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. 2011 Mar 22;60(4):1354–1359. doi: 10.2337/db10-0885

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© 2011 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 3. — A polymorphic gene(s) in close linkage with the D11Mit48 microsatellite marker controls susceptibility to AI4 T-cell–induced diabetes through effects on a CD4 T-cell population other than CD25⁺ Tregs. A: Mice homozygous for the B6 allele (B6/B6) vs. heterozygous (NOD/B6) for D11Mit48 were, respectively, highly susceptible and resistant to AI4 T-cell–induced diabetes. Results represent three independent experiments. B: Insulitis scores are shown for nondiabetic heterozygous and homozygous BC1 NOD.Rag1^null.AI4 splenocyte recipients. C and D: B6.H2^g7 mice previously reconstituted with bone marrow from D11Mit48^B6/B6 or D11Mit48^NOD/B6 BC1 segregants are, respectively, susceptible or resistant to diabetes and insulitis induced by subsequently infused AI4 T-cells. E: Incidence of diabetes in 6- to 8-week-old female B6.H2^g7.Rag1^null, NOD.Rag1^null, and F1.Rag1^null recipients of 1 × 10⁷ NOD.Rag1^null.AI4 splenocytes. F: Incidence of diabetes in 6- to 8-week-old sublethally irradiated NOD and F1 recipients of 1 × 10⁷ NOD.Rag1^null.AI4 splenocytes. Recipients were also injected intraperitoneally with a CD25-depleting antibody (PC61 250 μg/mouse) 1 day before AI4 T-cell transfer. G and H: B6.H2^g7.Rag1^null mice infused with purified CD4⁺ T-cells from D11Mit48^B6/B6 or D11Mit48^NOD/B6 BC1 segregants are, respectively, susceptible or resistant to diabetes and insulitis induced by subsequently infused AI4 T-cells.