Phenotypes Associated with This Genotype

Genotype
MGI:3590228

• Allelic Composition: Tg(H2-Ea-Ins2)1Wehi/0
• Genetic Background: NOD/ShiLtJWehi-Tg(H2-Ea-Ins2)1Wehi

• ♀: phenotype observed in females
• ♂: phenotype observed in males
• N: normal phenotype

endocrine/exocrine glands

endocrine/exocrine gland phenotype ( J:100232 )

N • unlike wild-type NOD mice, transgenic NOD/LtWehi mice do not develop spontaneous diabetes

N • whereas wildtype NOD mice are susceptible to diabetes induction by cyclophosphamide, no transgenic NOD/LtWehi mice became diabetic (defined as blood glucose > 11 mmol/l) after a single cyclophosphamide injection; following a second injection only one of ten developed diabetes, and it was more slowly progressive than in wild-type controls

N • pancreata of transgenic NOD/LtWehi mice are almost entirely free of insulitis: 90% of 244 islets from 100-day-old female mice and 98% of 259 islets from 147-day-old males had no cellular infiltration, and the rest exhibited only a minimal degree of insulitis

salivary gland inflammation ( J:100232 )

• the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates

immune system

immune system phenotype ( J:100232 )

N • pancreata of transgenic NOD/LtWehi mice are almost entirely free of insulitis: 90% of islets from 100-day-old female mice and 98% of those from 147-day-old males have no cellular infiltration, and the rest exhibit only a minimal degree of insulitis

abnormal T cell proliferation ( J:100232 )

• spleen- and draining lymph node-derived T cells from wild-type and transgenic NOD/LtWehi mice exhibit statistically similar in vitro proliferative responses to peptides derived from proinsulin and GAD2 (GAD65) following immunization with these self antigens

salivary gland inflammation ( J:100232 )

• the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates

digestive/alimentary system

salivary gland inflammation ( J:100232 )

• the transgene does not affect the characteristic susceptibility of NOD mice to sialitis, the degree of which does not differ significantly between transgenic NOD/LtWis mice and control littermates

hematopoietic system

abnormal T cell proliferation ( J:100232 )

• spleen- and draining lymph node-derived T cells from wild-type and transgenic NOD/LtWehi mice exhibit statistically similar in vitro proliferative responses to peptides derived from proinsulin and GAD2 (GAD65) following immunization with these self antigens

cellular

abnormal T cell proliferation ( J:100232 )

• spleen- and draining lymph node-derived T cells from wild-type and transgenic NOD/LtWehi mice exhibit statistically similar in vitro proliferative responses to peptides derived from proinsulin and GAD2 (GAD65) following immunization with these self antigens

Mouse Models of Human Disease		DO ID	OMIM ID(s)	Ref(s)
type 1 diabetes mellitus		DOID:9744	OMIM:222100	J:100251