Catalog No.	PA007164.r2b
Product Name	Anti-mouse PD-L1 Antibody (B7-H1, 10F.9G2.1) | PA007164.r2b
Supplier Name	Syd Labs, Inc.
Brand Name	Syd Labs
Synonyms	Programmed Death Ligand 1, B7-H1, CD274, 10F.9G2 antibody
Summary	The in vivo grade recombinant anti-mouse PD-L1 / B7-H1 monoclonal antibody (rat IgG2b kappa) was produced in mammalian cells.
Clone	10F.9G2.1, the same variable region and constant region sequences as the rat anti-mouse PD-L1 monoclonal antibody (clone: 10F.9G2)
Isotype	Mouse IgG1, kappa
Applications	immunohistochemistry (IHC), Flow Cytometry (FC), and various in vitro and in vivo functional assays.
Immunogen	The original rat hybridoma (clone: 10F.9G2) was generated by immunizing rats with the mouse PD-L1 cDNA and mouse PD-L1 CHO transfectants.
Form Of Antibody	0.2 μM filtered solution of 1x PBS.
Endotoxin	Less than 1 EU/mg of protein as determined by LAL method.
Purity	>95% by SDS-PAGE under reducing conditions.
Shipping	The in vivo grade recombinant anti-mouse PD L1/B7-H1 monoclonal antibodies are shipped with ice pack. Upon receipt, store it immediately at the temperature recommended below.
Stability & Storage	Use a manual defrost freezer and avoid repeated freeze-thaw cycles. 1 month from date of receipt, 2 to 8°C as supplied. 3 months from date of receipt, -20°C to -70°C as supplied.
Note	Recombinant anti-mouse PD L1/B7-H1 monoclonal antibodies, which share the same variable region sequences with the rat anti-mouse PD L1 monoclonal antibody (clone number: 10F.9G2), are produced from mammalian cells and good for in vitro and in vivo studies.
Order Offline	Phone: 1-617-401-8149 Fax: 1-617-606-5022 Email: message@sydlabs.com Or leave a message with a formal purchase order (PO) Or credit card.

Description

PA007164.r2b: Recombinant Anti-mouse PD-L1 Antibody (Clone: 10F.9G2.1), Mouse IgG1, kappa, In Vivo Grade

The rat anti-mouse PD-L1 monoclonal antibody 10F.9G2 (rat IgG2b kappa) reacts with the mouse PD-L1 protein (programmed death ligand-1, B7-H1 or CD274 antibody), a member of the B7 family of the Ig superfamily. PD-1 has two ligands, PD-L1 and PD-L2. It has been shown that in mouse models of melanoma, tumor growth can be transiently arrested via treatment with the anti-mouse PD-1 and anti-mouse PD-L1 antibodies which block the interaction between the PD-L1 protein and its receptor PD-1 protein. The 10F.9G2 monoclonal antibody blocks the binding of the mouse PD-L1 protein to the mouse PD-1 protein.

Our recombinant 10F.9G2 antibodies have a part (variable regions) or complete amino acid sequences of the rat anti-mouse PD L1 monoclonal antibody (hybridoma clone name or number: 10F.9G2).

References for Anti-mouse PD-L1 Antibody(10F.9G2.1):

1、Organotypic tumor slice cultures provide a versatile platform for immuno-oncology and drug discovery.
Ramya Sivakumar et al.. Oncoimmunology. 2019 Oct 10;8(12):e1670019. doi: 10.1080/2162402X.2019.1670019. PMID: 31741771.
“Tissue slices were treated with 1000 and 10,000U of mouse IFN-γ (Shenandoah Biotechnology, 200-16AF) for 48–60 hr; 10 μg of human anti PD-L1 antibody (Bioxcell, BE0285), mouse anti-PD-L1 antibody (Bioxcell, BE0101), anti-cytotoxic T lymphocyte antigen 4 (CTLA-4) antibody (Bioxcell, BE0164), rat IgG2b,K (Bioxcell, BE0090) or mouse IgG2b (Bioxcell, BE0086) for 48 hr. …Protein microarrays were printed and processed as described previously. …Organotypic tumor tissue slices can be used to investigate multiple hypotheses through diverse experimental approaches. …Organotypic tumor slices represent a physiologically-relevant culture system for studying the tumor microenvironment. …We found that the immune cell compositions of organotypic tumor slices prepared on the same day as the tumor cores were harvested are similar.”

2、The Antitumor Activity of Combinations of Cytotoxic Chemotherapy and Immune Checkpoint Inhibitors Is Model-Dependent.
Chloé Grasselly, et al.. Front Immunol. 2018 Oct 9;9:2100. doi: 10.3389/fimmu.2018.02100. PMID: 30356816.
“For the metastatic 4T1 breast cancer mouse model, the combination was cyclophosphamide (Baxter) injected i.p. once a week at a dose of 100 mg/kg + doxorubicin (Accord Healthcare) injected i.p. once a week at a dose of 2 mg/kg + anti-PD-1 (RMP1-14, BioXCell) or anti-PD-L1 (10F.9G2, BioXCell), injected i.p. once a week at a dose of 12.5 mg/kg. …In spite of impressive response rates in multiple cancer types, immune checkpoint inhibitors (ICIs) are active in only a minority of patients. …Here, we performed a study of PD-1 or PDL-1 blockade in combination with reference chemotherapies in four fully immunocompetent mouse models of cancer. …We observed enhanced antitumor effects of the combination of immunotherapy with chemotherapy in the MC38 colon and MB49 bladder models, a lack of response in the 4T1 breast model, and an inhibition of ICIs activity in the MBT-2 bladder model. …We found that the balance between effector cells and immunosuppressive cells in the tumor microenvironment could be altered with some treatment combinations, but this effect was not always correlated with an impact on in vivo tumor growth.”

3、PD-1 Inhibitory Receptor Downregulates Asparaginyl Endopeptidase and Maintains Foxp3 Transcription Factor Stability in Induced Regulatory T Cells.
Chaido Stathopoulou et al.. Immunity. 2018 Aug 21;49(2):247-263.e7. doi: 10.1016/j.immuni.2018.05.006. PMID: 30054205.
“Flow cytometry staining antibodies for CD4 (clone: RM4-4), CXCR3 (clone: CXCR3-173), PD-1 (clone: 29F.1A12), PDL-1 (clone: 10F.9G2), CD44 (clone: IM7), CD45.1 (clone: A20), CD45.2 (clone: 104), H-2Kb (AF6-88.5), CD62L (clone: MEL-14), CD8 (clone: 53-6.7), CCR4 (clone: 2G12), Neuropilin-1 (clone: 3E12), Helios (clone: 22F6), CD25 (clone: PC61) and CD127 (clone: A7R34) were purchased from BioLegend. …CD4+ T cell differentiation into multiple T helper (Th) cell lineages is critical for optimal adaptive immune responses. …This report identifies an intrinsic mechanism by which programmed death-1 receptor (PD-1) signaling imparted regulatory phenotype to Foxp3+ Th1 cells (denoted as Tbet+iTregPDL1 cells) and inducible regulatory T (iTreg) cells. …Programmed death ligand-1 (PDL-1) binding to PD-1 imparted regulatory function to Tbet+iTregPDL1 cells and iTreg cells by specifically downregulating endo-lysosomal protease asparaginyl endopeptidase (AEP). …Functional plasticity of cells belonging to the innate and adaptive immune system is necessary for the generation of robust immune responses while minimizing detrimental effects toward the host.”

4、Follicular regulatory T cells can be specific for the immunizing antigen and derive from naive T cells.
Aloulou M, et al. Nat Commun. 2016 Jan 28;7:10579. doi: 10.1038/ncomms10579. PMID: 26818004.
“We show that, in addition to developing from thymic derived Treg cells, Tfr cells can also arise from Foxp3− precursors in a PD-L1-dependent manner, if the adjuvant used is one that supports T-cell plasticity. …To decipher whether PD-L1 was a mechanism by which Tfr cells can differentiate from Foxp3− precursors after immunization with protein emulsified in IFA, but not CFA, we first assessed PD-L1 expression at the surface of dendritic cells (DCs). …This is striking as we have previously shown that moDCs are the main cells presenting the Ag through MHCII molecules after protein immunization. …T follicular regulatory (Tfr) cells are a subset of Foxp3+ regulatory T (Treg) cells that form in response to immunization or infection, which localize to the germinal centre where they control the magnitude of the response. …Despite an increased interest in the role of Tfr cells in humoral immunity, many fundamental aspects of their biology remain unknown, including whether they recognize self- or foreign antigen.”

5、Programmed death-1 controls T cell survival by regulating oxidative metabolism.
Victor Tkachev et al. J Immunol. 2015 Jun 15;194(12):5789-800. doi: 10.4049/jimmunol.1402180. PMID: 25972478.
“We found that both murine and human alloreactive T cells concomitantly upregulated PD-1 expression and increased levels of reactive oxygen species (ROS) following allogeneic bone marrow transplantation. …Blockade of PD-1 signaling decreased both mitochondrial H2O2 and total cellular ROS levels, and PD-1–driven increases in ROS were dependent upon the oxidation of fatty acids, because treatment with etomoxir nullified changes in ROS levels following PD-1 blockade. …Downstream of PD-1, elevated ROS levels impaired T cell survival in a process reversed by antioxidants. …These data indicate that PD-1 facilitates apoptosis in alloreactive T cells by increasing ROS in a process dependent upon the oxidation of fat. …In addition, blockade of PD-1 undermines the potential for subsequent metabolic inhibition, an important consideration given the increasing use of anti–PD-1 therapies in the clinic.”

6、Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer.
Christina Twyman-Saint Victor et al. Nature. 2015 Apr 16;520(7547):373-7. doi: 10.1038/nature14292. PMID: 25754329.
“This raises fundamental questions about mechanisms of non-redundancy and resistance. …Here we report major tumour regressions in a subset of patients with metastatic melanoma treated with an anti-CTLA4 antibody (anti-CTLA4) and radiation, and reproduced this effect in mouse models. …Unbiased analyses of mice revealed that resistance was due to upregulation of PD-L1 on melanoma cells and associated with T-cell exhaustion. …Radiation enhances the diversity of the T-cell receptor (TCR) repertoire of intratumoral T cells. …Thus, PD-L1 on melanoma cells allows tumours to escape anti-CTLA4-based therapy, and the combination of radiation, anti-CTLA4 and anti-PD-L1 promotes response and immunity through distinct mechanisms.”

7、PD-1 Co-inhibitory and OX40 Co-stimulatory Crosstalk Regulates Helper T Cell Differentiation and Anti-Plasmodium Humoral Immunity.
Ryan A Zander, et al. Cell Host Microbe. 2015 May 13;17(5):628-41. doi: 10.1016/j.chom.2015.03.007. PMID: 25891357.
“At the indicated times, mice were injected i.p. with 200 μg α-CD4 (GK1.5), 500 μg of α-IFN-γ (XMG1.2), 200 μg α-PD-L1 (10F.9G2), 50 μg of α-OX40 Ab (OX86), 200 μg α-PD-L1 and 50 μg α-OX40, or 200 μg α-PD-1 (RMP1-14) and 50 μg α-OX40, or equivalent amounts of rat IgG. All biologics were acquired from BioXcell. Recombinant IFN-γ was acquired from Tonbo. …The Ethics Committee of the Faculty of Medicine, Pharmacy and Dentistry at the University of Sciences, Technique and Technology of Bamako and the IRB of the NIAID, NIH approved the human components of this study. …Collectively, our results reveal the profound impact that crosstalk between PD-1 co-inhibitory and OX40 co-stimulatory pathways has on immune modulation during experimental malaria. …The differentiation and protective capacity of Plasmodium-specific T cells are regulated by both positive and negative signals during malaria, but the molecular and cellular details remain poorly defined. …However, these beneficial effects of OX40 signaling are abrogated following coordinate blockade of PD-1 co-inhibitory pathways, which are also upregulated during malaria and associated with elevated parasitemia.”

8、Memory programming in CD8(+) T-cell differentiation is intrinsic and is not determined by CD4 help.
Juhyun Kim et al. Nat Commun. 2015 Aug 14;6:7994. doi: 10.1038/ncomms8994. PMID: 26272364.
“Rat anti-mouse PD-L1 antibody (200 μg per mouse; 10 F:9G2; Bio X Cells, West Lebanon, NH, USA) or rat IgG2b isotype control (Bio X Cells) were administered i.p. five times every 3 days beginning on day 14 after immunization for PD-L1 blockade. …Magnetic bead-based enrichment of T cells was performed as described previously. …CD8+ T cells activated without CD4+ T-cell help are impaired in memory expansion. …Contrary to the general consensus that CD4 help encodes memory programmes in CD8+ T cells and helper-deficient CD8+ T cells are abortive, these cells can differentiate into effectors and memory precursors. …These results suggest that the memory programme is CD8+ T-cell-intrinsic, and provide insight into the role of CD4 help in CD8+ T-cell responses.”

9、Both PD-1 ligands protect the kidney from ischemia reperfusion injury.
Jaworska K, et al. J Immunol. 2015 Jan 1;194(1):325-33. doi: 10.4049/jimmunol.1400497. PMID: 25404361.
“Acute kidney injury (AKI) is a common problem in hospitalized patients that enhances morbidity and mortality and promotes the development of chronic and end-stage renal disease. …Our recent studies demonstrated that regulatory T cells (Tregs) protect the kidney from ischemia reperfusion–induced inflammation and injury. …The present study was designed to investigate the role of the known PD-1 ligands, PD-L1 and PD-L2, in kidney IRI. …Interestingly, blockade of both PD-1 ligands resulted in worse injury, dysfunction, and inflammation than did blocking either ligand alone. …These findings suggest that PD-L1 and PD-L2 are nonredundant aspects of the natural protective response to ischemic injury and may be novel therapeutic targets for AKI.”

10、Irradiation and anti-PD-L1 treatment synergistically promote antitumor immunity in mice.
Liufu Deng, et al. J Clin Invest. 2014 Feb;124(2):687-95. doi: 10.1172/JCI67313. PMID: 24382348.
“Tumors locally received one 12-Gy dose on day 14 and/or 200 μg anti–PD-L1 (clone 10F.9G2) or isotype control i.p. every three days for a total of four times. **P < 0.01; ***P < 0.001. (B) Combination therapy greatly delayed MC38 tumor growth compared with single treatments. …The tumor microenvironment is populated by various types of inhibitory immune cells including Tregs, alternatively activated macrophages, and myeloid-derived suppression cells (MDSCs), which suppress T cell activation and promote tumor outgrowth. …High-dose ionizing irradiation (IR) results in direct tumor cell death and augments tumor-specific immunity, which enhances tumor control both locally and distantly. …Here, we demonstrate that PD-L1 was upregulated in the tumor microenvironment after IR. Administration of anti–PD-L1 enhanced the efficacy of IR through a cytotoxic T cell–dependent mechanism. …Our data provide evidence for a close interaction between IR, T cells, and the PD-L1/PD-1 axis and establish a basis for the rational design of combination therapy with immune modulators and radiotherapy.”

Related Recombinant IgG Reference Antibodies:
Recombinant Mouse IgG1 Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2a Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Mouse IgG2c Isotype Control Antibody and Mutants, In vivo Grade
Recombinant Rat IgG2a Isotype Control Antibody, In vivo Grade

Syd Labs provides the following anti-mouse PD-L1 / PD-1 antibodies:
Recombinant anti-mouse PD1 antibodies (Clone 29F.1A12.1), In vivo grade
Recombinant anti-mouse PD-1 antibodies (Clone RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-L1 antibodies (Clone 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-1 bispecific antibodies (Clone RMP1-14.1 / 29F.1A12.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-1 bispecific antibodies (Clone 29F.1A12.1 / RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-L1 bispecific antibodies (Clone RMP1-14.1 / 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-L1 / PD-1 bispecific antibodies (Clone 10F.9G2.1 / RMP1-14.1), In vivo grade
Recombinant anti-mouse PD-1 / PD-L1 bispecific antibodies (Clone 29F.1A12.1 / 10F.9G2.1), In vivo grade
Recombinant anti-mouse PD-L1 / PD-1 bispecific antibodies (Clone 10F.9G2.1 / 29F.1A12.1), In vivo grade

Questions and Answers about anti-mouse PD-L1 antibody (Clone 10F.9G2):

Question: Do you produce Fc-silenced 10F.9G2 antibody?
Answer: Sure, we provide various recombinant Fc slient 10F.9G2 antibodies, such as mIgG2c LALAPG, mIgG2a LALAPG, and mIgG1 D265A. We also provide custom recombinant antibody production service to produce other engineered versions of recombinant 10F.9G2 antibodies.

Question: What is the difference among PA007164.r2b and PA007164.m2cLA?
Answer: PA007164.r2a is the recombinant anti-mouse PD L1 monoclonal antibody (rat IgG2b kappa, clone 10F.9G2.1) produced in CHO cells or HEK293 cells if needed. It has the same variable region and constant region sequences as the rat anti-mouse PD-L1 monoclonal antibody from the hybridoma clone of 10F.9G2. Rat antibodies may cause high immuogenicity in mice; thus, at least recombinant antibodies with mouse antibody constant regions should be used to replace the rat antibody constant regions. PA007164.m2cLA is the recombinant anti-mouse PD-L1 antibody (clone 10F.9G2.1) whose constant regions are mouse IgG2c LALAPG kappa.

Anti-mouse PD-L1 antibody (10F.9G2.1) from: Recombinant Anti-Myc-Tag Mouse IgG1 Monoclonal Antibody (clone 9E10): PA007164.r2b Syd Labs

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