登录 | 注册    关注公众号  
微信公众号
搜索
 >  Cell>IL-7 R alpha & TSLP R >CHEK-ATF045

Human TSLP R (Luc) HEK293 Reporter Cell

For research use only.

  1. Genetically modified cell lines best reflect MOA (Mechanism of Action)
  2. Higher activity and larger assay window for robust and reproducible cell-based bioassay
  3. Comprehensive application data to support assay development and validation
  4. Full tracible record, stringent quality control and validated cell passage stability
  5. Parental cell line legally obtained from internationally recognized cell resource bank and commercially licensed
  6. Global commercial license assistance whenever regulatory filing is required

描述(Description)

The Human TSLP R (Luc) HEK293 Reporter Cell was engineered to not only express STAT5 signaling response element, but also express the receptors full length human TSLP R (Uniprot: Q9HC73-1) and IL-7 R alpha (Uniprot: P16871-1). When stimulated with human TSLP protein, the TSLP/TSLP R interaction drives STAT5-mediated luminescence. Inhibition of TSLP binding to TSLP R by either anti-TSLP or anti-TSLP R antibodies results in a decrease in luminescence.

应用说明(Application)

Screen for anti-human TSLP or anti-human TSLP R neutralizing antibody

IL-7 R alpha & TSLP R Assay Principles

生长特性(Growth Properties)

Adherent

筛选标记(Selection Marker)

Zeocin (100 μg/mL) + Puromycin (2 μg/mL)

培养基(Complete Growth Medium)

DMEM medium + 10% FBS

冻存液(Freeze Medium)

Serum-free cell cryopreservation medium

装量(Quantity)

1 vial contains at least 5×10^6 cells in 1 mL serum-free cryopreservation medium

存储(Storage)

Frozen in liquid nitrogen.

支原体检测(Mycoplasma Testing)

Negative

无菌检测(Sterility Testing)

Negative

使用说明(Instructions for Use)

See data sheet for detailed culturing and assay protocol.

质量管理控制体系(QMS)

  1. 质量管理体系(ISO, GMP)
  2. 质量优势
  3. 质控流程
 

Receptor Assay

IL-7 R alpha & TSLP R FACS

Co-expression analysis of human TSLP R and IL-7 R alpha on Human TSLP R (Luc) HEK293 Reporter Cell by FACS.
Cell surface staining was performed on Human TSLP R (Luc) HEK293 Reporter Cell or negative control cell using PE-labeled anti-TSLP R antibody and FITC-labeled anti-IL-7 R alpha antibody.

Protocol

 

Application

IL-7 R alpha & TSLP R APPLICATION

Inhibition of human TSLP protein-induced reporter activity by anti-human TSLP neutralizing antibody.
This reporter cell was incubated with serial dilutions of antibodies in the presence of human TSLP protein (Cat. No. TSP-H52Hb) with a final concentration of 0.3 μg/mL. The EC50 of anti-human TSLP neutralizing antibody is approximately 0.55 μg/mL.

Protocol

 

Signaling Bioassay

IL-7 R alpha & TSLP R SIGNALING

Response to human TSLP protein (RLU).
The Human TSLP R (Luc) HEK293 Reporter Cell was stimulated with serial dilutions of human TSLP protein (Cat. No. TSP-H52Hb). The EC50 was approximately 0.1392 μg/mL.

Protocol

IL-7 R alpha & TSLP R SIGNALING

Response to human TSLP protein (Fold).
The Human TSLP R (Luc) HEK293 Reporter Cell was stimulated with serial dilutions of human TSLP protein (Cat. No. TSP-H52Hb). The max induction fold was approximately 45.15

Protocol

 

Passage Stability

IL-7 R alpha & TSLP R PASSAGE

Passage stability analysis by Signaling Bioassay.
The continuously growing Human TSLP R (Luc) HEK293 Reporter Cell was stimulated with serial dilutions of human TSLP protein. Human TSLP protein stimulated response demonstrates passage stabilization (fold induction and EC50) across passage 10-26.

Protocol

如有相关细胞池需求请联系我们

 
评论(1)
  1. 131XXXXXXX5
  2. 2人赞
  3. 我们购买了human TSLPR (luc) reporter cell line,用于抗体筛选实验的开发。对于这个细胞系,我们已经完成了细胞膜表面受体表达的验证和质控.
  4. 2024-12-5
 
ACRO质量管理体系
 
 

背景(Background)

Thymic stromal lymphopoietin (TSLP) is a pleiotropic cytokine and takes multi-functions via binding to a high-affinity heteromeric complex composed of thymic stromal lymphopoietin receptor (TSLPR) chain and IL-7Rα. The receptor complex on cells co-expressing TSLPR and IL-7Rα activated downstream genes expression and initiate proinflammatory signaling. TSLP involved in a variety of allergic diseases (e.g., atopic dermatitis, bronchial asthma). Further investigation indicated that TSLP is also involved in chronic inflammatory (i.e., chronic obstructive pulmonary disease and celiac disease) and autoimmune (e.g., psoriasis, rheumatoid arthritis) disorders and several cancers.

Limited Use&License Disclosure

BY USE OF THIS PRODUCT, RESEARCHER AGREES TO BE BOUND BY THE FOLLOWING TERMS OF LIMITED USE OF THIS CELL LINE PRODUCT.

  1. If the researcher is not willing to accept the terms of limited use of this cell line product, and the product is unused, ACRO will accept return of the unused product.
  2. Researchers may use this product for research use only, no commercial use is allowed. "Commercial use" means any and all uses of this product and derivatives by a party for profit or other consideration and may include but is not limited to use in: (1) product manufacture; and (2) to provide a service, information or data; and/or resale of the product or its derivatives, whether or not such product or derivatives are resold for use in research.
  3. This cell line is neither intended for any animal or human therapeutic purposes nor for any direct human in vivo use . You have no right to share, modify, transfer, distribute, sell, sublicense, or otherwise make the cell line available for use to other researchers, laboratories, research institutions, hospitals, universities, or service organizations.
  4. ACROBIOSYSTEMS MAKES NO WARRANTIES OR REPRESENTATIONS OF ANY KIND, EITHER EXPRESSED OR IMPLIED, WITH RESPECT TO THE SUITABILITY OF THE CELL LINE FOR ANY PARTICULAR USE.
  5. ACROBIOSYSTEMS ACCEPTS NO LIABILITY IN CONNECTION WITH THE HANDLING OR USE OF THE CELL LINE.
  6. Modifications of the cell line, transfer to a third party, or commercial use of the cell line may require a separate license and additional fees. Please contact order.cn@acrobiosystems.com for further details.

 

前沿进展

Steroid resistance of airway type 2 innate lymphoid cells from patients with severe asthma: The role of thymic stromal lymphopoietin
Liu, Verma, Michalec et al
J Allergy Clin Immunol (2018) 141 (1), 257-268.e6
Abstract: Type 2 innate lymphoid cells (ILC2s) represent an important type 2 immune cell. Glucocorticoid regulation of human ILC2s is largely unknown.We sought to assess steroid resistance of human blood and airway ILC2s from asthmatic patients and to examine its mechanism of induction.We studied human blood and lung ILC2s from asthmatic patients and control subjects using flow cytometry and ELISA.Dexamethasone inhibited (P = .04) chemoattractant receptor-homologous molecule expressed on TH2 lymphocytes and type 2 cytokine expression by blood ILC2s stimulated with IL-25 and IL-33. However, it did not do so when ILC2s were stimulated with IL-7 and thymic stromal lymphopoietin (TSLP), 2 ligands of IL-7 receptor α. Unlike blood ILC2s, bronchoalveolar lavage (BAL) fluid ILC2s from asthmatic patients were resistant to dexamethasone. BAL fluid from asthmatic patients had increased TSLP but not IL-7 levels. BAL fluid TSLP levels correlated (r = 0.74) with steroid resistance of ILC2s. TSLP was synergistically induced in epithelial cells by IL-13 and human rhinovirus. Mechanistically, dexamethasone upregulated ILC2 expression of IL-7 receptor α, which augmented and sustained signal transducer and activator of transcription (STAT) 5 signaling by TSLP. TSLP induced mitogen-activated protein kinase kinase (MEK), c-Fos, inhibitor of DNA binding 3, phosphorylated signal transducer and activator of transcription (pSTAT) 3, and pSTAT5, molecules linked to steroid resistance. Dexamethasone inhibited c-Fos, inhibitor of DNA binding 3, and pSTAT3 but not pSTAT5 and MEK. The MEK inhibitor trametinib, the Janus kinase-STAT inhibitor tofacitinib, and the STAT5 inhibitor pimozide reversed steroid resistance of BAL ILC2s.Dexamethasone inhibited type 2 cytokine production by blood ILC2s. IL-7 and TSLP abrogated this inhibition and induced steroid resistance of ILC2s in a MEK- and STAT5-dependent manner. BAL fluid ILC2s from asthmatic patients with increased TSLP levels were steroid resistant, which was reversed by clinically available inhibitors of MEK and STAT5.Copyright © 2017 American Academy of Allergy, Asthma & Immunology. Published by Elsevier Inc. All rights reserved.
Structure and antagonism of the receptor complex mediated by human TSLP in allergy and asthma
Verstraete, Peelman, Braun et al
Nat Commun (2017) 8, 14937
Abstract: The pro-inflammatory cytokine thymic stromal lymphopoietin (TSLP) is pivotal to the pathophysiology of widespread allergic diseases mediated by type 2 helper T cell (Th2) responses, including asthma and atopic dermatitis. The emergence of human TSLP as a clinical target against asthma calls for maximally harnessing its therapeutic potential via structural and mechanistic considerations. Here we employ an integrative experimental approach focusing on productive and antagonized TSLP complexes and free cytokine. We reveal how cognate receptor TSLPR allosterically activates TSLP to potentiate the recruitment of the shared interleukin 7 receptor α-chain (IL-7Rα) by leveraging the flexibility, conformational heterogeneity and electrostatics of the cytokine. We further show that the monoclonal antibody Tezepelumab partly exploits these principles to neutralize TSLP activity. Finally, we introduce a fusion protein comprising a tandem of the TSLPR and IL-7Rα extracellular domains, which harnesses the mechanistic intricacies of the TSLP-driven receptor complex to manifest high antagonistic potency.
Genetic Variants of Thymic Stromal Lymphopoietin in Nonsteroidal Anti-Inflammatory Drug-Induced Urticaria/Angioedema
Plaza-Serón, Blanca-López, Pérez-Sánchez et al
Int Arch Allergy Immunol (2016) 169 (4), 249-55
Abstract: Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent agents involved in hypersensitivity drug reactions, with NSAID-induced urticaria and/or angioedema (NIUA) being the most common entity. Mast cells are key players in NIUA and are activated by thymic stromal lymphopoietin (TSLP). This cytokine functions through recognition by its receptor, composed of IL7Rα (interleukin-7 receptor alpha) and TSLPR (TSLP receptor). These genes have been previously associated with other inflammatory diseases.We assessed the genetic association between single nucleotide polymorphisms (SNPs) in TSLP, IL7R and TSLPR and NIUA in Spanish individuals, using genotyped and imputed data. A total of 369 unrelated NIUA patients and 580 NSAID-tolerant control subjects were included, and 6 SNPs in TSLP, 6 in IL7R and 3 in TSLPR were genotyped. Further variants were imputed using Mach and the 1,000 Genomes Project (Phase 3) data. Association testing and statistical analyses were performed with Mach2dat and R.A total of 139 SNPs were tested for association following quality control. Two SNPs in TSLP (rs1816678 and rs764917) showed a nominal association (p = 0.033 and 0.024, respectively) with NIUA, although these results were not statistically significant after correcting for multiple comparisons.Although TSLP, IL7R and TSLPR are important genes involved in the development of the inflammatory response, we found no significant genetic association with NIUA in our population for common SNPs in these genes.© 2016 S. Karger AG, Basel.
Altered responses to homeostatic cytokines in patients with idiopathic CD4 lymphocytopenia
Bugault, Benati, Mouthon et al
PLoS One (2013) 8 (1), e55570
Abstract: Idiopathic CD4 lymphocytopenia (ICL) is a rare immune deficiency characterized by a protracted CD4(+) T cell loss of unknown etiology and by the occurrence of opportunistic infections similar to those seen in AIDS. We investigated whether a defect in responses to cytokines that control CD4(+) T cell homeostasis could play a role in ICL. Immunophenotype and signaling responses to interleukin-7 (IL-7), IL-2, and thymic stromal lymphopoietin (TSLP) were analyzed by flow cytometry in CD4(+) T cells from 15 ICL patients and 15 healthy blood donors. The induction of phospho-STAT5 after IL-7 stimulation was decreased in memory CD4(+) T cells of some ICL patients, which correlated with a decreased expression of the IL-7Rα receptor chain (R = 0.74, p<0.005) and with lower CD4(+) T cell counts (R = 0.69, p<0.005). IL-2 responses were also impaired, both in the Treg and conventional memory subsets. Decreased IL-2 responses correlated with decreased IL-7 responses (R = 0.75, p<0.005), pointing to combined defects that may significantly perturb CD4(+) T cell homeostasis in a subset of ICL patients. Unexpectedly, responses to the IL-7-related cytokine TSLP were increased in ICL patients, while they remained barely detectable in healthy controls. TSLP responses correlated inversely with IL-7 responses (R = -0.41; p<0.05), suggesting a cross-regulation between the two cytokine systems. In conclusion, IL-7 and IL-2 signaling are impaired in ICL, which may account for the loss of CD4(+) T cell homeostasis. Increased TSLP responses point to a compensatory homeostatic mechanism that may mitigate defects in γc cytokine responses.
Showing 1-4 of 6 papers.
Powered by BizGenius
 
 
货号/价格
文档
联系电话:
+86 400-682-2521(全国)
010-53681107(北京)
021-50850665(上海)
运输方式
订单邮箱:
order.cn@acrobiosystems.com
技术支持邮箱:
tech.cn@acrobiosystems.com
IL-7 R alpha & TSLP R靶点信息
英文全称:Interleukin-7 receptor subunit alpha
中文全称:白细胞介素-7受体α亚基
种类:Homo sapiens
上市药物数量:0详情
临床药物数量:7详情
最高研发阶段:临床二期
查看更多信息
前沿进展
点击查看详细

消息提示

请输入您的联系方式,再点击提交!

确定