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Article ; Online: IL-9 exerts biological function on antigen-experienced murine T cells and exacerbates colitis induced by adoptive transfer.

de Heusch, Magali / Steenwinckel, Valérie / Cochez, Perrine M / Louahed, Jamila / Warnier, Guy / Lemaire, Muriel M / Renauld, Jean-Christophe / Dumoutier, Laure

European journal of immunology

2020 Volume 50, Issue 7, Page(s) 1034–1043

Abstract: IL-9 is involved in various T cell-dependent inflammatory models including colitis, encepahlitis, and asthma. However, the regulation and specificity of IL-9 responsiveness by T cells during immune responses remains poorly understood. Here, we addressed ... ...

Abstract	IL-9 is involved in various T cell-dependent inflammatory models including colitis, encepahlitis, and asthma. However, the regulation and specificity of IL-9 responsiveness by T cells during immune responses remains poorly understood. Here, we addressed this question using two different models: experimental colitis induced by transfer of naive CD4
MeSH term(s)	Adoptive Transfer/adverse effects ; Animals ; Colitis/etiology ; Colitis/genetics ; Colitis/immunology ; Colitis/pathology ; Disease Models, Animal ; Hyaluronan Receptors/genetics ; Hyaluronan Receptors/immunology ; Interleukin-2/genetics ; Interleukin-2/immunology ; Interleukin-9/genetics ; Interleukin-9/immunology ; Mice ; Mice, Knockout ; Mice, SCID ; Receptors, Interleukin-9/genetics ; Receptors, Interleukin-9/immunology ; Th17 Cells/immunology ; Th17 Cells/pathology ; Th17 Cells/transplantation ; Th2 Cells/immunology ; Th2 Cells/pathology ; Th2 Cells/transplantation
Chemical Substances	Cd44 protein, mouse ; Hyaluronan Receptors ; Il9r protein, mouse ; Interleukin-2 ; Interleukin-9 ; Receptors, Interleukin-9
Language	English
Publishing date	2020-03-18
Publishing country	Germany
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	120108-6
ISSN	1521-4141 ; 0014-2980
ISSN (online)	1521-4141
ISSN	0014-2980
DOI	10.1002/eji.201948430
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Article: 054 Manufactured Cells: C-Wash for C3BS clinical application

Steenwinckel, Valerie / Awidekian, R / Daro, D / De Waele, P / Deblandre, G / Link, O / Saccavino, I / Sunnanväder, A

Cryobiology. 2013 Dec., v. 67, no. 3

2013

Abstract: Cardio3 BioSciences (C3BS) is a Belgian biotechnology company focused on the discovery, development and commercialization of regenerative and protective therapies for the treatment of cardiac diseases. The challenge is to provide the injured heart with ... ...

Abstract	Cardio3 BioSciences (C3BS) is a Belgian biotechnology company focused on the discovery, development and commercialization of regenerative and protective therapies for the treatment of cardiac diseases. The challenge is to provide the injured heart with stem cells that have the capacity to act as if they are cardiac-specific progenitor cells. Therefore, C3BS developed a GMP therapy based on autologous bone marrow-derived and cardiogenically oriented mesenchymal stem cells (MSCs). The procedures used to prepare MSCs for clinical applications are based on enrichment of MSCs present in bone marrow mononuclear cells by plastic adherence, followed by in vitro expansion before injection to the patient. Since MSCs constitute a relatively rare subset of bone marrow cells, preparations for clinical purposes require a minimal cell loss during manufacturing steps including preservation of the cells. Two methodologies commonly used to facilitate cellular preservation are hypothermic storage (+2/+8°C) and cryopreservation (−80 to −196°C). The primary differences lie in their storage interval and their respective physical environments: storage in either a liquid or a solid/frozen state. Cardio3 BioSciences performed its phase I/II clinical trial using a hypothermic approach. If hypothermic storage is a simple and broadly applicable method for enhancing cell stability, it also lead to logistic burden linked to the short shelf life of the product. Ideally the hypothermic preservation solution should also serve as an excipient enabling administration of the product without additional manipulation at the clinical site. This first clinical experience led C3BS to develop a cryopreservation-reconditioning process, allowing to extended shelf-life, eliminate logistics problems and make commercialization success far more attainable. However, if cryopreservation of cellular product was relatively straightforward, development of a reconditioning method for final drug product, on clinical site and ready for injection, was more challenging. In that perspective, the Sepax 2 device from BioSafe S.A. (Switzerland) was evaluated as a washing device for removal of Me2SO and other manufacturing related impurities prior to cell injection. Sepax 2 is a fully-automated, portable, closed capacity system for processing of bone-marrow, peripheral blood or blood-like material, including stem cells. C3BS in collaboration with Biosafe developed a dedicated washing program, called C-Wash. This protocol is designed to concentrate the ready-to-use drug product in a range from 8 to 20mL, compatible with injection into the heart. This reconditioning process does not affect the quality attributes of the cells i.e. QC release test (homogeneity, identity, purity and potency) or viability. Shelf-life of therapeutic form of C3BS-MSCs was demonstrated as the ready-to-use drug product could be stored for up to 8h after thawing without significant deterioration. The system is suitable for large amounts of cells (up to one billion), in closed system and simple manipulation at clinical site (without clean room). Finally C3BS’ cryopreservation-reconditioning process can be considered as safe for the patients in term of sterility, mycoplasma and endotoxin, and is currently used in the pivotal clinical phase III CHART-1 trial.Source of funding: None declared.Conflict of interest: None declared.v.steenwinckel@c3bs.com
Keywords	blood ; bone marrow ; bone marrow cells ; clinical trials ; commercialization ; cryopreservation ; drugs ; endotoxins ; extended shelf life ; heart ; heart diseases ; liquids ; manufacturing ; mesenchymal stromal cells ; Mycoplasma ; patients ; stem cells ; thawing ; therapeutics ; viability ; washing
Language	English
Dates of publication	2013-12
Size	p. 412-413.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	80098-3
ISSN	1090-2392 ; 0011-2240
ISSN (online)	1090-2392
ISSN	0011-2240
DOI	10.1016/j.cryobiol.2013.09.060
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Overcoming Target Driven Fratricide for T Cell Therapy.

Breman, Eytan / Demoulin, Benjamin / Agaugué, Sophie / Mauën, Sebastien / Michaux, Alexandre / Springuel, Lorraine / Houssa, Julien / Huberty, Fanny / Jacques-Hespel, Céline / Marchand, Céline / Marijsse, Jérôme / Nguyen, Thuy / Ramelot, Nancy / Violle, Benjamin / Daro, Dorothée / De Waele, Peter / Gilham, David E / Steenwinckel, Valérie

Frontiers in immunology

2018 Volume 9, Page(s) 2940

Abstract: Chimeric Antigen Receptor (CAR) T cells expressing the fusion of the NKG2D protein with CD3ζ (NKG2D-CAR T Cells) acquire a specificity for stress-induced ligands expressed on hematological and solid cancers. However, these stress ligands are also ... ...

Abstract	Chimeric Antigen Receptor (CAR) T cells expressing the fusion of the NKG2D protein with CD3ζ (NKG2D-CAR T Cells) acquire a specificity for stress-induced ligands expressed on hematological and solid cancers. However, these stress ligands are also transiently expressed by activated T cells implying that NKG2D-based T cells may undergo self-killing (fratricide) during cell manufacturing or during the freeze thaw cycle prior to infusion in patients. To avoid target-driven fratricide and enable the production of NKG2D-CAR T cells for clinical application, two distinct approaches were investigated. The first focused upon the inclusion of a Phosphoinositol-3-Kinase inhibitor (LY294002) into the production process. A second strategy involved the inclusion of antibody blockade of NKG2D itself. Both processes impacted T cell fratricide, albeit at different levels with the antibody process being the most effective in terms of cell yield. While both approaches generated comparable NKG2D-CAR T cells, there were subtle differences, for example in differentiation status, that were fine-tuned through the phasing of the inhibitor and antibody during culture in order to generate a highly potent NKG2D-CAR T cell product. By means of targeted inhibition of NKG2D expression or generic inhibition of enzyme function, target-driven CAR T fratricide can be overcome. These strategies have been incorporated into on-going clinical trials to enable a highly efficient and reproducible manufacturing process for NKG2D-CAR T cells.
MeSH term(s)	Antibodies, Blocking/immunology ; Antibodies, Blocking/pharmacology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cells, Cultured ; Chromones/pharmacology ; Cytotoxicity, Immunologic/drug effects ; Cytotoxicity, Immunologic/immunology ; Enzyme Inhibitors/pharmacology ; Humans ; Immunotherapy, Adoptive/methods ; K562 Cells ; Ligands ; Morpholines/pharmacology ; NK Cell Lectin-Like Receptor Subfamily K/antagonists & inhibitors ; NK Cell Lectin-Like Receptor Subfamily K/immunology ; NK Cell Lectin-Like Receptor Subfamily K/metabolism ; Phosphatidylinositol 3-Kinases/metabolism ; Phosphoinositide-3 Kinase Inhibitors ; Receptors, Antigen, T-Cell/immunology ; Receptors, Antigen, T-Cell/metabolism ; T-Lymphocytes/immunology ; T-Lymphocytes/metabolism
Chemical Substances	Antibodies, Blocking ; Chromones ; Enzyme Inhibitors ; KLRK1 protein, human ; Ligands ; Morpholines ; NK Cell Lectin-Like Receptor Subfamily K ; Phosphoinositide-3 Kinase Inhibitors ; Receptors, Antigen, T-Cell ; 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (31M2U1DVID)
Language	English
Publishing date	2018-12-12
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2018.02940
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Article ; Online: Guidelines for translational research in heart failure.

Lara-Pezzi, Enrique / Menasché, Philippe / Trouvin, Jean-Hugues / Badimón, Lina / Ioannidis, John P A / Wu, Joseph C / Hill, Joseph A / Koch, Walter J / De Felice, Albert F / de Waele, Peter / Steenwinckel, Valérie / Hajjar, Roger J / Zeiher, Andreas M

Journal of cardiovascular translational research

2015 Volume 8, Issue 1, Page(s) 3–22

Abstract: Heart failure (HF) remains a major cause of death and hospitalization worldwide. Despite medical advances, the prognosis of HF remains poor and new therapeutic approaches are urgently needed. The development of new therapies for HF is hindered by ... ...

Abstract	Heart failure (HF) remains a major cause of death and hospitalization worldwide. Despite medical advances, the prognosis of HF remains poor and new therapeutic approaches are urgently needed. The development of new therapies for HF is hindered by inappropriate or incomplete preclinical studies. In these guidelines, we present a number of recommendations to enhance similarity between HF animal models and the human condition in order to reduce the chances of failure in subsequent clinical trials. We propose different approaches to address safety as well as efficacy of new therapeutic products. We also propose that good practice rules are followed from the outset so that the chances of eventual approval by regulatory agencies increase. We hope that these guidelines will help improve the translation of results from animal models to humans and thereby contribute to more successful clinical trials and development of new therapies for HF.
MeSH term(s)	Animals ; Cardiology/standards ; Disease Models, Animal ; Guidelines as Topic ; Heart Failure/diagnosis ; Heart Failure/physiopathology ; Heart Failure/therapy ; Humans ; Research Design/standards ; Translational Medical Research/standards
Language	English
Publishing date	2015-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2422411-X
ISSN	1937-5395 ; 1937-5387
ISSN (online)	1937-5395
ISSN	1937-5387
DOI	10.1007/s12265-015-9606-8
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Article ; Online: Optimized delivery system achieves enhanced endomyocardial stem cell retention.

Behfar, Atta / Latere, Jean-Pierre / Bartunek, Jozef / Homsy, Christian / Daro, Dorothee / Crespo-Diaz, Ruben J / Stalboerger, Paul G / Steenwinckel, Valerie / Seron, Aymeric / Redfield, Margaret M / Terzic, Andre

Circulation. Cardiovascular interventions

2013 Volume 6, Issue 6, Page(s) 710–718

Abstract: Background: Regenerative cell-based therapies are associated with limited myocardial retention of delivered stem cells. The objective of this study is to develop an endocardial delivery system for enhanced cell retention.: Methods and results: Stem ... ...

Abstract	Background: Regenerative cell-based therapies are associated with limited myocardial retention of delivered stem cells. The objective of this study is to develop an endocardial delivery system for enhanced cell retention. Methods and results: Stem cell retention was simulated in silico using 1- and 3-dimensional models of tissue distortion and compliance associated with delivery. Needle designs, predicted to be optimal, were accordingly engineered using nitinol, a nickel and titanium alloy displaying shape memory and superelasticity. Biocompatibility was tested with human mesenchymal stem cells. Experimental validation was performed with species-matched cells directly delivered into Langendorff-perfused porcine hearts or administered percutaneously into the endocardium of infarcted pigs. Cell retention was quantified by flow cytometry and real-time quantitative polymerase chain reaction methodology. Models, computing optimal distribution of distortion calibrated to favor tissue compliance, predicted that a 75°-curved needle featuring small-to-large graded side holes would ensure the highest cell retention profile. In isolated hearts, the nitinol curved needle catheter (C-Cath) design ensured 3-fold superior stem cell retention compared with a standard needle. In the setting of chronic infarction, percutaneous delivery of stem cells with C-Cath yielded a 37.7±7.1% versus 10.0±2.8% retention achieved with a traditional needle without effect on biocompatibility or safety. Conclusions: Modeling-guided development of a nitinol-based curved needle delivery system with incremental side holes achieved enhanced myocardial stem cell retention.
MeSH term(s)	Alloys ; Animals ; Cell- and Tissue-Based Therapy ; Computer Simulation ; Disease Models, Animal ; Drug Delivery Systems/instrumentation ; Drug Delivery Systems/methods ; Endocardium/cytology ; Equipment Design ; Male ; Myocardial Infarction/pathology ; Myocardial Infarction/therapy ; Needles ; Stem Cell Transplantation ; Stem Cells/cytology ; Swine ; Treatment Outcome
Chemical Substances	Alloys ; nitinol (2EWL73IJ7F)
Language	English
Publishing date	2013-12-10
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2450797-0
ISSN	1941-7632 ; 1941-7640
ISSN (online)	1941-7632
ISSN	1941-7640
DOI	10.1161/CIRCINTERVENTIONS.112.000422
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Article: IL-13 mediates in vivo IL-9 activities on lung epithelial cells but not on hematopoietic cells.

Steenwinckel, Valérie / Louahed, Jamila / Orabona, Ciriana / Huaux, François / Warnier, Guy / McKenzie, Andrew / Lison, Dominique / Levitt, Roy / Renauld, Jean-Christophe

Journal of immunology (Baltimore, Md. : 1950)

2007 Volume 178, Issue 5, Page(s) 3244–3251

Abstract: Increased IL-9 expression, either systemically or under the control of lung-specific promoter, induces an asthma-like phenotype, including mucus overproduction, mastocytosis, lung eosinophilia, and airway hyperresponsiveness. These activities correlate ... ...

Abstract	Increased IL-9 expression, either systemically or under the control of lung-specific promoter, induces an asthma-like phenotype, including mucus overproduction, mastocytosis, lung eosinophilia, and airway hyperresponsiveness. These activities correlate with increased production of other Th2 cytokines such as IL-4, IL-5, and IL-13 in IL-9 Tg mice. To determine the exact role of IL-13 in this phenotype, mice overexpressing IL-9 were crossed with IL-13-deficient mice. In these animals, IL-9 could still induce mastocytosis and B lymphocyte infiltration of the lungs. Although IL-9-induced eosinophilia in the peritoneal cavity was not diminished in the absence of IL-13, IL-13 was required for IL-9 to increase eotaxin expression and lung eosinophilia. Mucus production and up-regulation of lung epithelial genes upon IL-9 overexpression were completely abolished in the absence of IL-13. Using hemopoietic cell transfer experiments with recipients that overexpressed IL-9 but were deficient in the IL-9 receptor (IL-9R), we could demonstrate that the effect of IL-9 on lung epithelial cells is indirect and could be fully restored by transfer of hemopoietic cells expressing IL-9R. Mucus production by lung epithelial cells was only up-regulated when hemopoietic cells simultaneously expressed functional IL-9R and IL-13 genes, indicating that IL-13 is not a cofactor but a direct mediator of the effect of IL-9 on lung epithelial cells. Taken together, these data indicate that IL-9 can promote asthma through IL-13-independent pathways via expansion of mast cells, eosinophils, and B cells, and through induction of IL-13 production by hemopoietic cells for mucus production and recruitment of eosinophils by lung epithelial cells.
MeSH term(s)	Animals ; Asthma/genetics ; Asthma/immunology ; Asthma/metabolism ; Asthma/pathology ; Chemokine CCL11 ; Chemokines, CC/biosynthesis ; Chemokines, CC/immunology ; Epithelial Cells/immunology ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Hematopoietic Stem Cell Transplantation ; Hematopoietic Stem Cells/immunology ; Hematopoietic Stem Cells/metabolism ; Hematopoietic Stem Cells/pathology ; Interleukin-13/deficiency ; Interleukin-13/immunology ; Interleukin-9/deficiency ; Interleukin-9/immunology ; Leukocytes/immunology ; Leukocytes/metabolism ; Leukocytes/pathology ; Lung/immunology ; Lung/metabolism ; Lung/pathology ; Mice ; Mice, Knockout ; Mucus/immunology ; Mucus/metabolism ; Pulmonary Eosinophilia/genetics ; Pulmonary Eosinophilia/immunology ; Pulmonary Eosinophilia/metabolism ; Pulmonary Eosinophilia/pathology ; Receptors, Interleukin-9/deficiency ; Receptors, Interleukin-9/immunology ; Up-Regulation/immunology
Chemical Substances	Ccl11 protein, mouse ; Chemokine CCL11 ; Chemokines, CC ; Il9r protein, mouse ; Interleukin-13 ; Interleukin-9 ; Receptors, Interleukin-9
Language	English
Publishing date	2007-02-20
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.178.5.3244
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Article ; Online: IL-9 promotes IL-13-dependent paneth cell hyperplasia and up-regulation of innate immunity mediators in intestinal mucosa.

Steenwinckel, Valérie / Louahed, Jamila / Lemaire, Muriel M / Sommereyns, Caroline / Warnier, Guy / McKenzie, Andrew / Brombacher, Frank / Van Snick, Jacques / Renauld, Jean-Christophe

Journal of immunology (Baltimore, Md. : 1950)

2009 Volume 182, Issue 8, Page(s) 4737–4743

Abstract: IL-9 contributes to lung inflammatory processes such as asthma, by promoting mast cell differentiation, B cell activation, eosinophilia, and mucus production by lung epithelial cells. The observation that IL-9 overexpressing mice show increased mast cell ...

Abstract	IL-9 contributes to lung inflammatory processes such as asthma, by promoting mast cell differentiation, B cell activation, eosinophilia, and mucus production by lung epithelial cells. The observation that IL-9 overexpressing mice show increased mast cell numbers in the intestinal mucosa suggests that this cytokine might also play a role in intestinal inflammation. In colons from IL-9 transgenic mice, the expression of Muc2, a major intestinal mucin gene, was up-regulated, together with that of CLCA3 chloride channel and resistin like alpha, which are goblet cell-associated genes. Additional IL-9 up-regulated genes were identified and included innate immunity genes such as angiogenin 4 and the PLA2g2a phospholipase A(2), which are typical Paneth cell markers. Histochemical staining of Paneth cells by phloxine/tartrazine showed that IL-9 induces Paneth cell hyperplasia in Lieberkühn glands of the small intestine, and in the colonic mucosa, where this cell type is normally absent. Expression of Paneth cell markers, including angiogenin 4, PLA2g2a, and cryptdins, was induced in the colon of wild-type mice after two to four daily administrations of IL-9. By crossing IL-9 transgenic mice with IL-13(-/-) mice, or by injecting IL-9 into IL-4R(-/-) mice, we showed that IL-13 was required for the up-regulation of these Paneth cell-specific genes by IL-9. Taken together, our data indicate that Paneth cell hyperplasia and expression of their various antimicrobial products contribute to the immune response driven by TH2 cytokines, such as IL-9 and IL-13 in the intestinal mucosa.
MeSH term(s)	Animals ; Biomarkers ; Hyperplasia/genetics ; Hyperplasia/immunology ; Hyperplasia/metabolism ; Hyperplasia/pathology ; Immunity, Innate/immunology ; Interleukin-13/deficiency ; Interleukin-13/genetics ; Interleukin-13/immunology ; Interleukin-13/metabolism ; Interleukin-9/genetics ; Interleukin-9/immunology ; Interleukin-9/metabolism ; Intestinal Mucosa/immunology ; Kinetics ; Mice ; Mice, Knockout ; Paneth Cells/immunology ; Phospholipases A2/metabolism ; Ribonuclease, Pancreatic/metabolism ; Up-Regulation/immunology
Chemical Substances	Biomarkers ; Interleukin-13 ; Interleukin-9 ; Phospholipases A2 (EC 3.1.1.4) ; Ang4 protein, mouse (EC 3.1.27.5) ; Ribonuclease, Pancreatic (EC 3.1.27.5)
Language	English
Publishing date	2009-04-02
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.0801941
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Article ; Online: IL-9 exerts biological function on antigen-experienced murine T cells and exacerbates colitis induced by adoptive transfer.

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Article: 054 Manufactured Cells: C-Wash for C3BS clinical application

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Article ; Online: Overcoming Target Driven Fratricide for T Cell Therapy.

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Article ; Online: Guidelines for translational research in heart failure.

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Article ; Online: Optimized delivery system achieves enhanced endomyocardial stem cell retention.

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Article: IL-13 mediates in vivo IL-9 activities on lung epithelial cells but not on hematopoietic cells.

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Article ; Online: IL-9 promotes IL-13-dependent paneth cell hyperplasia and up-regulation of innate immunity mediators in intestinal mucosa.

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