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      Oral histone deacetylase inhibitor synergises with T cell targeted immunotherapy to preserve beta cell metabolic function and induce stable remission of new-onset autoimmune diabetes in NOD mice.

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          Abstract

          Combination therapy targeting the major actors involved in the immune-mediated destruction of pancreatic beta cells appears to be an indispensable approach to treat type 1 diabetes effectively. We hypothesised that the combination of an orally active pan-histone deacetylase inhibitor (HDACi: givinostat) with subtherapeutic doses of CD3 antibodies may provide ideal synergy to treat ongoing autoimmunity.

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          Author and article information

          Journal
          Diabetologia
          Diabetologia
          Springer Nature America, Inc
          1432-0428
          0012-186X
          February 2018
          : 61
          : 2
          Affiliations
          [1 ] University Paris Descartes, Sorbonne Paris Cité, Paris, France.
          [2 ] INSERM U1151, Institut Necker-Enfants Malades, Hôpital Necker, Bâtiment Hamburger, 5ème étage, 149 rue de Sèvres, 75015, Paris, France.
          [3 ] CNRS UMR 8253, Institut Necker-Enfants Malades, Paris, France.
          [4 ] Laboratory for Immuno-Endocrinology, Department of Biomedical Sciences, University of Copenhagen, Copenhagen, Denmark.
          [5 ] University Paris Descartes, Sorbonne Paris Cité, Paris, France. sylvaine.you@inserm.fr.
          [6 ] INSERM U1151, Institut Necker-Enfants Malades, Hôpital Necker, Bâtiment Hamburger, 5ème étage, 149 rue de Sèvres, 75015, Paris, France. sylvaine.you@inserm.fr.
          [7 ] CNRS UMR 8253, Institut Necker-Enfants Malades, Paris, France. sylvaine.you@inserm.fr.
          Article
          10.1007/s00125-017-4459-0
          10.1007/s00125-017-4459-0
          29030662
          9f63fee7-7490-4618-9346-719b45099e5f
          History

          Humanised NOD mice,Type 1 diabetes,Insulin secretion,Human CD3 antibodies,HDACi,Glucose tolerance,Beta cells

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