Journal of Clinical and Cellular Immunology
Open Access
ISSN: 2155-9899
+44 1223 790975
ISSN: 2155-9899
+44 1223 790975
Sahar Tahvili, Marie Torngren, Dan Holmberg, Tomas Leanderson and Fredrik Ivars
Lund University, Sweden
Personalmatsalen Active Biotech, Sweden
Posters & Accepted Abstracts: J Clin Cell Immunol
The NOD mouse spontaneously developed type 1 diabetes (T1D). At the age of 3-4 weeks, there was detectable infiltration of mononuclear cells in the pancreatic islets of Langerhans of these mice. This process known as insulitis, causes selective cell death of the insulin producing �?²-cells in the islets. Female NOD mice displayed severe insulitis at about 15 weeks of age and developed hyper-glycaemia at around 15-30 weeks of age. We have previously shown that the immunomodulatory compound paquinimod can reduce the influx of monocytes to sites of inflammation. Since monocyte-derived macrophages are known to be involved in pathogenesis in NOD pancreas, we have in here investigated the impact of paquinimod treatment on the development of T1D in the NOD mouse. In cohorts of mice treated between weeks 10 to 20 of age and followed up until 40 weeks of age, we observed dosedependent reduction of incidence of disease as well as delayed onset of disease. Further, in mice treated with paquinimod from 15 weeks of age, most of the treated mice had not developed glycosuria at 30 weeks of age and displayed strongly reduced insulitis. Importantly, in these treated mice there were significantly more non-infiltrated islets than in untreated controls. Collectively, these data indicate that paquinimod treatment inhibits progression of insulitis to overt diabetes in the NOD mouse.
Email: sahar.tahvili@med.lu.se