InVivoMAb anti-rat CD80 (B7-1)
About InVivoMAb anti-rat CD80 (B7-1)
The 3H5 monoclonal antibody reacts with rat CD80 also known as B7-1. CD80 is a 60 kDa Ig superfamily member and is expressed by activated B cells and constitutively by monocytes and dendritic cells. This ligand binds to CD28 to provide a costimulatory signal necessary for T cell activation and survival, and cytokine production. Additionally, CD80 binds to CTLA-4 which inhibits T cells. The 3H5 antibody has been shown to block CD80-mediated co-stimulation of rat T cells in vitro.
InVivoMAb anti-rat CD80 (B7-1) Specifications
Mouse IgG1, κ
|Recommended Isotype Control(s)||InVivoMAb mouse IgG1 isotype control, unknown specificity(BE0083)|
|Recommended InVivoPure Dilution Buffer||InVivoPure pH 7.0 Dilution Buffer(IP0070)|
HTLV-1-transformed Lewis-S1 rat T cell line
0.2 μM filtered
Purified from tissue culture supernatant in an animal free facility
The antibody solution should be stored at the stock concentration at 4°C. Do not freeze.
InVivoMAb anti-rat CD80 (B7-1) (Clone: 3H5)Dolen, Y., et al. (2015). "Granulocytic subset of myeloid derived suppressor cells in rats with mammary carcinoma." Cell Immunol 295(1): 29-35. PubMed
Limited knowledge is available on myeloid derived suppressor cells (MDSCs) of rat origin. We examined the myeloid cells from peripheral blood, bone marrow and spleens of healthy and mammary tumor bearing rats employing a novel immunophenotyping strategy with CD172a, HIS48, and Rp-1 antibodies. We addressed rat granulocytes by Rp-1 positivity and used HIS48 in discrimination of two mononuclear cell subsets. An expansion of granulocyte numbers was detected in peripheral blood and spleens of mammary tumor-bearing animals. The purified granulocytes were able to impair antigen-specific helper T-cell proliferation, and therefore nominated as granulocytic MDSCs of this rat tumor model. HIS48(+) mononuclear cell numbers were also increased in the blood and spleens of mammary tumor bearing rats with a lower MHC class II positivity. Despite the lack of an antigen specific suppression of CD4(+) T cells, HIS48(+) monocytes resemble monocytic MDSCs with their inflammatory phenotype. Together, these results provide evidence for the existence and phenotypic characterization of a granulocytic MDSC subset in a rat model of mammary carcinoma.
Zhu, X. M., et al. (2014). "Anti-RAGE antibody ameliorates severe thermal injury in rats through regulating cellular immune function." Acta Pharmacol Sin 35(9): 1167-1176. PubMed
AIM: The receptor of advanced glycation end products (RAGE) participates in a variety of pathophysiological processes and inflammatory responses. The aim of this study was to investigate the therapeutic potential of an anti-RAGE neutralizing antibody for severe thermal injury in rats, and to determine whether the treatment worked via modulating cellular immune function. METHODS: Full-thickness scald injury was induced in Wistar rats, which were treated with the anti-RAGE antibody (1 mg/kg, iv) at 6 h and 24 h after the injury. The rats were sacrificed on d 1, 3, 5, and 7. Blood and spleen samples were harvested to monitor organ function and to analyze dendritic cell (DC) and T cell cytokine profiles. The survival rate was analyzed up to d 7 after the injury. RESULTS: Administration of the antibody significantly increased the 7 d survival rate in thermally injured rats (6.67% in the model group; 33.33% in anti-RAGE group). Treatment with the antibody also attenuated the multiple organ dysfunction syndrome (MODS) following the thermal injury, as shown by significant decreases in the organ dysfunction markers, including serum ALT, AST, blood urea nitrogen, creatinine and CK-MB. Moreover, treatment with the antibody significantly promoted DC maturation and T cell activation in the spleens of thermally injured rats. CONCLUSION: Blockade of the RAGE axis by the antibody effectively ameliorated MODS and improved the survival rate in thermally injured rats, which may be due to modulation of cellular immune function.
Dingle, B. M., et al. (2013). "FoxP3(+) regulatory T cells attenuate experimental necrotizing enterocolitis." PLoS One 8(12): e82963. PubMed
Necrotizing enterocolitis (NEC) results from severe intestinal inflammation in premature infants. FoxP3(+) regulatory T cells (Tregs) are central to gut homeostasis. While Treg proportions are significantly reduced in the ileums of premature infants with NEC, it is unknown whether they play a critical function in preventing NEC. This study investigated Treg development in newborn rat pups and their role in experimental NEC induction. Utilizing an established rat model of experimental NEC, the ontogeny of T cells and Tregs in newborn pups was characterized by flow cytometry. To investigate the functions of Tregs, newborn pups were given Tregs harvested from adult rats prior to NEC induction to assess clinical improvement and mechanisms of immune regulation. The results revealed that there were few Treg numbers in the terminal ileums of newborn rats and 8-fold reduction after NEC. Adoptive transfer of Tregs significantly improved weight loss, survival from 53% to 88%, and NEC incidence from 87% to 35%. The Tregs modulated the immune response as manifested in reduced CD80 expression on antigen presenting cells and decreased T cell activation within the mesenteric lymph nodes. These findings suggest that while Tregs are present in the intestines, their numbers might be insufficient to dampen the excessive inflammatory state in NEC. Adoptive transfer of Tregs attenuates the severity of NEC by limiting the immune response. Strategies to enhance Tregs have a therapeutic potential in controlling the development of NEC.
Gao, X. W., et al. (2013). "Mechanism of immune tolerance induced by donor derived immature dendritic cells in rat high-risk corneal transplantation." Int J Ophthalmol 6(3): 269-275. PubMed
AIM: To study the role of immature dendritic cells (imDCs) on immune tolerance in rat penetrating keratoplasty (PKP) in high-risk eyes and to investigate the mechanism of immune hyporesponsiveness induced by donor-derived imDCs. METHODS: Seventy-five SD rats (recipient) and 39 Wistar rats (donor) were randomly divided into 3 groups: control, imDC and mature dendritic cell (mDC) group respectively. Using a model of orthotopic corneal transplantation in which allografts were placed in neovascularized high-risk eyes of recipient rat. Corneal neovascularization was induced by alkaline burn in the central cornea of recipient rat. Recipients in imDC group or mDC group were injected donor bone marrow-derived imDCs or mDCs of 1x10(6) respectively 1 week before corneal transplantation via tail vein. Control rat received the same volume of PBS. In each group, 16 recipients were kept for determination of survival time and other 9 recipients were executed on day 3, 7 and 14 after transplantation. Cornea was harvested for hematoxylin-eosin staining and acute rejection evaluation, Western blot was used to detect the expression level of Foxp3. RESULTS: The mean survival time of imDC group was significantly longer than that of control and mDC groups (all P<0.05). The expression level of Foxp3 on CD4(+)CD25(+)T cells of imDC group (2.24+/-0.18) was significantly higher than that in the control (1.68+/-0.09) and mDC groups (1.46+/-0.13) (all P<0.05). CONCLUSION: Donor-derived imDC is an effective treatment in inducing immune hyporesponsiveness in rat PKP. The mechanism of immune tolerance induced by imDC might be inhibit T lymphocytes responsiveness by regulatory T cells.
Maeda, K., et al. (1997). "Characterization of rat CD80 and CD86 by molecular cloning and mAb." Int Immunol 9(7): 993-1000. PubMed
The CD28/B7 pathway provides a critical co-stimulatory signal for T cell activation. In the present study, we cloned rat CD80 and CD86 cDNA from a HTLV-1-transformed rat T cell line, Lewis-S1, expressing a high level of CTLA-4-Ig binding proteins. The predicted CD80 and CD86 polypeptides were composed of 321 and 313 amino acids respectively, and exhibited features common to human and mouse B7 family proteins. Both CD80 and CD86 mRNAs were abundantly detected in HTLV-1-transformed rat T cell lines but not in a thymic lymphoma cell line. To further explore the function of rat CD80 and CD86, we generated cDNA transfectants and anti-rat CD80 (3H5) and anti-rat CD86 (24F) mAb. Rat CD80 or CD86 transfectants exhibited a potent co-stimulatory activity for rat T cell proliferation, which was blocked by 3H5 and 24F mAb respectively. 3H5 or 24F immunoprecipitated a 80-90 or 90-100 kDa surface protein from Lewis-S1 cells. HTLV-1-transformed rat T cell lines expressed high levels of both CD80 and CD86 as estimated by staining with 3H5 and 24F, which acted co-stimulatory for allogeneic T cell activation as estimated by blocking with 3H5 and 24F. These mAb will be useful for investigating the pathophysiological functions of CD80 and CD86 in transplantation, autoimmune diseases and HTLV-1-associated pathologies in the rat system.