LCMV gp33-41
目录号 : GC31901
LCMVgp33-41是来源于淋巴细胞性脑脊髓膜炎病毒(LCMV)糖蛋白gp33的H-2Db限制性表位残基33至41。
Cas No.:151705-84-9
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
LCMV gp33-41 is the H-2Db restricted epitope derived from the lymphocytic choreomeningitis virus (LCMV) glycoprotein gp 33; residues 33 to 41.
| Cas No. | 151705-84-9 | SDF | |
| Canonical SMILES | Lys-Ala-Val-Tyr-Asn-Phe-Ala-Thr-Met | ||
| 分子式 | C48H73N11O13S | 分子量 | 1044.22 |
| 溶解度 | Soluble in Water | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 0.9577 mL | 4.7883 mL | 9.5765 mL |
| 5 mM | 0.1915 mL | 0.9577 mL | 1.9153 mL |
| 10 mM | 0.0958 mL | 0.4788 mL | 0.9577 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
The LCMV gp33-specific memory T cell repertoire narrows with age
Immun Ageing.2012 Aug 15;9(1):17.PMID:22894656DOI: 10.1186/1742-4933-9-17.
Background: The memory response to LCMV in mice persists for months to years with only a small decrease in the number of epitope specific CD8 T cells. This long persistence is associated with resistance to lethal LCMV disease. In contrast to studies focused on the number and surface phenotype of the memory cells, relatively little attention has been paid to the diversity of TCR usage in these cells. CD8+ T cell responses with only a few clones of identical specificity are believed to be relatively ineffective, presumably due to the relative ease of virus escape. Thus, a broad polyclonal response is associated with an effective anti-viral CD8+ T cell response. Results: In this paper we show that the primary CD8+ T cell response to the LCMV gp33-41 epitope is extremely diverse. Over time while the response remains robust in terms of the number of gp33-tetramer+ T cells, the diversity of the response becomes less so. Strikingly, by 26 months after infection the response is dominated by a small number TCRβ sequences. In addition, it is of note the gp33 specific CD8+ T cells sorted by high and low tetramer binding populations 15 and 22 months after infection. High and low tetramer binding cells had equivalent diversity and were dominated by a small number of clones regardless of the time tested. A similar restricted distribution was seen in NP396 specific CD8+ T cells 26 months after infection. The identical TCRVβ sequences were found in both the tetramerhi and tetramerlo binding populations. Finally, we saw no evidence of public clones in the gp33-specific response. No CDR3 sequences were found in more than one mouse. Conclusions: These data show that following LCMV infection the CD8+ gp33-specific CD8 T cell response becomes highly restricted with enormous narrowing of the diversity. This narrowing of the repertoire could contribute to the progressively ineffective immune response seen in aging.
Phenotypic and functional analysis of LCMV gp33-41-specific CD8 T cells elicited by multiple peptide immunization in mice revealed the up-regulation of PD-1 expression on antigen-specific CD8 T cells
Cell Mol Immunol.2007 Dec;4(6):431-7.PMID:18163954
The phenotype and function of antigen-specific CD8 T cells are closely associated with the efficacy of a therapeutic vaccination. Here we showed that multiple immunizations with LCMV gp33-41 peptide (KAV) in Freund's adjuvant could induce KAV-specific CD8 T cells with low expression of CD127 and CD62L molecules. The inhibitory receptor PD-1 was also expressed on a substantial part of KAV-specific CD8 T cells, and its expression level on KAV-specific CD8 T cells in spleen and lymph nodes was much higher when compared to those in peripheral blood. Furthermore, KAV-specific CD8 T cells could specifically kill KAV-pulsed target cells in vivo but the efficiency was low. These data suggest that prime-boost vaccination schedule with peptide in Freund's adjuvant can elicit antigen-specific CD8 T cells of effector-like phenotype with partial functional exhaustion, which may only provide short-term protection against the pathogen.
Generation and function of bone marrow-derived dendritic cells from CD4/CD8(-/-) double-knockout mice
Immunol Lett.1999 Apr 15;67(3):243-9.PMID:10369133DOI: 10.1016/s0165-2478(99)00018-8.
We present a novel, simple and straightforward method to obtain mouse bone marrow-derived dendritic cells (DC) from C57Bl/6 CD4/CD8(-/-) double knock-out mice. This new method, involving culture of bone marrow cells in medium supplemented with Interleukin 4 and Granulocyte-Macrophage Colony-Stimulating Factor, does not involve negative immunodepletion of CD4+ and CD8+ populations, or extensive prior manipulations of the starting population. The resulting, loosely adherent cell population, exhibited the morphological characteristics and typical surface markers of DCs, and were endowed with the functional activities characteristic of bone marrow-derived DCs of wild-type mice. Interestingly, LCMV GP33-41 peptide-loaded CD4/CD8(-/-) DCs were efficiently lysed by peptide-specific activated CTLs in vitro. Furthermore, these peptide-loaded CD4/CD8(-/-) DCs induced a peptide-specific CTL response upon immunization of wild-type C57Bl/6 mice.
Molecular anatomy and number of antigen specific CD8 T cells required to cause type 1 diabetes
PLoS Pathog.2012;8(11):e1003044.PMID:23209415DOI: 10.1371/journal.ppat.1003044.
We quantified CD8 T cells needed to cause type 1 diabetes and studied the anatomy of the CD8 T cell/beta (β) cell interaction at the immunologic synapse. We used a transgenic model, in situ tetramer staining to distinguish antigen specific CD8 T cells from total T cells infiltrating islets and a variety of viral mutants selected for functional deletion(s) of various CD8 T cell epitopes. Twenty percent of CD8 T cells in the spleen were specific for all immunodominant and subdominant viral glycoprotein (GP) epitopes. CTLs to the immunodominant LCMV GP33-41 epitope accounted for 63% of the total (12.5% of tetramers). In situ hybridization analysis demonstrated only 1 to 2% of total infiltrating CD8 T cells were specific for GP33 CD8 T cell epitope, yet diabetes occurred in 94% of mice. The immunologic synapse between GP33 CD8 CTL and β cell contained LFA-1 and perforin. Silencing both immunodominant epitopes (GP33, GP276-286) in the infecting virus led to a four-fold reduction in viral specific CD8 CTL responses, negligible lymphocyte infiltration into islets and absence of diabetes.
Cooperativity between CD8+ T cells, non-neutralizing antibodies, and alveolar macrophages is important for heterosubtypic influenza virus immunity
PLoS Pathog.2013 Mar;9(3):e1003207.PMID:23516357DOI: 10.1371/journal.ppat.1003207.
Seasonal epidemics of influenza virus result in ∼36,000 deaths annually in the United States. Current vaccines against influenza virus elicit an antibody response specific for the envelope glycoproteins. However, high mutation rates result in the emergence of new viral serotypes, which elude neutralization by preexisting antibodies. T lymphocytes have been reported to be capable of mediating heterosubtypic protection through recognition of internal, more conserved, influenza virus proteins. Here, we demonstrate using a recombinant influenza virus expressing the LCMV GP33-41 epitope that influenza virus-specific CD8+ T cells and virus-specific non-neutralizing antibodies each are relatively ineffective at conferring heterosubtypic protective immunity alone. However, when combined virus-specific CD8 T cells and non-neutralizing antibodies cooperatively elicit robust protective immunity. This synergistic improvement in protective immunity is dependent, at least in part, on alveolar macrophages and/or other lung phagocytes. Overall, our studies suggest that an influenza vaccine capable of eliciting both CD8+ T cells and antibodies specific for highly conserved influenza proteins may be able to provide heterosubtypic protection in humans, and act as the basis for a potential "universal" vaccine.