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【产品名称】
 anti m PD-L1 抗体 免疫治疗研究的重要工具 美国BioXcell原装进口
【订购货号】
 B657087
【产品CAS号码】
 无
【规格/价格】
 
【预计到货时间】
 30 天
【产品详细说明】
【本产品仅供科学研究使用】
【更新日期】 2015-5-20  
InVivoMAb anti m PD-L1
 
克隆号: 10F.9G2

货号: BE0101
背景知识

程序性死亡分子1及其配体(PD-1/PD-L1)是一对负性免疫共刺激分子,正常情况下,组织细胞表面的PD-L1与淋巴细胞表面的PD-1结合后,可抑制淋巴细胞功能,诱导活化的淋巴细胞凋亡,从而在自身免疫耐受及防止自身免疫性疾病中发挥重要作用。多种肿瘤细胞表面也表达PD-L1,肿瘤细胞表达的PD-L1,可与肿瘤浸润淋巴细胞表面的PD-1分子结合,抑制淋巴细胞的功能及细胞因子的释放,并诱导淋巴细胞凋亡,从而抵抗淋巴细胞的杀伤作用,最终导致肿瘤发生免疫逃逸。

产品描述
· 内毒素:<2.0 EU/mg
· 成分:PBS, pH 7
· 灭菌:0.2 µm filtration
· 纯度:> 95%
  • 采用消光系数等于1.33来确定浓度
  • 采用LAL凝胶凝血实验确定内毒素水平
  • SDS-PAGE确定纯度
储存
未稀释液黑暗储存于4度
生产
组织培养
纯化
Protein G
同型
Rat IgG2b
推荐的同型对照
产品名称:LTF-2
货号:BE0090
鼠科动物病原菌测试结果
Murine Pneumonia Virus: Negative
Mouse Hepatitis Virus: Negative
Mouse Minute Virus: Negative
Mouse Parvovirus: Negative
Sendai Virus: Negative
Murine Encephalomyelitis: Negative
 

Product Description
InVivoMAb anti m PD-L1
Clone: 10F.9G2
Catalog#: BE0101

Product

  • Endotoxin: <2.0 EU/mg
  • Formulation: PBS, pH 7
  • Sterile: 0.2 µm filtration
  • Purity: > 95%
  • Concentration is determined using an extinction coefficient equal to 1.33
  • Endotoxin level is determined using an LAL gel clotting test
  • Purity determined by SDS-PAGE.

Production

Tissue culture

Purification

Protein G

Isotype

Rat IgG2b

Storage

Undiluted at 4C in the dark.

If the antibody is to be stored for more than 6 months, aliquot and freeze at -20C in a non-frost free freezer.

Avoid freeze/thaw cycles.

 
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Human PD-L1 (CD274), FLAG-tag 71183 100 µg
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CD137[Biotinylated]:CD137L Inhibitor Screening Assay Kit 72025 96
CD28:B7-1[Biotinylated] Inhibitor Screening Assay Kit 72007 96
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CTLA4[Biotinylated]:B7-2 Inhibitor Screening Assay Kit 72024 96
IDO1 Inhibitor Screening Assay Kit 72021 96
IDO2 Inhibitor Screening Assay Kit 72022 96
PD-1:PD-L1[Biotinylated] Inhibitor Screening Assay Kit 72003 96
PD-1:PD-L1[Biotinylated] Inhibitor Screening Colorimetric Assay Kit 72016 96
PD-1:PD-L2 Homogeneous Assay Kit 72015 384
PD-1:PD-L2 TR-FRET Assay Kit 72012 384
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PD-1:PD-L2[Biotinylated] Inhibitor Screening Colorimetric Assay Kit 72017 96
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PD-1[Biotinylated]:PD-L1 Inhibitor Screening Colorimetric Assay Kit 72018 96
PD-1[Biotinylated]:PD-L2 Inhibitor Screening Assay Kit 72006 96
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PD1:PDL1 Homogeneous Assay Kit 72014 384
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PD-L1文献
 
Cho, H.-I., et al. (2010). “Interferon gamma limits the effectiveness of melanoma peptide vaccines.” Blood.
The development of effective therapeutic vaccines to generate tumor-reactive cytotoxic T lymphocytes (CTLs) continues to be a top research priority. However, in spite of some promising results, there are no clear examples of vaccines that eradicate established tumors. Most vaccines are ineffective because they generate low numbers of CTLs and because numerous immunosuppressive factors abound in tumor-bearing hosts. We designed a peptide vaccine that produces large numbers of tumor-reactive CTLs in a mouse melanoma model. Surprisingly, CTL tumor recognition and anti-tumor effects decreased in the presence of interferon gamma (IFNγ), a cytokine that can provide a therapeutic benefit. Tumors exposed to IFNγ evade CTLs by inducing large amounts of non-cognate MHC class I, which limit T cell activation and effector function. Our results demonstrate that peptide vaccines can eradicate large established tumors in circumstances where the inhibitory activities of IFNγ are curtailed.
 
Hafalla, J. C. R., et al. (2012). “The CTLA-4 and PD-1/PD-L1 Inhibitory Pathways Independently Regulate Host Resistance to Plasmodium-induced Acute Immune Pathology.” PLoS Pathog 8(2): e1002504.
T cells are part of the body’s defense system in response to infection. However, once the infection has been suitably controlled, these T cells must be switched off. Inhibitory pathways, such as CTLA-4 and PD-1, are known to send the ‘turn off’ signal to T cells during chronic infections. However, their roles in acute infections, such as malaria, are unclear. We compared the function of these inhibitory pathways in mice that are either susceptible or resistant to severe malarial disease (cerebral malaria). Strikingly, we found that receptors for CTLA-4 and PD-1 are more highly expressed in T cells from susceptible mice than from resistant mice. Therefore, cerebral malaria develops despite the high expression of these inhibitory receptors. Moreover, we demonstrated that blocking these inhibitory receptors in the resistant mice increased the function of T cells, which in turn led to the characteristic signs of cerebral malaria. Finally, reminiscent of what is known for the susceptible strain, we confirmed that certain T cells (CD8+) and molecules (IFN-γ) are crucial to the development of cerebral malaria in the otherwise resistant mice. Thus, the CTLA-4 and PD-1 inhibitory pathways have essential, independent and non-redundant roles in regulating the body’s complex response to malaria.
 
Reiley, W. W., et al. (2010). “Distinct functions of antigen-specific CD4 T cells during murine Mycobacterium tuberculosis infection.” Proceedings of the National Academy of Sciences 107(45): 19408-19413.
The immune response elicited after Mycobacterium tuberculosis (Mtb) infection is critically dependent on CD4 T cells during both acute and chronic infection. How CD4 T-cell responses are maintained throughout infection is not well understood, and evidence from other infection models has suggested that, under conditions of chronic antigen stimulation, T cells can undergo replicative exhaustion. These findings led us to determine whether subpopulations of CD4 T cells existed that displayed markers of terminal differentiation or exhaustion during murine Mtb infection. Analysis of antigen-specific effector CD4 T cells revealed that programmed death-1 (PD-1) and the killer cell lectin-like receptor G1 (KLRG1) delineated subpopulations of T cells. PD-1–expressing CD4 T cells were highly proliferative, whereas KLRG1 cells exhibited a short lifespan and secreted the cytokines IFNγ and TNFα. Adoptive transfer studies demonstrated that proliferating PD-1–positive CD4 T cells differentiated into cytokine-secreting KLRG1-positive T cells, but not vice versa. Thus, proliferating PD-1–positive cells are not exhausted, but appear to be central to maintaining antigen-specific effector T cells during chronic Mtb infection. Our findings suggest that antigen-specific T-cell responses are maintained during chronic mycobacterial infection through the continual production of terminal effector cells from a proliferating precursor population.
 
Rivas, M. N., et al. (2009). “Reviving Function in CD4+ T Cells Adapted to Persistent Systemic Antigen.” The Journal of Immunology 183(7): 4284-4291.
In bone marrow-transplanted patients, chronic graft-versus-host disease is a complication that results from the persistent stimulation of recipient minor histocompatibility Ag (mHA)-specific T cells contained within the graft. In this study, we developed a mouse model where persistent stimulation of donor T cells by recipient’s mHA led to multiorgan T cell infiltration. Exposure to systemic mHA, however, deeply modified T cell function and chronically stimulated T cells developed a long-lasting state of unresponsiveness, or immune adaptation, characterized by their inability to mediate organ immune damages in vivo. However, analysis of the gene expression profile of adapted CD4+ T cells revealed the specific coexpression of genes known to promote differentiation and function of Th1 effector cells as well as genes coding for proteins that control T cell activity, such as cell surface-negative costimulatory molecules and regulatory cytokines. Strikingly, blockade of negative costimulation abolished T cell adaptation and stimulated strong IFN-γ production and severe multiorgan wasting disease. Negative costimulation was also shown to control lethal LPS-induced toxic shock in mice with adapted T cells, as well as the capacity of adapted T cells to reject skin graft. Our results demonstrate that negative costimulation is the molecular mechanism used by CD4+ T cells to adapt their activity in response to persistent antigenic stimulation. The effector function of CD4+ T cells that have adapted to chronic Ag presentation can be activated by stimuli strong enough to overcome regulatory signals delivered to the T cells by negative costimulation.
 
Zhang, L., et al. (2009). “PD-1/PD-L1 interactions inhibit antitumor immune responses in a murine acute myeloid leukemia model.” Blood 114(8): 1545-1552.
Negative regulatory mechanisms within the solid tumor microenvironment inhibit antitumor T-cell function, leading to evasion from immune attack. One inhibitory mechanism is up-regulation of programmed death-ligand 1 (PD-L1) expressed on tumor or stromal cells which binds to programmed death-1 (PD-1) on activated T cells. PD-1/PD-L1 engagement results in diminished antitumor T-cell responses and correlates with poor outcome in murine and human solid cancers. In contrast to available data in solid tumors, little is known regarding involvement of the PD-1/PD-L1 pathway in immune escape by hematopoietic cancers, such as acute myeloid leukemia (AML). To investigate this hypothesis, we used the murine leukemia, C1498. When transferred intravenously, C1498 cells grew progressively and apparently evaded immune destruction. Low levels of PD-L1 expression were found on C1498 cells grown in vitro. However, PD-L1 expression was up-regulated on C1498 cells when grown in vivo. PD-1−/− mice challenged with C1498 cells generated augmented antitumor T-cell responses, showed decreased AML burden in the blood and other organs, and survived significantly longer than did wild-type mice. Similar results were obtained with a PD-L1 blocking antibody. These data suggest the importance of the PD-1/PD-L1 pathway in immune evasion by a hematologic malignancy, providing a rationale for clinical trials targeting this pathway in leukemia patients.
 
 
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