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Contrary to expectations based on in vitro experiments, we previously found that pancreatic IL-10 did not inhibit autoimmune diabetes but accelerated it in an MHC-dependent manner. Therefore, the ability of IL-10 to overcome the absence of all non-MHC diabetes susceptibility (Idd) alleles was studied in transgenic mice expressing pancreatic IL-10 backcrossed to B10.H2g7 congenic mice, which have no Idd alleles other than NOD MHC (H2g7). IL-10 transgenic backcross 1 (BC1) mice with H2g7/g7 haplotype developed clear-cut insulitis and diabetes, but neither transgenic mice with the H2g/b haplotype nor nontransgenic BC1 mice did so. Further implicating IL-10 in autoimmune diabetes, anti-IL-10 antibody treatment inhibited the development of insulitis in NOD mice. These results suggest that IL-10 may be necessary and sufficient for producing autoimmune diabetes in conjunction with NOD MHC homozygosity and that some Idd genes may be related to the regulation of IL-10.

Original publication




Journal article


The Journal of experimental medicine

Publication Date





2663 - 2668


Department of Neuropharmacology, Scripps Research Institute, La Jolla, California 92037, USA.


Islets of Langerhans, B-Lymphocytes, Animals, Mice, Inbred Strains, Mice, Inbred C57BL, Mice, Inbred NOD, Mice, Transgenic, Mice, Diabetes Mellitus, Type 1, Genetic Predisposition to Disease, DNA Primers, Interleukin-10, Histocompatibility Antigens Class II, Crosses, Genetic, Polymerase Chain Reaction, Major Histocompatibility Complex, Base Sequence, Homozygote, Alleles, Molecular Sequence Data, Female, Male