InVivoMAb anti-mouse/rat MHC Class II (I-Ek/RT1-D)
|14-4-4S (HB32)||BE0167||InVivoMab Antibodies|
About InVivoMAb anti-mouse/rat MHC Class II (I-Ek/RT1-D)
The 14-4-4S monoclonal antibody reacts with mouse MHC Class II alloantigen I-Ek and the rat MHC class II alloantigen RT1D. These MHC class II molecules are expressed primarily on the surface of B lymphocytes, macrophages, dendritic cells and other antigen presenting cells as well as a subset of T cells from H-2k bearing mice. These MHC molecules play a role in antigen presentation to T cells. The 14-4-4S antibody has been reported to block antigen presentation and induce differentiation of mouse cells expressing I-Ek.
InVivoMAb anti-mouse/rat MHC Class II (I-Ek/RT1-D) Specifications
Mouse IgG2a, κ
|Recommended Isotype Control(s)||InVivoMAb mouse IgG2a isotype control, unknown specificity(BE0085)|
|Recommended InVivoPure Dilution Buffer||InVivoPure pH 7.0 Dilution Buffer(IP0070)|
C3H mouse skin graft and spleen cells
0.2 μM filtered
Purified from tissue culture supernatant in an animal free facility
The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
InVivoMAb anti-mouse/rat MHC Class II (I-Ek/RT1-D) (Clone: 14-4-4S (HB32))Haag, S., et al. (2015). "Positional identification of RT1-B (HLA-DQ) as susceptibility locus for autoimmune arthritis." J Immunol 194(6): 2539-2550. PubMed
Rheumatoid arthritis (RA) is associated with amino acid variants in multiple MHC molecules. The association to MHC class II (MHC-II) has been studied in several animal models of RA. In most cases these models depend on T cells restricted to a single immunodominant peptide of the immunizing Ag, which does not resemble the autoreactive T cells in RA. An exception is pristane-induced arthritis (PIA) in the rat where polyclonal T cells induce chronic arthritis after being primed against endogenous Ags. In this study, we used a mixed genetic and functional approach to show that RT1-Ba and RT1-Bb (RT1-B locus), the rat orthologs of HLA-DQA and HLA-DQB, determine the onset and severity of PIA. We isolated a 0.2-Mb interval within the MHC-II locus of three MHC-congenic strains, of which two were protected from severe PIA. Comparison of sequence and expression variation, as well as in vivo blocking of RT1-B and RT1-D (HLA-DR), showed that arthritis in these strains is regulated by coding polymorphisms in the RT1-B genes. Motif prediction based on MHC-II eluted peptides and structural homology modeling suggested that variants in the RT1-B P1 pocket, which likely affect the editing capacity by RT1-DM, are important for the development of PIA.