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Home > Antibodies > Anti-Mouse Antibodies (In Vivo) > Anti-Mouse CD80 (B7-1) Monoclonal Antibodies

Anti-Mouse CD80 (B7-1) Monoclonal Antibodies

B7-1, Cd28l, Ly-53, Ly53, MIC17, TSA1, B7, BB1

Catalog No. Product Name Size List Price (US$) Quantity
PA007579.r2a In Vivo Grade Recombinant Anti-mouse CD80 (B7-1) Monoclonal Antibody (Clone: 1G10), Rat IgG2a Kappa 1 mg 150.00
PA007579.r2a In Vivo Grade Recombinant Anti-mouse CD80 (B7-1) Monoclonal Antibody (Clone: 1G10), Rat IgG2a Kappa 5 mg 350.00
PA007579.r2a In Vivo Grade Recombinant Anti-mouse CD80 (B7-1) Monoclonal Antibody (Clone: 1G10), Rat IgG2a Kappa 25 mg 900.00
Description

PA007579.r2a: In Vivo Grade Recombinant Anti-mouse CD80 (B7-1) Monoclonal Antibody (Clone: 1G10), Rat IgG2a Kappa

Recombinant Rat IgG2a Monoclonal Antibody.
Clone: 1G10.
Isotype: Rat IgG2a Kappa.
Source: The anti-mouse CD80 (B7-1) monoclonal antibody (clone: 1G10) was produced in mammalian cells.
Specificity/Sensitivity: The in vivo grade recombinant rat monoclonal antibody (clone: 1G10) specifically binds to mouse CD80 (B7-1).
Applications: ELISA, neutralization, functional assays such as bioanalytical PK and ADA assays, and those assays for studying biological pathways affected by the mouse CD80 (B7-1) protein.
Form of Antibody: 0.2 uM filtered solution, pH 7.4, no stabilizers or preservatives.
Endotoxin: < 1 EU per 1 mg of the protein by the LAL method.
Purity: >95% by SDS-PAGE under reducing conditions and HPLC.

Shipping: The in vivo grade recombinant anti-mouse CD80 (B7-1) monoclonal antibody of clone 1G10 is 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.
12 months from date of receipt, -20 to -70°C as supplied.
1 month from date of receipt, 2 to 8°C as supplied.

References of anti-mouse CD80 (B7-1) antibody (Clone: 1G10):


Post-immunotherapy CTLA-4 Ig treatment improves antitumor efficacy
Khan, O., et al. Proc Natl Acad Sci U S A. 2024 Jul 9;121(28):e2404184121. doi: 10.1073/pnas.2404184121. PMID: 38923991
Mice were injected intraperitoneally with 200 μg of anti-mouse CD80 (clone 1G10, BioXCell) every 3 days starting from day 7 post-tumor inoculation. Immune checkpoint therapies (ICT) improve overall survival of patients with cancer but may cause immune-related adverse events (irAEs) such as myocarditis. In mouse tumor models, we administered CTLA-4 Ig 1) concomitantly with ICT or 2) after ICT completion. Concomitant treatment reduced antitumor efficacy, while post-ICT administration improved efficacy without affecting frequency and function of CD8 T cells. The frequency of Tregs was significantly decreased with CTLA-4 Ig.
Tags: anti-mouse CD80 (B7-1) 1G10; anti-mouse CD80 (B7-1) 1G10 in vivo

Unregulated antigen-presenting cell activation by T cells breaks self tolerance
Bacchetta, R., et al. Proc Natl Acad Sci U S A. 2019 Jan 15;116(3):1137-1145. doi: 10.1073/pnas.1812749116. PMID: 30598454
To block CD80 signaling in vivo, mice received 100 μg of anti-mouse CD80 antibody (1G10 clone, BioXCell) intravenously on days 0, 2, and 4 after Treg depletion. T cells proliferate vigorously following acute depletion of CD4+ Foxp3+ T regulatory cells [natural Tregs (nTregs)] and also when naive T cells are transferred to syngeneic, nTreg-deficient Rag1-/- hosts. Here, using mice raised in an antigen-free (AF) environment, we show that the proliferation of transferred T cells in nTreg-deficient Rag1-/- hosts is a consequence of the loss of Treg-mediated inhibition of antigen-presenting cell (APC) activation. The data support a model in which self tolerance is imposed via modulation of CD28 signaling and explains the pathological effects of superagonistic CD28 antibodies. Hence, in both DT-Foxp3-DTR mice and Rag1−/− mice, the lack of Tregs broke self tolerance and caused a proportion of normal T cells to become strongly responsive to autologous antigens.
Tags: anti-mouse CD80 (B7-1) 1G10 antibody in vivo; anti-mouse CD80 (B7-1) 1G10 in animal model

Plasma membrane vesicles decorated with glycolipid-anchored antigens and adjuvants via protein transfer as an antigen delivery platform for inhibition of tumor growth
Cai, H., et al. Biomaterials. 2016 Jan;75:71-80. doi: 10.1016/j.biomaterials.2015.10.019. PMID: 26461116
For in vivo blockade, C57BL/6 mice were treated with anti-mouse CD80 (1G10, 150 μg per dose, i.p.) on days -1, 1, and 3 relative to PMV vaccination. Antigen delivered within particulate materials leads to enhanced antigen-specific immunity compared to soluble administration of antigen. However, current delivery approaches for antigen encapsulated in synthetic particulate materials are limited by the complexity of particle production that affects scalability. Further incorporation of the immunostimulatory molecules IL-12 and B7-1 onto the PMVs by protein transfer enhanced tumor protection and induced beneficial Th1 and Th2-type HER-2-specific immune responses. Since protein antigens can be easily converted to GPI-anchored forms, these results demonstrate that isolated plasma membrane vesicles can be modified with desired antigens along with immunostimulatory molecules by protein transfer and used as a vaccine delivery vehicle to elicit potent antigen-specific immunity.
Tags: anti-mouse CD80 (B7-1) 1G10 in cancer research; anti-mouse CD80 (B7-1) 1G10 in mouse tumor model

PD-L1 limits the mucosal CD8+ T cell response to Chlamydia trachomatis
Johnson, R. M., et al. J Immunol. 2014 Jan 1;192(1):446-55. doi: 10.4049/jimmunol.1302709. PMID: 24353266
Anti-mouse CD80 (clone 1G10, BioXCell) was administered at 150 μg i.p. every other day starting 1 day prior to infection to block costimulatory signals in vivo. Chlamydia trachomatis infection is the most common bacterial sexually transmitted disease in the United States. Repeated infections with C. trachomatis lead to serious sequelae, such as infertility. It is unclear why the adaptive immune system, specifically the CD8(+) T cell response, is unable to protect against subsequent C. trachomatis infections. In this article, we characterize the mucosal CD8(+) T cell response to C. trachomatis genital infection.
Tags: function of anti-mouse CD80 (B7-1) 1G10 antibody; bioactivity of anti-mouse CD80 (B7-1) 1G10

B7-1 and B7-2 co-stimulatory molecules are required for mercury-induced autoimmunity
Gillespie, K. M., et al. Clin Exp Immunol. 2002 Feb;127(2):270-8. doi: 10.1046/j.1365-2249.2002.01789.x. PMID: 11882027
Mice were injected i.p. with 250 μg anti-B7-1 (CD80; clone 1G10) or anti-B7-2 (CD86; clone GL1) every 3 days concurrently with HgCl2 treatment to neutralize costimulatory signals in vivo. B7-1 (CD80) and B7-2 (CD86) molecules on antigen presenting cells play important roles in providing co-stimulatory signals required for activation and expansion of autoreactive T cells. Moreover, some reports have suggested that these molecules may have distinct functions in the differentiation of Th1 and Th2 cells. Mercury-induced autoimmunity in H-2s mice is characterized by lymphoproliferation of T and B cells, serum increases in IgG1 and IgE and production of antinucleolar antibodies (ANoA). To examine the contributions of B7 co-stimulatory molecules to this model, susceptible mice were treated with antibodies to B7-1, B7-2, or both during the development of mercury-induced autoimmunity.
Tags: anti-mouse CD80 (B7-1) antibody (1G10); anti-CD80 (B7-1) clone 1G10

For more references about anti-mouse CD80 (B7-1) antibody (Clone: 1G10), please contact our scientific support team with message@sydlabs.com.

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