Genieplex Quantitative Multiplex Immunoassays
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Human Angiogenin Fused to Human CD30 Ligand (Ang-CD30L) Exhibits Specific Cytotoxicity Against CD30-Positive Lymphoma1
[CANCER RESEARCH 61, 8737–8742, December 15, 2001] Human Angiogenin Fused to Human CD30 Ligand (Ang-CD30L) Exhibits Specific Cytotoxicity against CD30-positive Lymphoma1 Michael Huhn, Stephanie Sasse, Mehmet K. Tur, Ba¨rbel Matthey, Timo Schinko¨the, Susanna M. Rybak, Stefan Barth,2 and Andreas Engert Fraunhofer IME, Department of Pharmaceutical Product Development, 52074 Aachen, Germany [M. K. T., M. H., S. B.]; Laboratory of Immunotherapy, Department I of Internal Medicine, University Hospital Cologne, 50931 Cologne, Germany [S. S., B. M., T. S., A. E.]; Developmental Therapeutics Program, Division of Cancer Treatment and Diagnosis, National Cancer Institute-Frederick Cancer Research and Development Center, Frederick, MD 21702 [S. M. R.] ABSTRACT first and then to administer ITs to kill residual H-RS cells. One of the most promising target antigens for immunotherapy of malignant lym- A number of different immunotoxins composed of cell-specific target- phoma such as Hodgkin’s lymphoma or anaplastic large cell lym- ing structures coupled to plant or bacterial toxins have increasingly been phoma is the CD30 receptor. This antigen was originally discovered evaluated for immunotherapy. Because these foreign proteins are highly immunogenic in humans, we have developed a new CD30 ligand-based on cultured H-RS cells using the moab Ki-1 (1). The gene encoding fusion toxin (Ang-CD30L) using the human RNase angiogenin. The com- the CD30 receptor molecule (2) is located on chromosome 1p36. The pletely human fusion gene was inserted into a pET-based expression naturally occurring CD30 ligand has also been identified and cloned plasmid. Transformed Escherichia coli BL21(DE3) were grown under (3). -
The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology
Cell, Vol. 104, 487±501, February 23, 2001, Copyright 2001 by Cell Press The TNF and TNF Receptor Review Superfamilies: Integrating Mammalian Biology Richard M. Locksley,*²³k Nigel Killeen,²k The receptors and ligands in this superfamily have and Michael J. Lenardo§k unique structural attributes that couple them directly to *Department of Medicine signaling pathways for cell proliferation, survival, and ² Department of Microbiology and Immunology differentiation. Thus, they have assumed prominent ³ Howard Hughes Medical Institute roles in the generation of tissues and transient microen- University of California, San Francisco vironments. Most TNF/TNFR SFPs are expressed in the San Francisco, California 94143 immune system, where their rapid and potent signaling § Laboratory of Immunology capabilities are crucial in coordinating the proliferation National Institute of Allergy and Infectious Diseases and protective functions of pathogen-reactive cells. National Institutes of Health Here, we review the organization of the TNF/TNFR SF Bethesda, Maryland 20892 and how these proteins have been adapted for pro- cesses as seemingly disparate as host defense and or- ganogenesis. In interpreting this large and highly active Introduction area of research, we have focused on common themes that unite the actions of these genes in different tissues. Three decades ago, lymphotoxin (LT) and tumor necro- We also discuss the evolutionary success of this super- sis factor (TNF) were identified as products of lympho- familyÐsuccess that we infer from its expansion across cytes and macrophages that caused the lysis of certain the mammalian genome and from its many indispens- types of cells, especially tumor cells (Granger et al., able roles in mammalian biology. -
Tools for Cell Therapy and Immunoregulation
RnDSy-lu-2945 Tools for Cell Therapy and Immunoregulation Target Cell TIM-4 SLAM/CD150 BTNL8 PD-L2/B7-DC B7-H1/PD-L1 (Human) Unknown PD-1 B7-1/CD80 TIM-1 SLAM/CD150 Receptor TIM Family SLAM Family Butyrophilins B7/CD28 Families T Cell Multiple Co-Signaling Molecules Co-stimulatory Co-inhibitory Ig Superfamily Regulate T Cell Activation Target Cell T Cell Target Cell T Cell B7-1/CD80 B7-H1/PD-L1 T cell activation requires two signals: 1) recognition of the antigenic peptide/ B7-1/CD80 B7-2/CD86 CTLA-4 major histocompatibility complex (MHC) by the T cell receptor (TCR) and 2) CD28 antigen-independent co-stimulation induced by interactions between B7-2/CD86 B7-H1/PD-L1 B7-1/CD80 co-signaling molecules expressed on target cells, such as antigen-presenting PD-L2/B7-DC PD-1 ICOS cells (APCs), and their T cell-expressed receptors. Engagement of the TCR in B7-H2/ICOS L 2Ig B7-H3 (Mouse) the absence of this second co-stimulatory signal typically results in T cell B7-H1/PD-L1 B7/CD28 Families 4Ig B7-H3 (Human) anergy or apoptosis. In addition, T cell activation can be negatively regulated Unknown Receptors by co-inhibitory molecules present on APCs. Therefore, integration of the 2Ig B7-H3 Unknown B7-H4 (Mouse) Receptors signals transduced by co-stimulatory and co-inhibitory molecules following TCR B7-H5 4Ig B7-H3 engagement directs the outcome and magnitude of a T cell response Unknown Ligand (Human) B7-H5 including the enhancement or suppression of T cell proliferation, B7-H7 Unknown Receptor differentiation, and/or cytokine secretion. -
Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes
Journal of Clinical Medicine Article Tacrolimus Prevents TWEAK-Induced PLA2R Expression in Cultured Human Podocytes Leticia Cuarental 1,2, Lara Valiño-Rivas 1,2, Luis Mendonça 3, Moin Saleem 4, Sergio Mezzano 5, Ana Belen Sanz 1,2 , Alberto Ortiz 1,2,* and Maria Dolores Sanchez-Niño 1,2,* 1 IIS-Fundacion Jimenez Diaz, Universidad Autonoma de Madrid, Fundacion Renal Iñigo Alvarez de Toledo-IRSIN, 28040 Madrid, Spain; [email protected] (L.C.); [email protected] (L.V.-R.); [email protected] (A.B.S.) 2 Red de Investigación Renal (REDINREN), Fundacion Jimenez Diaz, 28040 Madrid, Spain 3 Nephrology Department, Centro Hospitalar Universitário São João, 4200-319 Porto, Portugal; [email protected] 4 Bristol Renal, University of Bristol, Bristol BS8 1TH, UK; [email protected] 5 Laboratorio de Nefrologia, Facultad de Medicina, Universidad Austral de Chile, 5090000 Valdivia, Chile; [email protected] * Correspondence: [email protected] (A.O.); [email protected] (M.D.S.-N.); Tel.: +34-91-550-48-00 (A.O. & M.D.S.-N.) Received: 29 May 2020; Accepted: 7 July 2020; Published: 10 July 2020 Abstract: Primary membranous nephropathy is usually caused by antibodies against the podocyte antigen membrane M-type phospholipase A2 receptor (PLA2R). The treatment of membranous nephropathy is not fully satisfactory. The calcineurin inhibitor tacrolimus is used to treat membranous nephropathy, but recurrence upon drug withdrawal is common. TNF superfamily members are key mediators of kidney injury. We have now identified key TNF receptor superfamily members in podocytes and explored the regulation of PLA2R expression and the impact of tacrolimus. -
Autologous T Cells Expressing CD30 Chimeric Antigen Receptors For
Published OnlineFirst August 31, 2016; DOI: 10.1158/1078-0432.CCR-16-1365 Cancer Therapy: Clinical Clinical Cancer Research Autologous T Cells Expressing CD30 Chimeric Antigen Receptors for Relapsed or Refractory Hodgkin Lymphoma: An Open-Label Phase I Trial Chun-Meng Wang1, Zhi-Qiang Wu2,YaoWang3, Ye-Lei Guo3,Han-RenDai3, Xiao-Hui Wang2, Xiang Li2, Ya-Jing Zhang1,Wen-YingZhang1, Mei-Xia Chen1, Yan Zhang1, Kai-Chao Feng1,YangLiu4,Su-XiaLi4, Qing-Ming Yang1, and Wei-Dong Han3 Abstract Purpose: Relapsed or refractory Hodgkin lymphoma is a chal- tolerated, with grade 3 toxicities occurring only in two of 18 lenge for medical oncologists because of poor overall survival. We patients. Of 18 patients, seven achieved partial remission and six aimed to assess the feasibility, safety, and efficacy of CD30- achieved stable disease. An inconsistent response of lymphoma targeting CAR T cells in patients with progressive relapsed or was observed: lymph nodes presented a better response than refractory Hodgkin lymphoma. extranodal lesions and the response of lung lesions seemed to Experimental Design: Patients with relapsed or refractory be relatively poor. Lymphocyte recovery accompanied by an Hodgkin lymphoma received a conditioning chemotherapy fol- increase of circulating CAR T cells (peaking between 3 and 9 days lowed by the CART-30 cell infusion. The level of CAR transgenes after infusion) is a probable indictor of clinical response. Analysis in peripheral blood and biopsied tumor tissues was measured of biopsied tissues by qPCR and immunohistochemistry revealed periodically according to an assigned protocol by quantitative the trafficking of CAR T cells into the targeted sites and reduction PCR (qPCR). -
A Computational Approach for Defining a Signature of Β-Cell Golgi Stress in Diabetes Mellitus
Page 1 of 781 Diabetes A Computational Approach for Defining a Signature of β-Cell Golgi Stress in Diabetes Mellitus Robert N. Bone1,6,7, Olufunmilola Oyebamiji2, Sayali Talware2, Sharmila Selvaraj2, Preethi Krishnan3,6, Farooq Syed1,6,7, Huanmei Wu2, Carmella Evans-Molina 1,3,4,5,6,7,8* Departments of 1Pediatrics, 3Medicine, 4Anatomy, Cell Biology & Physiology, 5Biochemistry & Molecular Biology, the 6Center for Diabetes & Metabolic Diseases, and the 7Herman B. Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN 46202; 2Department of BioHealth Informatics, Indiana University-Purdue University Indianapolis, Indianapolis, IN, 46202; 8Roudebush VA Medical Center, Indianapolis, IN 46202. *Corresponding Author(s): Carmella Evans-Molina, MD, PhD ([email protected]) Indiana University School of Medicine, 635 Barnhill Drive, MS 2031A, Indianapolis, IN 46202, Telephone: (317) 274-4145, Fax (317) 274-4107 Running Title: Golgi Stress Response in Diabetes Word Count: 4358 Number of Figures: 6 Keywords: Golgi apparatus stress, Islets, β cell, Type 1 diabetes, Type 2 diabetes 1 Diabetes Publish Ahead of Print, published online August 20, 2020 Diabetes Page 2 of 781 ABSTRACT The Golgi apparatus (GA) is an important site of insulin processing and granule maturation, but whether GA organelle dysfunction and GA stress are present in the diabetic β-cell has not been tested. We utilized an informatics-based approach to develop a transcriptional signature of β-cell GA stress using existing RNA sequencing and microarray datasets generated using human islets from donors with diabetes and islets where type 1(T1D) and type 2 diabetes (T2D) had been modeled ex vivo. To narrow our results to GA-specific genes, we applied a filter set of 1,030 genes accepted as GA associated. -
CD226 T Cells Expressing the Receptors TIGIT and Divergent Phenotypes of Human Regulatory
The Journal of Immunology Divergent Phenotypes of Human Regulatory T Cells Expressing the Receptors TIGIT and CD226 Christopher A. Fuhrman,*,1 Wen-I Yeh,*,1 Howard R. Seay,* Priya Saikumar Lakshmi,* Gaurav Chopra,† Lin Zhang,* Daniel J. Perry,* Stephanie A. McClymont,† Mahesh Yadav,† Maria-Cecilia Lopez,‡ Henry V. Baker,‡ Ying Zhang,x Yizheng Li,{ Maryann Whitley,{ David von Schack,x Mark A. Atkinson,* Jeffrey A. Bluestone,‡ and Todd M. Brusko* Regulatory T cells (Tregs) play a central role in counteracting inflammation and autoimmunity. A more complete understanding of cellular heterogeneity and the potential for lineage plasticity in human Treg subsets may identify markers of disease pathogenesis and facilitate the development of optimized cellular therapeutics. To better elucidate human Treg subsets, we conducted direct transcriptional profiling of CD4+FOXP3+Helios+ thymic-derived Tregs and CD4+FOXP3+Helios2 T cells, followed by comparison with CD4+FOXP32Helios2 T conventional cells. These analyses revealed that the coinhibitory receptor T cell Ig and ITIM domain (TIGIT) was highly expressed on thymic-derived Tregs. TIGIT and the costimulatory factor CD226 bind the common ligand CD155. Thus, we analyzed the cellular distribution and suppressive activity of isolated subsets of CD4+CD25+CD127lo/2 T cells expressing CD226 and/or TIGIT. We observed TIGIT is highly expressed and upregulated on Tregs after activation and in vitro expansion, and is associated with lineage stability and suppressive capacity. Conversely, the CD226+TIGIT2 population was associated with reduced Treg purity and suppressive capacity after expansion, along with a marked increase in IL-10 and effector cytokine production. These studies provide additional markers to delineate functionally distinct Treg subsets that may help direct cellular therapies and provide important phenotypic markers for assessing the role of Tregs in health and disease. -
TRAIL and Cardiovascular Disease—A Risk Factor Or Risk Marker: a Systematic Review
Journal of Clinical Medicine Review TRAIL and Cardiovascular Disease—A Risk Factor or Risk Marker: A Systematic Review Katarzyna Kakareko 1,* , Alicja Rydzewska-Rosołowska 1 , Edyta Zbroch 2 and Tomasz Hryszko 1 1 2nd Department of Nephrology and Hypertension with Dialysis Unit, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] (A.R.-R.); [email protected] (T.H.) 2 Department of Internal Medicine and Hypertension, Medical University of Białystok, 15-276 Białystok, Poland; [email protected] * Correspondence: [email protected] Abstract: Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) is a pro-apoptotic protein showing broad biological functions. Data from animal studies indicate that TRAIL may possibly contribute to the pathophysiology of cardiomyopathy, atherosclerosis, ischemic stroke and abdomi- nal aortic aneurysm. It has been also suggested that TRAIL might be useful in cardiovascular risk stratification. This systematic review aimed to evaluate whether TRAIL is a risk factor or risk marker in cardiovascular diseases (CVDs) focusing on major adverse cardiovascular events. Two databases (PubMed and Cochrane Library) were searched until December 2020 without a year limit in accor- dance to the PRISMA guidelines. A total of 63 eligible original studies were identified and included in our systematic review. Studies suggest an important role of TRAIL in disorders such as heart failure, myocardial infarction, atrial fibrillation, ischemic stroke, peripheral artery disease, and pul- monary and gestational hypertension. Most evidence associates reduced TRAIL levels and increased TRAIL-R2 concentration with all-cause mortality in patients with CVDs. It is, however, unclear Citation: Kakareko, K.; whether low TRAIL levels should be considered as a risk factor rather than a risk marker of CVDs. -
Single-Cell RNA Sequencing Demonstrates the Molecular and Cellular Reprogramming of Metastatic Lung Adenocarcinoma
ARTICLE https://doi.org/10.1038/s41467-020-16164-1 OPEN Single-cell RNA sequencing demonstrates the molecular and cellular reprogramming of metastatic lung adenocarcinoma Nayoung Kim 1,2,3,13, Hong Kwan Kim4,13, Kyungjong Lee 5,13, Yourae Hong 1,6, Jong Ho Cho4, Jung Won Choi7, Jung-Il Lee7, Yeon-Lim Suh8,BoMiKu9, Hye Hyeon Eum 1,2,3, Soyean Choi 1, Yoon-La Choi6,10,11, Je-Gun Joung1, Woong-Yang Park 1,2,6, Hyun Ae Jung12, Jong-Mu Sun12, Se-Hoon Lee12, ✉ ✉ Jin Seok Ahn12, Keunchil Park12, Myung-Ju Ahn 12 & Hae-Ock Lee 1,2,3,6 1234567890():,; Advanced metastatic cancer poses utmost clinical challenges and may present molecular and cellular features distinct from an early-stage cancer. Herein, we present single-cell tran- scriptome profiling of metastatic lung adenocarcinoma, the most prevalent histological lung cancer type diagnosed at stage IV in over 40% of all cases. From 208,506 cells populating the normal tissues or early to metastatic stage cancer in 44 patients, we identify a cancer cell subtype deviating from the normal differentiation trajectory and dominating the metastatic stage. In all stages, the stromal and immune cell dynamics reveal ontological and functional changes that create a pro-tumoral and immunosuppressive microenvironment. Normal resident myeloid cell populations are gradually replaced with monocyte-derived macrophages and dendritic cells, along with T-cell exhaustion. This extensive single-cell analysis enhances our understanding of molecular and cellular dynamics in metastatic lung cancer and reveals potential diagnostic and therapeutic targets in cancer-microenvironment interactions. 1 Samsung Genome Institute, Samsung Medical Center, Seoul 06351, Korea. -
Clinical Trials of CAR-T Cells in China Bingshan Liu1,2, Yongping Song2* and Delong Liu2*
Liu et al. Journal of Hematology & Oncology (2017) 10:166 DOI 10.1186/s13045-017-0535-7 RAPID COMMUNICATION Open Access Clinical trials of CAR-T cells in China Bingshan Liu1,2, Yongping Song2* and Delong Liu2* Abstract Novel immunotherapeutic agents targeting tumor-site microenvironment are revolutionizing cancer therapy. Chimeric antigen receptor (CAR)-engineered T cells are widely studied for cancer immunotherapy. CD19-specific CAR-T cells, tisagenlecleucel, have been recently approved for clinical application. Ongoing clinical trials are testing CAR designs directed at novel targets involved in hematological and solid malignancies. In addition to trials of single-target CAR-T cells, simultaneous and sequential CAR-T cells are being studied for clinical applications. Multi-target CAR-engineered T cells are also entering clinical trials. T cell receptor-engineered CAR-T and universal CAR-T cells represent new frontiers in CAR-T cell development. In this study, we analyzed the characteristics of CAR constructs and registered clinical trials of CAR-T cells in China and provided a quick glimpse of the landscape of CAR-T studies in China. Background “third generation chimeric,” and “fourth generation chimeric”; Novel immunotherapeutic agents targeting CTLA-4, country: China. All relevant trials registered at the Clinical- programmed cell death-1 protein receptor (PD-1), and the Trials.gov prior to July 18, 2017, were included in the analysis. ligand PD-L1 are revolutionizing cancer therapy [1–7]. One trial was excluded (NCT03121625) because the target Cancer immunotherapy by re-igniting T cells through antigen was not disclosed. A search of the PubMed blocking PD-1 and PD-L1 is highly potent in a variety of databasewasalsodonetoincludethosetrialsand malignancies [8–12]. -
Mouse TWEAK/TNFSF12 Antibody Antigen Affinity-Purified Polyclonal Goat Igg Catalog Number: AF1237
Mouse TWEAK/TNFSF12 Antibody Antigen Affinity-purified Polyclonal Goat IgG Catalog Number: AF1237 DESCRIPTION Species Reactivity Mouse Specificity Detects TWEAK/TNFSF12 in direct ELISAs and Western blots. In direct ELISAs, approximately 30% crossreactivity with recombinant human TWEAK is observed and less than 1% crossreactivity with recombinant mouse (rm) BAFF, rmFas Ligand, rmOX40 Ligand, rmTNFα, and rmTRAIL is observed. Source Polyclonal Goat IgG Purification Antigen Affinitypurified Immunogen E. coliderived recombinant mouse TWEAK/TNFSF12 Arg105His249 Accession # O54907 Endotoxin Level <0.10 EU per 1 μg of the antibody by the LAL method. Formulation Lyophilized from a 0.2 μm filtered solution in PBS with Trehalose. See Certificate of Analysis for details. APPLICATIONS Please Note: Optimal dilutions should be determined by each laboratory for each application. General Protocols are available in the Technical Information section on our website. Recommended Sample Concentration Western Blot 0.1 µg/mL Recombinant Mouse TWEAK/TNFSF12 (Catalog # 1237TW) Neutralization Measured by its ability to neutralize TWEAK/TNFSF12induced inhibition of proliferation in the HT29 human colon adenocarcinoma cell line. Yu, K. Y. et al. (1999) J. Biol. Chem. 274:13733; Harrop, J. A. et al. (1998) J. Biol. Chem. 273:27548The Neutralization Dose (ND ) is typically 416 µg/mL in the presence of 2 µg/mL Recombinant 50 Mouse TWEAK/TNFSF12. DATA Neutralization TWEAK/TNFSF12 Inhibition of Cell Proliferation and Neutralization by Mouse TWEAK/TNFSF12 Antibody. Recombinant Mouse TWEAK/TNFSF12 (Catalog # 1237TW) inhibits proliferation in the the HT29 human colon adenocarcinoma cell line in a dosedependent manner (orange line). -
CD134/OX40 Code No
D125-3 For Research Use Only. Page 1 of 2 Not for use in diagnostic procedures. MONOCLONAL ANTIBODY CD134/OX40 Code No. Clone Subclass Quantity Concentration D125-3 W4-3 Rat IgG2a 100 L 1 mg/mL BACKGROUND: OX40 (CD134/TNFRSF4/ACT35) is SPECIES CROSS REACTIVITY: a 50 kDa of cell surface glycoprotein. OX40, a member of Species Human Mouse Rat the tumor necrosis factor (TNF) superfamily, is expressed primarily on activated CD4+ T cells. OX40 interacts with Cells MT2, HPB-MLT Not Tested Not Tested OX40 ligand antigen (OX40L, also known as CD252/gp34/CD134L) expressed on activated B cells and Reactivity on FCM + antigen presenting cells results in enhanced T cell proliferation and induction of IL-2 production. REFERENCES: OX40/OX40L interaction provides a costimulatory signal, 1) Kawamata, S., et al., J. Biol. Chem. 273, 5808-5814 (1998) resulting in enhanced T cell proliferation and cytokine 2) Latza, U., et al., Europ. J. Immun. 24, 677-683 (1994) production. Then, cell proliferation and immunoglobulin secretion in activated B cells are enhanced. OX40/OX40L system mediates the adhesion of activated or HTLV-I-transformed T cells to vascular endothelial cells. TRAF2 and TRAF5 binding to OX40 led to NF-B activation, and TRAF3 binding appeared to inhibit NF-B activation SOURCE: This antibody was purified from C.B-17 SCID mice ascites fluid using protein A agarose. This hybridoma (clone W4-3) was established by fusion of mouse myeloma cell SP2/0 with WKA/H rat splenocyte immunized with the human OX40 transfectant. Flow cytometric analysis of CD134 expression on HPB-MLT (left) and PM1 FORMULATION: 100 g IgG in 100 L volume of (right).