RecombiMAb anti-mouse PD-1 (CD279)
(switched from rat IgG2a)
Product Details
The RMP1-14-CP157 monoclonal antibody is a chimeric version of the original RMP1-14 antibody. The variable domain sequences are identical to the original RMP1-14 but the constant region sequences have been switched from rat IgG2a to mouse IgG2a. The RMP1-14-CP157 antibody contains no Fc mutations just as the original rat IgG2a antibody does not. RMP1-14-CP157 reacts with mouse PD-1 (programmed death-1) also known as CD279. PD-1 is a 50-55 kDa cell surface receptor encoded by the Pdcd1 gene that belongs to the CD28 family of the Ig superfamily. PD-1 is transiently expressed on CD4 and CD8 thymocytes as well as activated T and B lymphocytes and myeloid cells. PD-1 expression declines after successful elimination of antigen. Additionally, Pdcd1 mRNA is expressed in developing B lymphocytes during the pro-B-cell stage. PD-1ās structure includes a ITIM (immunoreceptor tyrosine-based inhibitory motif) suggesting that PD-1 negatively regulates TCR signals. PD-1 signals via binding its two ligands, PD-L1 and PD-L2 both members of the B7 family. Upon ligand binding, PD-1 signaling inhibits T-cell activation, leading to reduced proliferation, cytokine production, and T-cell death. Additionally, PD-1 is known to play key roles in peripheral tolerance and prevention of autoimmune disease in mice as PD-1 knockout animals show dilated cardiomyopathy, splenomegaly, and loss of peripheral tolerance. Induced PD-L1 expression is common in many tumors including squamous cell carcinoma, colon adenocarcinoma, and breast adenocarcinoma. PD-L1 overexpression results in increased resistance of tumor cells to CD8 T cell mediated lysis. In mouse models of melanoma, tumor growth can be transiently arrested via treatment with antibodies which block the interaction between PD-L1 and its receptor PD-1. For these reasons anti-PD-1 mediated immunotherapies are currently being explored as cancer treatments.Specifications
| Isotype | Mouse IgG2a,Ā Īŗ |
|---|---|
| Recommended Isotype Control(s) | InVivoPlus mouse IgG2a isotype control, unknown specificity |
| Recommended Dilution Buffer | InVivoPure pH 7.0 Dilution Buffer |
| Conjugation | This product is unconjugated. Conjugation is available via our Antibody Conjugation Services. |
| Immunogen | Syrian Hamster BKH cells transfected with mouse PD-1 cDNA |
| Reported Applications |
in vivo blocking of PD-1/PD-L signaling* *Reported for the original rat IgG2a RMP1-14 antibody |
| Formulation |
PBS, pH 7.0 Contains no stabilizers or preservatives |
| Endotoxin |
<1EU/mg (<0.001EU/Ī¼g) Determined by LAL gel clotting assay |
| Aggregation |
<5% Determined by SEC |
| Purity |
>95% Determined by SDS-PAGE |
| Sterility | 0.2 Āµm filtration |
| Production | Purified from CHO cell supernatant in an animal-free facility |
| Purification | Protein A |
| RRID | AB_2927526 |
| Molecular Weight | 150 kDa |
| Murine Pathogen Tests |
Ectromelia/Mousepox Virus: Negative Hantavirus: Negative K Virus: Negative Lactate Dehydrogenase-Elevating Virus: Negative Lymphocytic Choriomeningitis virus: Negative Mouse Adenovirus: Negative Mouse Cytomegalovirus: Negative Mouse Hepatitis Virus: Negative Mouse Minute Virus: Negative Mouse Norovirus: Negative Mouse Parvovirus: Negative Mouse Rotavirus: Negative Mycoplasma Pulmonis: Negative Pneumonia Virus of Mice: Negative Polyoma Virus: Negative Reovirus Screen: Negative Sendai Virus: Negative Theilerās Murine Encephalomyelitis: Negative |
| Storage | The antibody solution should be stored at the stock concentration at 4Ā°C. Do not freeze. |
Additional Formats
Recommended Products
-
Recommended Isotype Control(s)
InVivoPlus mouse IgG2a isotype control, unknown specificity
-
Recommended Dilution Buffer
InVivoPure pH 7.0 Dilution Buffer
See the references for the original rat IgG2a RMP1-14 antibody (https://bioxcell.com/catalogsearch/result/?q=BP0146).
- Cancer Research,
- Immunology and Microbiology
Forced intracellular degradation of xenoantigens as a modality for cell-based cancer immunotherapy.
In IScience on 21 March 2025 by Bikorimana, J. P., Farah, R., et al.
Given recent leverage of mesenchymal stromal cells (MSCs) as a potent vaccination platform, we investigated whether forced degradation of an expressed experimental antigen fused to small degron sequences could prime potent antitumoral responses. Retrovirally gene-engineered MSCs were evaluated for their in-vitro antigen presentation capacity, nature of generated peptide repertoire and therapeutic potency in syngeneic immunocompetent mice with pre-established solid TĀ cell lymphoma. Despite lack of noticeable changes in gene expression, MSC-UBvR-OVA vaccination triggered potent TĀ cell activation which can be attributable to the enriched cell surface presentation of OVA-derived peptides added to elevated mitochondrial reactive oxidative species (ROS) production, the latter being associated with efficient antigen processing. Where MSC-UBvR-OVA vaccination successfully controlled tumor growth in cancer-bearing mice, the effect is further enhanced using tranylcypromine-stimulated MSCs and anti-PD-1 combination. Such anti-tumoral response relies on efferocytosis by endogenous phagocytes. Altogether, UBvR facilitated forced antigen degradation represents a plausible modality for future development of tumor antigen-expressing MSC-based vaccine. Ā© 2025 The Author(s).
- Mus musculus (House mouse)
A1-reprogrammed mesenchymal stromal cells prime potent antitumoral responses.
In IScience on 15 March 2024 by GonƧalves, M. P., Farah, R., et al.
Mesenchymal stromal cells (MSCs) have been modified via genetic or pharmacological engineering into potent antigen-presenting cells-like capable of priming responding CD8 TĀ cells. In this study, our screening of a variant library of Accum molecule revealed a molecule (A1) capable of eliciting antigen cross-presentation properties in MSCs. A1-reprogrammed MSCs (ARM) exhibited improved soluble antigen uptake and processing. Our comprehensive analysis, encompassing cross-presentation assays and molecular profiling, among other cellular investigations, elucidated A1's impact on endosomal escape, reactive oxygen species production, and cytokine secretion. By evaluating ARM-based cellular vaccine in mouse models of lymphoma and melanoma, we observe significant therapeutic potency, particularly in allogeneic setting and in combination with anti-PD-1 immune checkpoint inhibitor. Overall, this study introduces a strong target for developing an antigen-adaptable vaccination platform, capable of synergizing with immune checkpoint blockers to trigger tumor regression, supporting further investigation of ARMs as an effective and versatile anti-cancer vaccine. Ā© 2024 The Author(s).
