Anti-Mouse CD8a Antibody (2.43) | PA007167.m2a
$150.00 – $900.00
Recombinant anti-mouse CD8a monoclonal antibodies from the variable region sequences of the rat anti-mouse CD8a monoclonal antibody (clone number: 2.43) are produced from mammalian cells and good for in vitro and in vivo studies.
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| Catalog No. | PA007167.m2a |
|---|---|
| Product Name | Anti-Mouse CD8a Antibody (2.43) | PA007167.m2a |
| Supplier Name | Syd Labs, Inc. |
| Brand Name | Syd Labs |
| Synonyms | CD8 alpha, T-cell surface glycoprotein CD8 alpha chain, CD_antigen CD8a |
| Summary | The in vivo grade recombinant anti-mouse CD8a mouse IgG2a monoclonal antibody was produced in mammalian cells. |
| Clone | 2.43. |
| Isotype | mouse IgG2a, kappa. |
| Specificity/Sensitivity | CD8a. |
| Applications | Western blot, immunohistochemistry (IHC), Flow Cytometry (FC), and in vivo CD8+ T cell depletion. |
| 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 CD8a antibodies (clone of 2.43) 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 CD8a monoclonal antibodies from the variable region sequences of the rat anti-mouse CD8a monoclonal antibody (clone number: 2.43) 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
PA007167.m2a: Recombinant Anti-Mouse CD8a Monoclonal Antibody(Clone 2.43), Mouse IgG2a Kappa,In vivo Grade
The rat anti-mouse CD8a monoclonal antibody 2.43 (rat IgG2b kappa) reacts with the mouse CD8a protein (T-cell surface glycoprotein CD8 alpha chain) encoded by the mouse CD8A gene that encodes the CD8a chain of the dimeric CD8 protein. The mouse CD8 protein is primarily responsible for cell-mediated immune defense and T-cell development. CD8A has been widely reported as a potential prognosis and diagnostic marker for several diseases, such as inflammatory disorders and tumors. It was shown that the anti-mouse CD8a rat monoclonal antibody (clone number: 2.43) can be used for depleting activity in vivo.
Our recombinant 2.43 antibodies have a part (variable regions) or complete amino acid sequences of the rat anti-mouse CD8a monoclonal antibody (hybridoma clone name or number: 2.43).
References for Anti-Mouse CD8a Antibody (2.43):
1、Macrophage Migration Inhibitory Factor protects cancer cells from immunogenic cell death and impairs anti-tumor immune responses
Balogh, K. N., et al. PLoS One. 2018 Jun 4;13(6):e0197702. doi: 10.1371/journal.pone.0197702. PMID: 29864117
“The MIF protein has an enzymatic activity, functioning as a keto-enol tautomerase, with the N-terminal proline required for this activity. …The Macrophage Migration Inhibitory Factor (MIF) was first described in the 1960’s as a T cell secreted factor capable of inhibiting the random migration of macrophages in vitro. …Recently, several studies, including our own, strongly suggest that MIF exerts its pro-tumorigenic effects through modulation of the immunosuppressive tumor microenvironment. …The Macrophage Migration Inhibitory Factor (MIF) is an inflammatory cytokine that is overexpressed in a number of cancer types, with increased MIF expression often correlating with tumor aggressiveness and poor patient outcomes. …We subsequently discovered that loss of MIF expression in 4T1 cells led to decreased cell numbers and increased apoptosis in vitro under reduced serum culture conditions.”
2、Co-inhibitory Molecule B7 Superfamily Member 1 Expressed by Tumor-Infiltrating Myeloid Cells Induces Dysfunction of Anti-tumor CD8+ T Cells
Li, J., et al. Immunity. 2018 Apr 17;48(4):773-786.e5. doi: 10.1016/j.immuni.2018.03.018. PMID: 29625896
“To deplete CD4+ or CD8+ T cells, 100 μg of anti-CD4 (GK 1.5, Bioxcell) or anti-CD8 (2.43, Bioxcell) was injected i.p. on Day −1, 2, 7, 12 and 17. To deplete NK cells, 20 μg of anti-asialo GM1 was injected i.v. on Day −1, 4, 9, 14 and 19. The depletion efficiency was up to 85%. …Fresh specimens and matched blood of HCC patients were provided by China-Japan Friendship Hospital. …Hepa1-6 or E.G7 tumors were digested with 1mg/mL collagenase D supplemented with 10U/mL DNase I for 40 min at 37°C prior to centrifugation on a discontinuous Percoll gradient (GE Healthcare). …The molecular mechanisms whereby CD8+ T cells become “exhausted” in the tumor microenvironment remain unclear. …Putative B7S1 receptor was co-expressed with PD-1 but not T cell immunoglobulin and mucin-domain containing-3 (Tim-3) at an activated state of early tumor-infiltrating CD8+ T cells, and B7S1 promoted T cell exhaustion, possibly through Eomes overexpression.”
3、Eradication of large established tumors in mice by combination immunotherapy that engages innate and adaptive immune responses
Moynihan, K. D., et al. Nat Med. 2016 Dec;22(12):1402-1410. doi: 10.1038/nm.4200. PMID: 27775706
“Checkpoint blockade with antibodies specific for cytotoxic T lymphocyte–associated protein (CTLA)-4 or programmed cell death 1 (PDCD1; also known as PD-1) elicits durable tumor regression in metastatic cancer, but these dramatic responses are confined to a minority of patients. …This suboptimal outcome is probably due in part to the complex network of immunosuppressive pathways present in advanced tumors, which are unlikely to be overcome by intervention at a single signaling checkpoint. …Here we describe a combination immunotherapy that recruits a variety of innate and adaptive immune cells to eliminate large tumor burdens in syngeneic tumor models and a genetically engineered mouse model of melanoma; to our knowledge tumors of this size have not previously been curable by treatments relying on endogenous immunity. …Maximal antitumor efficacy required four components: a tumor-antigen-targeting antibody, a recombinant interleukin-2 with an extended half-life, anti-PD-1 and a powerful T cell vaccine. …Depletion experiments revealed that CD8+ T cells, cross-presenting dendritic cells and several other innate immune cell subsets were required for tumor regression.”
4、VEGF-A modulates expression of inhibitory checkpoints on CD8+ T cells in tumors
Voron, T., et al. J Exp Med. 2015 Feb 9;212(2):139-48. doi: 10.1084/jem.20140559. PMID: 25601652
“For CD8+ T cell depletion studies, anti-CD8 antibody (clone 2.43; BioXcell) or isotype control antibody (rat IgG2a) was administered at 100 µg i.p. to CT26-tumor bearing mice the day before starting anti-VEGFA treatment. CD8 depletion was checked by flow cytometry. …Immune escape is a prerequisite for tumor development. …The recent development of therapies targeting PD-1 and CTLA-4 have raised great interest since they induced long-lasting objective responses in patients suffering from advanced metastatic tumors. …Thus, induction of cells with immunosuppressive properties, such as regulatory T (T reg) cells or myeloid-derived suppressor cells (MDSCs), and promotion of T cell exhaustion are key mechanisms of immune evasion. …We first analyzed the impact of VEGF-A–VEGFR blockade on PD-1 expression on tumor-infiltrating CD8+ T cells in a mouse model of colorectal cancer (CT26).”
5、TGFβ Is a Master Regulator of Radiation Therapy-Induced Antitumor Immunity
Vanpouille-Box, C., et al. Cancer Res. 2015 Jun 1;75(11):2232-42. doi: 10.1158/0008-5472.CAN-14-3511. PMID: 25858148
“Depletion of CD4+ and CD8+ T cells was achieved by injecting GK1.5 or 2.43 mAb (BioXCell) given i.p. at 100 μg/mouse on 3 consecutive days, starting at day 10, and was maintained by weekly injections. …The unpaired Student t test was used for analysis of IFNγ levels, cell number, and phenotype. …All reported P values are two sided and are declared as significant at the level of 5%. The statistical computations were carried out using SAS for windows, version 9.3 (SAS Institute). …T cells directed to endogenous tumor antigens are powerful mediators of tumor regression. …We hypothesized that TGFβ activity is a major obstacle hindering the ability of radiation to generate an in situ tumor vaccine.”
6、Suppression of Fcγ-receptor-mediated antibody effector function during persistent viral infection
Yamada, D. H., et al. Immunity. 2015 Feb 17;42(2):379-390. doi: 10.1016/j.immuni.2015.01.005. PMID: 25680277
“Target cell depletion was performed by intraperitoneal (i.p.) or i.v. injection of 100 μg or 1 mg (unless otherwise stated) of the following Abs: anti-CD4 clone GK1.5, anti-CD4 clone YTS191, anti-CD8 clone 53.6.72, anti-CD8 clone 2.43, anti-NK1.1 clone PK136, anti-Ly6G clone 1A8 (BioXcell); anti-mouse CD20 (clone MB20; 50 μg/mouse) and anti-platelet (clone 6A6; 4 μg/mouse); and anti-human CD20 (Rituximab; 250 μg/mouse). …For studies targeting LCMV-infected cells in vivo, the DC cell line DC2.4 was infected with LCMV-M1 in vitro for 3 days. …Splenocytes isolated on day 21 of LCMV-Cl13 infection were pooled from multiple mice and then B cell and T cell-depleted using anti-CD19, anti-Thy1.2, and anti-CD4 magnetic beads (Miltenyi Biotec) and allowed to recover for 1 hr at 37°C in complete media. …Understanding how viruses subvert host immunity and persist is essential for developing strategies to eliminate infection. …Suppression of FcγR activity was not due to inhibitory FcγRs or high concentrations of free antibody, and proper FcγR functions were restored when persistently infected mice specifically lacked immune complexes.”
7、Radiation and dual checkpoint blockade activate non-redundant immune mechanisms in cancer
Twyman-Saint Victor, C., et al. Nature. 2015 Apr 16;520(7547):373-7. doi: 10.1038/nature14292. PMID: 25754329
“Immune checkpoint inhibitors1 result in impressive clinical responses2,3,4,5, but optimal results will require combination with each other6 and other therapies. …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. …Although combined treatment improved responses in irradiated and unirradiated tumours, resistance was common. Unbiased analyses of mice revealed that resistance was due to upregulation of PD-L1 on melanoma cells and associated with T-cell exhaustion. …Accordingly, optimal response in melanoma and other cancer types requires radiation, anti-CTLA4 and anti-PD-L1/PD-1. Anti-CTLA4 predominantly inhibits T-regulatory cells (Treg cells), thereby increasing the CD8 T-cell to Treg (CD8/Treg) ratio.”
8、IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis
Coffelt, S. B., et al. Nature. 2015 Jun 18;522(7556):345-348. doi: 10.1038/nature14282. PMID: 25822788
“However, the precise contribution of tumour-induced systemic inflammation to metastasis and the mechanisms regulating systemic inflammation are poorly understood. …Here we show that tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis. …We mechanistically demonstrate that interleukin (IL)-1β elicits IL-17 expression from gamma delta (γδ) T cells, resulting in systemic, granulocyte colony-stimulating factor (G-CSF)-dependent expansion and polarization of neutrophils in mice bearing mammary tumours. …Tumour-induced neutrophils acquire the ability to suppress cytotoxic T lymphocytes carrying the CD8 antigen, which limit the establishment of metastases. …Moreover, the absence of γδ T cells or neutrophils profoundly reduces pulmonary and lymph node metastases without influencing primary tumour progression.”
9、Antibody Blockade of Semaphorin 4D Promotes Immune Infiltration into Tumor and Enhances Response to Other Immunomodulatory Therapies
Evans, E. E., et al. Cancer Immunol Res. 2015 Jun;3(6):689-701. doi: 10.1158/2326-6066.CIR-14-0171. PMID: 25614511
“Fluorescent-conjugated rat or hamster MAbs to CD3 (clone: 17A-2), CD8a (clone: 53-6.7), CD11b (clone: M1/70), Gr-1 (clone: RB6-8C5), CD69 (clone: H1.2F3), CD25 (clone: PC61) with appropriate isotype controls were purchased from BioLegend. …Tumor growth depends on dynamic interactions within a complex ecosystem, including the proliferating neoplastic cells, immune cells, and stroma that constitute the tumor microenvironment. …Semaphorin 4D (SEMA4D, CD100) and its receptor plexin-B1 (PLXNB1) are broadly expressed in murine and human tumors, and their expression has been shown to correlate with invasive disease in several human tumors. …We describe a novel immunomodulatory function of SEMA4D, whereby strong expression of SEMA4D at the invasive margins of actively growing tumors influences the infiltration and distribution of leukocytes in the TME. …Anti-SEMA4D monoclonal antibodies (MAb) were generated following immunization of SEMA4D−/− mice with rSEMA4D-his.”
10、The transcription factor IRF1 dictates the IL-21-dependent anticancer functions of TH9 cells
Végran, F., et al. Nat Immunol. 2014 Aug;15(8):758-66. doi: 10.1038/ni.2925. PMID: 24973819
“The TH9 subset of helper T cells was initially shown to contribute to the induction of autoimmune and allergic diseases, but subsequent evidence has suggested that these cells also exert antitumor activities. …However, the molecular events that account for their effector properties are elusive. …Here we found that the transcription factor IRF1 enhanced the effector function of TH9 cells and dictated their anticancer properties. …Under TH9-skewing conditions, interleukin 1β (IL-1β) induced phosphorylation of the transcription factor STAT1 and subsequent expression of IRF1, which bound to the promoters of Il9 and Il21 and enhanced secretion of the cytokines IL-9 and IL-21 from TH9 cells. Furthermore, IL-1β-induced TH9 cells exerted potent anticancer functions in an IRF1- and IL-21-dependent manner. …Our findings thus identify IRF1 as a target for controlling the function of TH9 cells.”
Syd Labs provides the following recombinant anti-human CD8a monoclonal antibodies:
Recombinant anti-human CD8a antibodies (clone OKT8),In vivo grade
Recombinant anti-human CD8a antibodies (clone OKT8) for flow cytometry
Syd Labs provides the following recombinant anti-mouse CD8a monoclonal antibodies:
Recombinant anti-mouse CD8a antibodies (clone 2.43), In vivo grade
Recombinant anti-mouse CD8a antibodies (clone YTS 169.4), In vivo grad.e
Recombinant anti-mouse CD8a antibodies (clone YTS 105.18), In vivo grade
Syd Labs provides the following recombinant anti-mouse CD8b monoclonal antibodies:
Recombinant anti-mouse CD8b antibodies (clone YTS 156.7), In vivo grade
Anti-Mouse CD8a Antibody (2.43) from: Anti-Mouse CD8a Monoclonal Antibodies (Clone: 2.43) | Recombinant, in vivo Grade – Syd Labs

