InVivoMAb anti-mouse MHC Class I (H-2Kd, H-2Dd)
About InVivoMAb anti-mouse MHC Class I (H-2Kd, H-2Dd)
The 34-1-2S monoclonal antibody is reported to react with the mouse H-2Kb and H-2Dd MHC class I alloantigens. MHC class I antigens are heterodimers consisting of one alpha chain (44 kDa) associated with β2 microglobulin (11.5 kDa). The antigen is expressed by all nucleated cells at varying levels. MHC Class I molecules present endogenously synthesized antigenic peptides to CD8 T cells.
InVivoMAb anti-mouse MHC Class I (H-2Kd, H-2Dd) 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)|
BDF mouse spleen cells
in vivo activation of APCs
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 MHC Class I (H-2Kd, H-2Dd) (Clone: 34-1-2S)Kapur, R., et al. (2015). "C-reactive protein (CRP) enhances murine antibody-mediated transfusion-related acute lung injury (TRALI)." Blood. pii: blood-2015-09-672592. PubMed
Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory distress triggered by blood transfusions and is the leading cause of transfusion-related mortality. TRALI has primarily been attributed to passive infusion of human leucocyte antigen (HLA) and/or human neutrophil antigen (HNA) antibodies present in transfused blood products and predisposing factors such as inflammation are known to be important for TRALI-initiation. Since the acute phase protein C-reactive protein (CRP) is highly up-regulated during infections and inflammation and can also enhance antibody-mediated responses such as in vitro phagocytosis, respiratory burst and in vivo thrombocytopenia, we investigated whether CRP affects murine antibody-mediated TRALI induced by the anti-MHC antibody, 34-1-2s. We found that BALB/c mice administered with 34-1-2s or CRP alone were resistant to TRALI, but mice injected with 34-1-2s together with CRP had significantly enhanced lung damage and pulmonary edema. Mechanistically, 34-1-2s injection with CRP resulted in a significant synergistic increase in plasma levels of the neutrophil chemoattractant, macrophage inflammatory protein-2 (MIP-2) and pulmonary neutrophil accumulation. Importantly, murine MIP-2 is the functional homologue of human IL-8, a known risk factor for human TRALI. These results suggest that elevated in vivo CRP levels, like those observed during infections, may significantly predispose recipients to antibody-mediated TRALI reactions and support the notion that modulating CRP levels is an effective therapeutic strategy to reduce TRALI-severity.