InVivoMAb anti-mouse MHC Class I (H-2Kk, H-2Dk)

Clone Catalog # Category
15-3-1S (HB13) BE0158 InVivoMab Antibodies
$95 - $3250

About InVivoMAb anti-mouse MHC Class I (H-2Kk, H-2Dk)

The 15-3-1S monoclonal antibody reacts with the mouse H-2Kk and H-2Dk 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-2Kk, H-2Dk) 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 spleen cells

Reported Applications
  • in vivo administration
  • Flow cytometry
  • <2EU/mg (<0.002EU/μg)
  • Determined by LAL gel clotting assay
  • >95%
  • Determined by SDS-PAGE
  • PBS, pH 7.0
  • Contains no stabilizers or preservatives

0.2 μM filtered


Purified from tissue culture supernatant in an animal free facility


Protein G


The antibody solution should be stored undiluted at 4°C, and protected from prolonged exposure to light. Do not freeze.



Molecular Weight

150 kDa

Application References

InVivoMAb anti-mouse MHC Class I (H-2Kk, H-2Dk) (Clone: 15-3-1S (HB13))

Hirohashi, T., et al. (2012). "A novel pathway of chronic allograft rejection mediated by NK cells and alloantibody." Am J Transplant 12(2): 313-321. PubMed

Chronic allograft vasculopathy (CAV) in murine heart allografts can be elicited by adoptive transfer of donor specific antibody (DSA) to class I MHC antigens and is independent of complement. Here we address the mechanism by which DSA causes CAV. B6.RAG1(-/-) or B6.RAG1(-/-)C3(-/-) (H-2(b)) mice received B10.BR (H-2(k)) heart allografts and repeated doses of IgG2a, IgG1 or F(ab')(2) fragments of IgG2a DSA (anti-H-2(k)). Intact DSA regularly elicited markedly stenotic CAV in recipients over 28 days. In contrast, depletion of NK cells with anti-NK1.1 reduced significantly DSA-induced CAV, as judged morphometrically. Recipients genetically deficient in mature NK cells (gamma-chain knock out) also showed decreased severity of DSA-induced CAV. Direct NK reactivity to the graft was not necessary. F(ab')(2) DSA fragments, even at doses twofold higher than intact DSA, were inactive. Graft microvascular endothelial cells responded to DSA in vivo by increased expression of phospho-extracellular signal-regulated kinase (pERK), a response not elicited by F(ab')(2) DSA. We conclude that antibody mediates CAV through NK cells, by an Fc dependent manner. This new pathway adds to the possible mechanisms of chronic rejection and may relate to the recently described C4d-negative chronic antibody-mediated rejection in humans.

Sheng-Tanner, X., et al. (2000). "Characterization of graft-versus-host disease in SCID mice and prevention by physicochemical stressors." Transplantation 70(12): 1683-1693. PubMed

BACKGROUND: Graft versus host disease (GVHD) prevents potentially curative allogeneic stem cell transplantation from being offered to cancer patients who lack a suitably matched donor. New methods to prevent GVHD are required to allow successful transplants across major histocompatibility complex barriers. METHODS: A model of GVHD in C.B-17 SCID mice was developed to allow the study of allo-activated donor T cells without confounding effects of host lymphocytes. The abilities of cyclosporin-A, anticytokine antibodies, and oxidative stress to prevent GVHD in this model was studied. RESULTS: T cells from major histocompatibility-mismatched donor mice caused severe GVHD in sublethally irradiated SCID hosts that could be ameliorated by coadministration of donor bone marrow but not by cyclosporine-A or anticytokine antibodies. In contrast, three-log more T cells could be injected without clinical consequences if they had been pretreated with a combination of heat, ultraviolet light, and oxygenation. The effect was not the trivial result of donor T cell destruction because T cell reconstitution, although delayed, recovered to normal levels within 2 weeks. Protection from GVHD required oxygenation and was associated with normalization of the CD4/CD8 donor T cell ratio, recovery of host hematopoiesis, and decreased inflammatory cytokine production. CONCLUSION: Pretreatment of donor T cells with a combination of physicochemical stressors effectively prevents GVHD caused by major major histocompatibility disparities and may facilitate the safe transplantation of patients without HLA-identical donors.

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