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Results: 4

1.
Figure 1

Figure 1. From: Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

Serum anti-insulin autoantibody levels. a, Insulin autoantibodies fail to occur in transgene+ mice in the absence of native insulin 1 and insulin 2 genes. b, Mice with insulin 1 gene (insulin 1+/-, insulin 2-/-, transgene+ or transgene-) produce insulin autoantibodies (IAA). Lines connect results for individual mice. mIAA, micro-IAA assay.

Maki Nakayama, et al. Nature. ;435(7039):220-223.
2.
Figure 2

Figure 2. From: Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

Histology of non-diabetic native insulin-negative mice (insulin 1-/-, insulin 2-/-, transgene+). Histology of pancreas and salivary gland of NOD mice lacking both native insulin 1 and 2 genes, with mutated (B16:alanine) preproinsulin transgene. a–c, Sections from a mouse killed at 26 weeks, showing islets stained for insulin (a), islets stained for glucagon (b) and salivary gland stained with haematoxylin and eosin (c). d, Islets from a mouse killed at 23 weeks, stained for insulin.

Maki Nakayama, et al. Nature. ;435(7039):220-223.
3.
Figure 3

Figure 3. From: Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

Histology of native insulin-positive mice. Histology showing marked insulitis of NOD mice with one or more copies of the insulin 1 or insulin 2 gene, with or without the mutated preproinsulin (B16:alanine) transgene. a, Insulin 1+/+, insulin 2-/-, transgene-, killed at 14 weeks, diabetic at 14 weeks. b, Insulin 1+/+, insulin 2-/-, transgene-, killed at 10.5 weeks, diabetic at 10.5 weeks. c, Insulin 1+/-, insulin 2-/-, transgene+, killed at 15 weeks, diabetic at 15 weeks. d, Insulin 1-/-, insulin 2+/+, transgene-, killed at 20 weeks, not diabetic. e, Insulin 1-/-, insulin 2+/+, transgene+, killed at 21 weeks, not diabetic. f, Insulin 1-/-, insulin 2+/-, transgene+, killed at 35 weeks, not diabetic.

Maki Nakayama, et al. Nature. ;435(7039):220-223.
4.
Figure 4

Figure 4. From: Prime role for an insulin epitope in the development of type 1 diabetes in NOD mice.

Life tables of diabetes development. a, Lack of progression to diabetes of NOD mice lacking both insulin native genes. b, c, Lack of difference in progression to diabetes for speed congenic female NOD mice with control regions from the 129 mouse surrounding the insulin genes (insulin 1 region (b); insulin 2 region (c)). d, Progression to diabetes of the four transgenic founder strains with the mutated preproinsulin gene on NOD background (insulin 1+/+, insulin 2+/+, transgene+). Founder strain F was significantly different (P < 0.01) from the others. e, NOD.SCID recipients of splenocytes from mice lacking both native insulin genes had delayed progression to diabetes compared with insulin 1+, insulin 2+ mice (P < 0.02). ins, insulin; Tg, transgene.

Maki Nakayama, et al. Nature. ;435(7039):220-223.

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