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Evidence for Contribution of CD4+CD25+ Regulatory T Cells in Maintaining Immune Tolerance to Human Factor IX following Perinatal Adenovirus Vector Delivery

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Title: Evidence for Contribution of CD4+CD25+ Regulatory T Cells in Maintaining Immune Tolerance to Human Factor IX following Perinatal Adenovirus Vector Delivery
Authors: Megha S. Nivsarkar, Suzanne M. K. Buckley, Alan L. Parker, Dany Perocheau, Tristan R. McKay, Ahad A. Rahim, Steven J. Howe, Simon N. Waddington
Source: Journal of Immunology Research, Vol 2015 (2015)
Publisher Information: Hindawi Limited, 2015.
Publication Year: 2015
Collection: LCC:Immunologic diseases. Allergy
Subject Terms: Immunologic diseases. Allergy, RC581-607
More Details: Following fetal or neonatal gene transfer in mice and other species immune tolerance of the transgenic protein is frequently observed; however the underlying mechanisms remain largely undefined. In this study fetal and neonatal BALB/c mice received adenovirus vector to deliver human factor IX (hFIX) cDNA. The long-term tolerance of hFIX was robust in the face of immune challenge with hFIX protein and adjuvant but was eliminated by simultaneous administration of anti-CD25+ antibody. Naive irradiated BALB/c mice which had received lymphocytes from donors immunised with hFIX developed anti-hFIX antibodies upon immune challenge. Cotransplantation with CD4+CD25+ cells isolated from neonatally tolerized donors decreased the antibody response. In contrast, cotransplantation with CD4+CD25− cells isolated from the same donors increased the antibody response. These data provide evidence that immune tolerance following perinatal gene transfer is maintained by a CD4+CD25+ regulatory population.
Document Type: article
File Description: electronic resource
Language: English
ISSN: 2314-8861
2314-7156
Relation: https://doaj.org/toc/2314-8861; https://doaj.org/toc/2314-7156
DOI: 10.1155/2015/397879
Access URL: https://doaj.org/article/ac77022689344402bb0548d5af363f32
Accession Number: edsdoj.77022689344402bb0548d5af363f32
Database: Directory of Open Access Journals
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  Data: Evidence for Contribution of CD4+CD25+ Regulatory T Cells in Maintaining Immune Tolerance to Human Factor IX following Perinatal Adenovirus Vector Delivery
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  Data: <searchLink fieldCode="AR" term="%22Megha+S%2E+Nivsarkar%22">Megha S. Nivsarkar</searchLink><br /><searchLink fieldCode="AR" term="%22Suzanne+M%2E+K%2E+Buckley%22">Suzanne M. K. Buckley</searchLink><br /><searchLink fieldCode="AR" term="%22Alan+L%2E+Parker%22">Alan L. Parker</searchLink><br /><searchLink fieldCode="AR" term="%22Dany+Perocheau%22">Dany Perocheau</searchLink><br /><searchLink fieldCode="AR" term="%22Tristan+R%2E+McKay%22">Tristan R. McKay</searchLink><br /><searchLink fieldCode="AR" term="%22Ahad+A%2E+Rahim%22">Ahad A. Rahim</searchLink><br /><searchLink fieldCode="AR" term="%22Steven+J%2E+Howe%22">Steven J. Howe</searchLink><br /><searchLink fieldCode="AR" term="%22Simon+N%2E+Waddington%22">Simon N. Waddington</searchLink>
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  Data: Journal of Immunology Research, Vol 2015 (2015)
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  Data: Hindawi Limited, 2015.
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  Data: Following fetal or neonatal gene transfer in mice and other species immune tolerance of the transgenic protein is frequently observed; however the underlying mechanisms remain largely undefined. In this study fetal and neonatal BALB/c mice received adenovirus vector to deliver human factor IX (hFIX) cDNA. The long-term tolerance of hFIX was robust in the face of immune challenge with hFIX protein and adjuvant but was eliminated by simultaneous administration of anti-CD25+ antibody. Naive irradiated BALB/c mice which had received lymphocytes from donors immunised with hFIX developed anti-hFIX antibodies upon immune challenge. Cotransplantation with CD4+CD25+ cells isolated from neonatally tolerized donors decreased the antibody response. In contrast, cotransplantation with CD4+CD25− cells isolated from the same donors increased the antibody response. These data provide evidence that immune tolerance following perinatal gene transfer is maintained by a CD4+CD25+ regulatory population.
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