Literature DB >> 21531013

Lentiviral-mediated gene therapy leads to improvement of B-cell functionality in a murine model of Wiskott-Aldrich syndrome.

Marita Bosticardo1, Elena Draghici, Francesca Schena, Aisha Vanessa Sauer, Elena Fontana, Maria Carmina Castiello, Marco Catucci, Michela Locci, Luigi Naldini, Alessandro Aiuti, Maria Grazia Roncarolo, Pietro Luigi Poliani, Elisabetta Traggiai, Anna Villa.   

Abstract

BACKGROUND: Wiskott-Aldrich syndrome (WAS) is an X-linked primary immunodeficiency characterized by thrombocytopenia, eczema, infections, autoimmunity, and lymphomas. Transplantation of hematopoietic stem cells from HLA-identical donors is curative, but it is not available to all patients. We have developed a gene therapy (GT) approach for WAS by using a lentiviral vector encoding for human WAS promoter/cDNA (w1.6W) and demonstrated its preclinical efficacy and safety.
OBJECTIVE: To evaluate B-cell reconstitution and correction of B-cell phenotype in GT-treated mice.
METHODS: We transplanted Was(-/-) mice sublethally irradiated (700 rads) with lineage marker-depleted bone marrow wild-type cells, Was(-/-) cells untransduced or transduced with the w1.6W lentiviral vector and analyzed B-cell reconstitution in bone marrow, spleen, and peritoneum.
RESULTS: Here we show that WAS protein(+) B cells were present in central and peripheral B-cell compartments from GT-treated mice and displayed the strongest selective advantage in the splenic marginal zone and peritoneal B1 cell subsets. After GT, splenic architecture was improved and B-cell functions were restored, as demonstrated by the improved antibody response to pneumococcal antigens and the reduction of serum IgG autoantibodies.
CONCLUSION: WAS GT leads to improvement of B-cell functions, even in the presence of a mixed chimerism, further validating the clinical application of the w1.6W lentiviral vector.
Copyright © 2011 American Academy of Allergy, Asthma & Immunology. Published by Mosby, Inc. All rights reserved.

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Year:  2011        PMID: 21531013     DOI: 10.1016/j.jaci.2011.03.030

Source DB:  PubMed          Journal:  J Allergy Clin Immunol        ISSN: 0091-6749            Impact factor:   10.793


  21 in total

1.  B cell-intrinsic deficiency of the Wiskott-Aldrich syndrome protein (WASp) causes severe abnormalities of the peripheral B-cell compartment in mice.

Authors:  Mike Recher; Siobhan O Burns; Miguel A de la Fuente; Stefano Volpi; Carin Dahlberg; Jolan E Walter; Kristin Moffitt; Divij Mathew; Nadine Honke; Philipp A Lang; Laura Patrizi; Hervé Falet; Marton Keszei; Masayuki Mizui; Eva Csizmadia; Fabio Candotti; Kari Nadeau; Gerben Bouma; Ottavia M Delmonte; Francesco Frugoni; Angela B Ferraz Fomin; David Buchbinder; Emma Maria Lundequist; Michel J Massaad; George C Tsokos; John Hartwig; John Manis; Cox Terhorst; Raif S Geha; Scott Snapper; Karl S Lang; Richard Malley; Lisa Westerberg; Adrian J Thrasher; Luigi D Notarangelo
Journal:  Blood       Date:  2012-02-01       Impact factor: 22.113

Review 2.  Hematopoietic stem cell gene therapy:assessing the relevance of preclinical models.

Authors:  Andre Larochelle; Cynthia E Dunbar
Journal:  Semin Hematol       Date:  2013-04       Impact factor: 3.851

3.  Autonomous role of Wiskott-Aldrich syndrome platelet deficiency in inducing autoimmunity and inflammation.

Authors:  Lucia Sereni; Maria Carmina Castiello; Francesco Marangoni; Achille Anselmo; Dario di Silvestre; Sara Motta; Elena Draghici; Stefano Mantero; Adrian J Thrasher; Silvia Giliani; Alessandro Aiuti; Pierluigi Mauri; Luigi D Notarangelo; Marita Bosticardo; Anna Villa
Journal:  J Allergy Clin Immunol       Date:  2018-02-06       Impact factor: 10.793

4.  Foamy virus vector-mediated gene correction of a mouse model of Wiskott-Aldrich syndrome.

Authors:  Toru Uchiyama; Marsilio Adriani; G Jayashree Jagadeesh; Adam Paine; Fabio Candotti
Journal:  Mol Ther       Date:  2012-01-03       Impact factor: 11.454

5.  Ubiquitous high-level gene expression in hematopoietic lineages provides effective lentiviral gene therapy of murine Wiskott-Aldrich syndrome.

Authors:  Alexander Astrakhan; Blythe D Sather; Byoung Y Ryu; Socheath Khim; Swati Singh; Stephanie Humblet-Baron; Hans D Ochs; Carol H Miao; David J Rawlings
Journal:  Blood       Date:  2012-03-19       Impact factor: 22.113

Review 6.  The contribution of mouse models to the understanding of constitutional thrombocytopenia.

Authors:  Catherine Léon; Arnaud Dupuis; Christian Gachet; François Lanza
Journal:  Haematologica       Date:  2016-08       Impact factor: 9.941

Review 7.  Advances in basic and clinical immunology in 2011.

Authors:  Javier Chinen; William T Shearer
Journal:  J Allergy Clin Immunol       Date:  2011-12-28       Impact factor: 10.793

8.  Deletion of WASp and N-WASp in B cells cripples the germinal center response and results in production of IgM autoantibodies.

Authors:  Carin I M Dahlberg; Magda-Liz Torres; Sven H Petersen; Marisa A P Baptista; Marton Keszei; Stefano Volpi; Emilie K Grasset; Mikael C I Karlsson; Jolan E Walter; Scott B Snapper; Luigi D Notarangelo; Lisa S Westerberg
Journal:  J Autoimmun       Date:  2015-07-02       Impact factor: 7.094

9.  Alterations in the adenosine metabolism and CD39/CD73 adenosinergic machinery cause loss of Treg cell function and autoimmunity in ADA-deficient SCID.

Authors:  Aisha V Sauer; Immacolata Brigida; Nicola Carriglio; Raisa Jofra Hernandez; Samantha Scaramuzza; Daniela Clavenna; Francesca Sanvito; Pietro L Poliani; Nicola Gagliani; Filippo Carlucci; Antonella Tabucchi; Maria Grazia Roncarolo; Elisabetta Traggiai; Anna Villa; Alessandro Aiuti
Journal:  Blood       Date:  2011-12-19       Impact factor: 22.113

10.  Wiskott-Aldrich syndrome protein-deficient hematopoietic cells can be efficiently mobilized by granulocyte colony-stimulating factor.

Authors:  Sabine Charrier; Michael Blundell; Gregory Cédrone; Fawzia Louache; William Vainchenker; Adrian J Thrasher; Anne Galy
Journal:  Haematologica       Date:  2013-02-26       Impact factor: 9.941

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