by the APC are thus readily available for presentation via MHC II molecules, and for this reason this antigen presentation pathway is usually referred to as exogenous. As membrane proteins on their way to degradation in lysosomes as part of their normal turn-over are also contained in the endosomal/lysosomal compartments, exogenous antigens must compete with those derived from endogenous components. Autophagy is also a source of endogenous peptides, autophagosomes constitutively fuse with MHC class II loading compartments. In addition to APCs, other cells of the gastrointestinal tract, such as epithelial cells, express MHC class II molecules and CD74 and act as APCs, which is an unusual trait of the GI tract. To produce a MHC class II molecule that presents an antigen, three MHC class II molecules (heterodimers of an alpha and a beta chain) associate with a CD74 trimer in the ER to form a heterononamer. Soon after the entry of this complex into the endosomal/lysosomal system where antigen processing occurs, CD74 undergoes a sequential degradation by various proteases, including CTSS and CTSL, leaving a small fragment termed CLIP (class-II-associated invariant chain peptide). The removal of CLIP is facilitated by HLA-DM via direct binding to the alpha-beta-CLIP complex so that CLIP is released. HLA-DM stabilizes MHC class II molecules until primary high affinity antigenic peptides are bound. The MHC II molecule bound to a peptide is then transported to the cell membrane surface.
PRODUCT SPECIFIC PUBLICATIONS
- Li et al. lncRNA Malat1 modulates the maturation process, cytokine secretion and apoptosis in airway epithelial cell-conditioned dendritic cells. (2018) Exp.Ther.Med. 16:3951-3958Read more>>
- Chengxiao Wang. et al. Dissolvable microneedles based on Panax notoginseng polysaccharide for transdermal drug delivery and skin dendritic cell activation. Carbohyd Polym. 2021 May;:118211Read more>>
- Yanqiao Wen. et al. Regulation of Yujin Powder alcoholic extracts on ILC3s-TD IgA-colonic mucosal flora axis of DSS-induced ulcerative colitis.. FRONT MICROBIOL. 2022 Oct;13:1039884-1039884Read more>>
VALIDATION IMAGES
Formalin-fixed and paraffin embedded human lung carcinoma labeled with Anti-MHC Class II/HLA-DPB1 Polyclonal Antibody, Unconjugated (bs-4107R) at 1:200 followed by conjugation to the secondary antibody and DAB staining.
Mouse lymph node lysates probed with MHC Class II/HLA DMB Polyclonal Antibody, Unconjugated (bs-4107R) at 1:500 dilution and 4˚C overnight incubation. Followed by conjugated secondary antibody incubation at 1:20000 for 60 min at 37˚C.
Mouse spleen cells were fixed with 4% PFA for 10min at room temperature, permeabilized with 20% PBST for 20 min at room temperature, and incubated in 5% BSA blocking buffer for 30 min at room temperature. Cells were then stained with HLA-DPB1 Polyclonal Antibody, ALEXA FLUOR® 647 Conjugated (bs-4107R-AF647) at 1:50 dilution in blocking buffer and incubated for 30 min at room temperature, washed twice with 2% BSA in PBS. Acquisitions of 20,000 events were performed. Cells stained with primary antibody (green) and isotype control (orange).