A CD2/CD28 Chimeric Receptor Triggers the CD28 Signaling Pathway in CTLL.2 Cells
Total Page:16
File Type:pdf, Size:1020Kb
Load more
Recommended publications
-
Costimulation of T-Cell Activation and Virus Production by B7 Antigen on Activated CD4+ T Cells from Human Immunodeficiency Virus Type 1-Infected Donors OMAR K
Proc. Natl. Acad. Sci. USA Vol. 90, pp. 11094-11098, December 1993 Immunology Costimulation of T-cell activation and virus production by B7 antigen on activated CD4+ T cells from human immunodeficiency virus type 1-infected donors OMAR K. HAFFAR, MOLLY D. SMITHGALL, JEFFREY BRADSHAW, BILL BRADY, NITIN K. DAMLE*, AND PETER S. LINSLEY Bristol-Myers Squibb Pharmaceutical Research Institute, Seattle, WA 98121 Communicated by Leon E. Rosenberg, August 3, 1993 (receivedfor review April 29, 1993) ABSTRACT Infection with the human immunodeficiency sequence (CTLA-4) (34), a protein structurally related to virus type 1 (HIV-1) requires T-cefl activation. Recent studies CD28 but only expressed on T cells after activation (12). have shown that interactions of the T-lymphocyte receptors CTLA-4 acts cooperatively with CD28 to bind B7 and deliver CD28 and CTLA-4 with their counter receptor, B7, on antigen- T-cell costimulatory signals (13). presenting cells are required for optimal T-cell activation. Here Because of the importance of the CD28/CTLA-4 and B7 we show that HIV-1 infection is associated with decreased interactions in immune responses, it is likely that these expression of CD28 and increased expression of B7 on CD4+ interactions are also important during HIV-1 infection. Stud- T-cell lines generated from seropositive donors by afloantigen ies with anti-CD28 monoclonal antibodies (mAbs) suggested stimulation. Loss of CD28 expression was not seen on CD4+ a role for CD28 in up-regulating HIV-1 long terminal repeat- T-ceU lines from seronegative donors, but up-regulation of B7 driven transcription of a reporter gene in leukemic cell lines expression was observed upon more prolonged culture. -
Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse
Welcome to More Choice CD Marker Handbook For more information, please visit: Human bdbiosciences.com/eu/go/humancdmarkers Mouse bdbiosciences.com/eu/go/mousecdmarkers Human and Mouse CD Marker Handbook Human and Mouse CD Marker Key Markers - Human Key Markers - Mouse CD3 CD3 CD (cluster of differentiation) molecules are cell surface markers T Cell CD4 CD4 useful for the identification and characterization of leukocytes. The CD CD8 CD8 nomenclature was developed and is maintained through the HLDA (Human Leukocyte Differentiation Antigens) workshop started in 1982. CD45R/B220 CD19 CD19 The goal is to provide standardization of monoclonal antibodies to B Cell CD20 CD22 (B cell activation marker) human antigens across laboratories. To characterize or “workshop” the antibodies, multiple laboratories carry out blind analyses of antibodies. These results independently validate antibody specificity. CD11c CD11c Dendritic Cell CD123 CD123 While the CD nomenclature has been developed for use with human antigens, it is applied to corresponding mouse antigens as well as antigens from other species. However, the mouse and other species NK Cell CD56 CD335 (NKp46) antibodies are not tested by HLDA. Human CD markers were reviewed by the HLDA. New CD markers Stem Cell/ CD34 CD34 were established at the HLDA9 meeting held in Barcelona in 2010. For Precursor hematopoetic stem cell only hematopoetic stem cell only additional information and CD markers please visit www.hcdm.org. Macrophage/ CD14 CD11b/ Mac-1 Monocyte CD33 Ly-71 (F4/80) CD66b Granulocyte CD66b Gr-1/Ly6G Ly6C CD41 CD41 CD61 (Integrin b3) CD61 Platelet CD9 CD62 CD62P (activated platelets) CD235a CD235a Erythrocyte Ter-119 CD146 MECA-32 CD106 CD146 Endothelial Cell CD31 CD62E (activated endothelial cells) Epithelial Cell CD236 CD326 (EPCAM1) For Research Use Only. -
T-Cell Antigen CD28 Mediates Adhesion with B Cells by Interacting with Activation Antigen B7/BB-1 PETER S
Proc. Nati. Acad. Sci. USA Vol. 87, pp. 5031-5035, July 1990 Immunology T-cell antigen CD28 mediates adhesion with B cells by interacting with activation antigen B7/BB-1 PETER S. LINSLEY*, EDWARD A. CLARKt, AND JEFFREY A. LEDBETTER* *Oncogen, 3005 First Avenue, Seattle, WA 98121; and tDepartment of Microbiology, University of Washington, Seattle, WA 98195 Communicated by Seymour J. Klebanoff, March 30, 1990 ABSTRACT Studies using monoclonal antibodies (mAbs) intercellular adhesion mediated by major histocompatibility have implicated the homodimeric glycoprotein CD28 as an complex (MHC) class I (13) and class II (14) molecules with important regulator of human T-cell activation, in part by the CD8 and CD4 accessory molecules, respectively. We posttranscriptional control ofcytokine mRNA levels. Although have expressed the CD28 antigen to high levels in Chinese the CD28 antigen has functional and structural characteristics hamster ovary (CHO) cells and have used these transfected of a receptor, a natural ligand for this molecule has not been cells to develop a CD28-mediated cell adhesion assay. By identified. Here we show that the CD28 antigen, expressed in using this assay as a screening method, we have demon- Chinese hamster ovary (CHO) cells, mediated specific inter- strated an interaction between CD28 and a natural ligand cellular adhesion with human lymphoblastoid and leukemic expressed on activated B lymphocytes, the B7/BB-1 antigen. B-cell lines and with activated primary murine B cells. CD28- mediated adhesion was not, dependant upon divalent cations. Several mAbs were identified that inhibited CD28-mediated MATERIALS AND METHODS adhesion, including mAb BB-1 against the B-cell activation mAbs. -
Papers J Clin Pathol: First Published As 10.1136/Jcp.49.7.539 on 1 July 1996
Clin Pathol 1996;49:539-544 539 Papers J Clin Pathol: first published as 10.1136/jcp.49.7.539 on 1 July 1996. Downloaded from Differential expression of T cell antigens in normal peripheral blood lymphocytes: a quantitative analysis by flow cytometry L Ginaldi, N Farahat, E Matutes, M De Martinis, R Morilla, D Catovsky Abstract diagnosis by comparison with findings in Aims-To obtain reference values of the normal counterparts. level of expression of T cell antigens on ( Clin Pathol 1996;49:539-544) normal lymphocyte subsets in order to disclose differences which could reflect Keywords: flow cytometry, T cell antigens, peripheral their function or maturation stages, or blood lymphocytes. both. Methods-Peripheral blood from 15 healthy donors was processed by flow The most common use of flow cytometry is to cytometry with triple colour analysis. For determine the percent of "positive" or "nega- each sample phycoerythrin (PE) conju- tive" cells for each antigen in different cell gated CD2, CD4, CD5, CD8, and CD56 populations. However, valuable information is monoclonal antibodies were combined lost when the relative intensities of the positive with Cy5-R-phycoerythrin (TC) conju- cells, reflecting antigenic densities, are not considered. A cell population with a well gated CD3 and fluorescein isothiocyanate http://jcp.bmj.com/ (FITC) conjugated CD7; CD2- and defined phenotype, positive for one antigen, CD7-PE were also combined with might be heterogeneous with regard to its level CD3-TC and CD4-FITC. Standard mi- of expression. This may reflect different crobeads with different capacities to bind functional or maturational states, or both, or mouse immunoglobulins were used to identify subpopulations on the basis of the dif- convert the mean fluorescence intensity ferent numbers of molecules of antigen per cell. -
Signaling Expression by IL-7 and TCR Α Receptor Differential Regulation
Differential Regulation of Human IL-7 Receptor α Expression by IL-7 and TCR Signaling This information is current as Nuno L. Alves, Ester M. M. van Leeuwen, Ingrid A. M. of September 24, 2021. Derks and René A. W. van Lier J Immunol 2008; 180:5201-5210; ; doi: 10.4049/jimmunol.180.8.5201 http://www.jimmunol.org/content/180/8/5201 Downloaded from References This article cites 36 articles, 19 of which you can access for free at: http://www.jimmunol.org/content/180/8/5201.full#ref-list-1 http://www.jimmunol.org/ Why The JI? Submit online. • Rapid Reviews! 30 days* from submission to initial decision • No Triage! Every submission reviewed by practicing scientists • Fast Publication! 4 weeks from acceptance to publication by guest on September 24, 2021 *average Subscription Information about subscribing to The Journal of Immunology is online at: http://jimmunol.org/subscription Permissions Submit copyright permission requests at: http://www.aai.org/About/Publications/JI/copyright.html Email Alerts Receive free email-alerts when new articles cite this article. Sign up at: http://jimmunol.org/alerts The Journal of Immunology is published twice each month by The American Association of Immunologists, Inc., 1451 Rockville Pike, Suite 650, Rockville, MD 20852 Copyright © 2008 by The American Association of Immunologists All rights reserved. Print ISSN: 0022-1767 Online ISSN: 1550-6606. The Journal of Immunology Differential Regulation of Human IL-7 Receptor ␣ Expression by IL-7 and TCR Signaling1 Nuno L. Alves,2* Ester M. M. van Leeuwen,3*† Ingrid A. M. Derks,* and Rene´A. -
CD18) in a Patient with Leukocyte Adhesion Molecule (Leu-CAM) Deficiency
Point mutations impairing cell surface expression of the common beta subunit (CD18) in a patient with leukocyte adhesion molecule (Leu-CAM) deficiency. M A Arnaout, … , D G Tenen, D M Fathallah J Clin Invest. 1990;85(3):977-981. https://doi.org/10.1172/JCI114529. Research Article The leukocyte adhesion molecules CD11a/CD18, CD11b/CD18, and CD11c/CD18 (Leu-CAM) are members of the integrin receptor family and mediate crucial adhesion-dependent functions in leukocytes. The molecular basis for their deficient cell surface expression was sought in a patient suffering from severe and recurrent bacterial infections. Previous studies revealed that impaired cell surface expression of Leu-CAM is secondary to heterogeneous structural defects in the common beta subunit (CD18). Cloning and sequencing of complementary DNA encoding for CD18 in this patient revealed two mutant alleles, each representing a point mutation in the coding region of CD18 and resulting in an amino acid substitution. Each mutant allele results in impaired CD18 expression on the cell surface membrane of transfected COS M6 cells. One substitution involves an arginine residue (Arg593----cysteine) that is conserved in the highly homologous fourth cysteine-rich repeats of other mammalian integrin subfamilies. The other substitution involves a lysine residue (Lys196----threonine) located within another highly conserved region in integrins. These data identify crucial residues and regions necessary for normal cell surface expression of CD18 and possibly other integrin beta subunits and define a molecular basis for impaired cell surface expression of CD18 in this patient. Find the latest version: https://jci.me/114529/pdf Rapid Publication Point Mutations Impairing Cell Surface Expression of the Common ,B Subunit (CD18) in a Patient with Leukocyte Adhesion Molecule (Leu-CAM) Deficiency M. -
CD40-Deficient Mice GEORG A
Proc. Natl. Acad. Sci. USA Vol. 93, pp. 4994-4998, May 1996 Immunology Induction of alloantigen-specific tolerance by B cells from CD40-deficient mice GEORG A. HOLLXNDER*t, EMANUELA CASTIGLIt, ROBERT KULBACKI§, MICHAEL SU*, STEVEN J. BURAKOFF*, JOSEI-CARLOS GUTIERREZ-RAMOS§, AND RAIF S. GEHAt *Division of Pediatric Oncology, Dana-Farber Cancer Institute, Department of Pediatrics, tDivision of Immunology, The Children's Hospital, Department of Pediatrics, §Center for Blood Research, Harvard Medical School, Boston, MA 02115 Communicated by Frederick W Alt, The Children's Hospital, Boston, MA, January 22, 1996 (received for review November 17, 1995) ABSTRACT Interaction between CD40 on B cells and The capacity of B cells to provide ligands for T-cell specific CD40 ligand molecules on T cells is pivotal for the generation costimulatory molecules determines the outcome of T-cell of a thymus-dependent antibody response. Here we show that activation. Resting B cells express only limited amounts of B cells deficient in CD40 expression are unable to elicit the costimulatory molecules compared to activated B cells (11) proliferation of allogeneic T cells in vitro. More importantly, and are thus ineffective as antigen presenting cells (12). This mice immunized with CD40-1- B cells become tolerant to concept has also been demonstrated in vivo. For instance, allogeneic major histocompatibility complex (MHC) antigens monovalent rabbit anti-mouse IgD when presented by small as measured by a mixed lymphocyte reaction and cytotoxic resting B cells rendered mice tolerant to rabbit Ig (13). T-cell assay. The failure of CD40-'- B cells to serve as antigen Polyclonal activation of antigen presenting B cells (e.g., by presenting cells in vitro was corrected by the addition of crosslinking with divalent rabbit anti-mouse IgD) prevented anti-CD28 mAb. -
The Immunological Synapse and CD28-CD80 Interactions Shannon K
© 2001 Nature Publishing Group http://immunol.nature.com ARTICLES The immunological synapse and CD28-CD80 interactions Shannon K. Bromley1,Andrea Iaboni2, Simon J. Davis2,Adrian Whitty3, Jonathan M. Green4, Andrey S. Shaw1,ArthurWeiss5 and Michael L. Dustin5,6 Published online: 19 November 2001, DOI: 10.1038/ni737 According to the two-signal model of T cell activation, costimulatory molecules augment T cell receptor (TCR) signaling, whereas adhesion molecules enhance TCR–MHC-peptide recognition.The structure and binding properties of CD28 imply that it may perform both functions, blurring the distinction between adhesion and costimulatory molecules. Our results show that CD28 on naïve T cells does not support adhesion and has little or no capacity for directly enhancing TCR–MHC- peptide interactions. Instead of being dependent on costimulatory signaling, we propose that a key function of the immunological synapse is to generate a cellular microenvironment that favors the interactions of potent secondary signaling molecules, such as CD28. The T cell receptor (TCR) interaction with complexes of peptide and as CD2 and CD48, which suggests that CD28 might have a dual role as major histocompatibility complex (pMHC) is central to the T cell an adhesion and a signaling molecule4. Coengagement of CD28 with response. However, efficient T cell activation also requires the partici- the TCR has a number of effects on T cell activation; these include pation of additional cell-surface receptors that engage nonpolymorphic increasing sensitivity to TCR stimulation and increasing the survival of ligands on antigen-presenting cells (APCs). Some of these molecules T cells after stimulation5. CD80-transfected APCs have been used to are involved in the “physical embrace” between T cells and APCs and assess the temporal relationship of TCR and CD28 signaling, as initiat- are characterized as adhesion molecules. -
(12) United States Patent (405
USOO6291239B1 (12) United States Patent (10) Patent No.: US 6,291,239 B1 Prodinger et al. (45) Date of Patent: Sep. 18, 2001 (54) MONOCLONAL ANTIBODY Recess Formed Between SCR1 and SCR 2 of Complement Receptor Type Two', Prodinger. (76) Inventors: Wolfgang Prodinger, Kirschentalgasse Immunopharmacology, vol. 38, No. 1-2, Dec., 1997, pp. 16, A-6020 Innsbruck; Michael 141-148, XP002089604, “Expression in Insect Cells of the Schwendinger, Semmelweisgasse 4, Functional Domain of CD21 (Complement Receptor Type A-7100 Neusiedl/See, both of (AT) Two) as a Truncated... ", Prodinger. Journal of Immunology, vol. 156, No. 7 Apr. 1, 1996, pp. (*) Notice: Subject to any disclaimer, the term of this 2580–2584, XP002089605, “Ligation of the Functional patent is extended or adjusted under 35 Domain of Complement Receptor Type 2 (CR2, CD21) is U.S.C. 154(b) by 0 days. Relevant for Complex . , Prodinger. Journal of Immunology, vol. 154, No. 10, May 15, 1995, pp. (21) Appl. No.: 09/276,296 5426–5435, XP002089606, “Characterization of a Comple (22) Filed: Mar. 25, 1999 ment Receptor 2 (CR2, CD21) Ligand Binding Site for C3”, H. Molina et al. (51) Int. Cl. ............................... C12N 5/06; C12O 1/70; Journal of Immunology, vol. 161, Nov. 1, 1998, pp. G01N 33/53; CO7K 16/00; A61K 39/395 4604–4610, XP002089607, “Characterization of C3dg Binding to a Recess Formed Between Short Consensus (52) U.S. Cl. ............................ 435/339.1; 435/5; 435/7.1; Repeats 1 and 2 ... ', Prodinger. 435/334; 530/388.1; 530/388.35; 424/141.1; 424/143.1; 424/159.1 Primary Examiner Hankyel T. -
CD20-Positive Peripheral T-Cell Lymphoma: Report of a Case After Nodular Sclerosis Hodgkin’S Disease and Review of the Literature Renee L
CD20-Positive Peripheral T-Cell Lymphoma: Report of a Case after Nodular Sclerosis Hodgkin’s Disease and Review of the Literature Renee L. Mohrmann, M.D., Daniel A. Arber, M.D. Division of Pathology, City of Hope National Medical Center, Duarte, California CASE REPORT We present a case of peripheral T-cell lymphoma co-expressing CD3 and CD20, as well as demon- A 47-year-old man presented in 1993 with a brief strating T-cell receptor gene rearrangement, in a history of right axillary lymph node enlargement patient who had been diagnosed with nodular scle- and mild fatigue. Biopsy showed nodular sclerosis rosis Hodgkin’s disease 5 years previously. Although Hodgkin’s disease. He was treated with six courses 15 cases of CD20-positive T-cell neoplasms have of mechlorethamine, vincristine, procarbazine, been previously reported in the literature, this is the prednisone/doxorubicin, bleomycin, vinblastine first report of CD20-positive T-cell lymphoma oc- chemotherapy over a period of 6 months. Clinical curring subsequent to treatment of Hodgkin’s dis- remission was achieved for 5 years. In early 1998, the patient noticed enlargement of lymph nodes in ease. The current case affords an opportunity to the posterior cervical region, which were followed review the rarely reported expression of CD20 in clinically for several months. Weight loss of 15 lbs., T-cell neoplasms as well as the relationship between fatigue, and flu-like symptoms ensued. The lymph Hodgkin’s disease and subsequently occurring non- nodes became firmer to palpation and were biop- Hodgkin’s lymphomas. In addition, the identifica- sied, showing peripheral T-cell lymphoma, diffuse tion of this case supports the suggestion that the use large-cell type. -
Development of Canine Chimeric Antigen Receptor T Cell Therapy for Treatment & Translation
University of Pennsylvania ScholarlyCommons Publicly Accessible Penn Dissertations 2017 Development Of Canine Chimeric Antigen Receptor T Cell Therapy For Treatment & Translation Mohammed Kazim Panjwani University of Pennsylvania, [email protected] Follow this and additional works at: https://repository.upenn.edu/edissertations Part of the Allergy and Immunology Commons, Immunology and Infectious Disease Commons, Medical Immunology Commons, and the Oncology Commons Recommended Citation Panjwani, Mohammed Kazim, "Development Of Canine Chimeric Antigen Receptor T Cell Therapy For Treatment & Translation" (2017). Publicly Accessible Penn Dissertations. 2513. https://repository.upenn.edu/edissertations/2513 This paper is posted at ScholarlyCommons. https://repository.upenn.edu/edissertations/2513 For more information, please contact [email protected]. Development Of Canine Chimeric Antigen Receptor T Cell Therapy For Treatment & Translation Abstract Chimeric antigen receptor (CAR) T cell therapy has had remarkable success targeting B cell leukemias in human patients, but unexpected toxicities and failures in other disease demonstrate the need for more predictive pre-clinical animal models than the murine ones currently used. Dogs develop spontaneous malignancies similar to humans in their tissues of origin, gene expression profiles, treatments, and disease courses, and have long been used as models for immunotherapy. I hypothesize that the development of CAR T cell therapy for dogs with spontaneous disease and that the -
Immunological Synapse Formation Licenses CD40-CD40L Accumulations at T-APC Contact Sites1
The Journal of Immunology Immunological Synapse Formation Licenses CD40-CD40L Accumulations at T-APC Contact Sites1 Judie Boisvert, Samuel Edmondson, and Matthew F. Krummel2 The maintenance of tolerance is likely to rely on the ability of a T cell to polarize surface molecules providing “help” to only specific APCs. The formation of a mature immunological synapse leads to concentration of the TCR at the APC interface. In this study, we show that the CD40-CD154 receptor-ligand pair is also highly concentrated into a central region of the synapse on mouse lymphocytes only after the formation of the TCR/CD3 c-SMAC. Concentration of this ligand was strictly dependent on TCR recognition, the binding of ICAM-1 to T cell integrins and the presence of an intact cytoskeleton in the T cells. This may provide a novel explanation for the specificity of T cell help directing the help signal to the site of Ag receptor signal. It may also serve as a site for these molecular aggregates to coassociate and/or internalize alongside other signaling receptors. The Journal of Im- munology, 2004, 173: 3647–3652. uring the onset and propagation of immune responses, T Interactions of T cells with Ag-bearing APCs is associated with cells send and receive signals via Ag-dependent and Ag- a coalescence of TCRs, other related receptors such as CD2, CD4, independent ligands. Whereas peptide-class II MHC CD28, and signaling molecules such as p56lck, fyn, linker for ac- D ϩ complexes on APC are recognized by the TCR on CD4 helper T tivation of T cells, and protein kinase C into the central portion of cells, separate cell surface receptors modulate T cell-APC inter- an “immunological synapse” (15–23).