These mice carry a transgene on a BALB/cBy background that expresses the influenza hemagglutinin (HA) on pancreatic islet beta cells that results in reduced class 1 and class II T-cell responses in cytotoxic lymphocyte (CTL) assays and adoptive transfer studies.
Linda Sherman, The Scripps Research Institute
Genetic Background | Generation |
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Allele Type |
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Transgenic (Inserted expressed sequence) |
Transgenic mice are viable, fertile, normal in size, normoglycemic and do not display any gross physical or behavioral abnormalities. Immunohistochemistry reveals pancreatic islet cell expression of the transgene and no expression in the spleen, kidney or thymus. Isolated islets stain normally for insulin and are morphologically indistinguishable from control islets. Additional functional studies found no expression in bone marrow. Histology revealed no insulitis and the single transgenic mice do not become diabetic. T-cell proliferation assays, Cytotoxic Lymphocyte (CTL) assays, and adoptive transfer studies performed using transgenic mice indicate significantly reduced class 1 and class II T-cell responses compared to controls. Hemagglutination inhibition assays of sera from HA primed transgenic mice indicate antibody titers slightly lower but nearly equivalent to HA primed control mice. Antibody titers of all transgenic mice tested were significantly higher than preimmune levels. When mated with Tg(TcraCl4,TcrbCl4) mice, the double transgenic neonates become spontaneously diabetic after birth and die within 10 days.
This is a good model for studying peripheral tolerance.
C.Cg-Tg(Ins2-HA)165Bri/ShrmJ expresses influenza hemagglutinin (HA) molecule from the well characterized influenza A/PR/8/34 under the control of the rat insulin 2 promoter (Ins2). This transgene was injected into (C57BL/6J x SJL)F2 oocytes. Resulting progeny from founder line 2917-5 was backcrossed to H2d strains BALB/cBy for 10 generations and B10.D2 for 10 generations or NOD/Shi, H2g7, for 13 generations prior to intercrossing. In 2005, the Jackson Laboratory received C.Cg-Tg(Ins2-HA)165Bri/ShrmJ at generation N10F20.
Expressed Gene | HA, influenza hemagglutinin, |
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Site of Expression |
Allele Name | transgene insertion 165, Ralph Brinster |
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Allele Type | Transgenic (Inserted expressed sequence) |
Allele Synonym(s) | 2917-5; InsHA; Ins-HA; RIP-HA; Tg(Ins-2,HA)Bri165 |
Gene Symbol and Name | Tg(Ins2-HA)165Bri, transgene insertion 165, Ralph Brinster |
Gene Synonym(s) | |
Promoter | Ins2, insulin 2, rat |
Expressed Gene | HA, influenza hemagglutinin, |
Strain of Origin | Not Specified |
Chromosome | UN |
Molecular Note | The transgenic construct consisted of the rat insulin 2 promoter fused to sequence encoding influenza hemagglutinin (HA) followed by the 3' untranslated region and polyadenylation signal from the H2-Ea. HA was from influenza A/PR/8/34. This rat insulin 2 promoter is active in pancreatic beta-cells. |
Mutations Made By | Dr. Ralph Brinster, University of Pennsylvania |
When using the BALB/c HA mouse strain in a publication, please cite the originating article(s) and include JAX stock #005533 in your Materials and Methods section.
Facility Barrier Level Descriptions
Service/Product | Description | Price |
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Hemizygous for Tg(Ins2-HA)165Bri/Shrm |
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