Premium
Diabetes Induction in C57BL/6 Mice Reconstituted with Lymphocytes of Nonobese Diabetic <−> C57BL/6 Mouse Embryo Aggregation Chimeras
Author(s) -
Francesco Colucci,
MarieLouise Bergman,
Kristina Lejon,
Dan Holmberg
Publication year - 1998
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1046/j.1365-3083.1998.00479.x
Subject(s) - insulitis , nod , diabetes mellitus , nod mice , chimera (genetics) , splenocyte , spleen , endocrinology , insulin , immunology , medicine , embryo , type 1 diabetes , biology , gene , genetics
To determine whether the genetic background of the insulin‐producing β cells of the pancreas contributes to autoimmune diabetes susceptibility, we have used a model of the disease based on tranferring spleen cells from nonobese diabetic (NOD) <−> C57BL/6 (B6) embryo aggregation (EA) chimeras into B6 and NOD irradiated mice. Insulitis and diabetes could be induced into both B6 and NOD hosts, albeit with low incidence. Cyclophosphamide (CY) treatment, known to accelerate diabetes in prediabetic NOD mice, was found to increase diabetes incidence up to 50–60% in both B6 and NOD mice reconstituted with chimeric splenocytes, while diabetes did not occur in CY‐treated B6 mice reconstituted with B6 splenocytes. We conclude that the genetic make‐up of the target organ does not affect the final stage of the pathogenesis of insulin‐dependent diabetes mellitus.