ISSN 1662-4009 (online)

ESPE Yearbook of Paediatric Endocrinology (2018) 15 10.21 | DOI: 10.1530/ey.15.10.21

Department of Immunology and Infectious Disease, The John Curtin School of Medical Research, The Australian National University, Canberra, Australian Capital Territory, Australia


To read the full abstract: PLoS One. 2018;13:e0191360

Up to now most studies to prevent autoimmune T1DM have focused on directly suppressing the autoimmune response rather than to better understanding the intrinsic requirements for beta cell survival. In this trial intracellular heparan sulfate was investigated as an essential requirement for the survival of beta cells and a marker for beta cell damage. Heparan sulfate depletion by heparanase plays an important role in the pathogenesis of T1DM. This opens the door for a possible intervention mechanism in T1DM development or progression. Replacement of heparin sulfate or inhibition of heparanase activity could improve the survival of beta cells. Such a scenario could be tested in a study in patients with new onset T1DM.

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