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Phenotypes Associated with This Genotype
Genotype
MGI:3588865
Allelic
Composition
Relbtm1Brv/Relbtm1Brv
Genetic
Background
either: (involves: 129S2/SvPas) or (involves: C57BL/6) or (involves: 129S2/SvPas * C57BL/6)
Find Mice Using the International Mouse Strain Resource (IMSR)
Mouse lines carrying:
Relbtm1Brv mutation (1 available); any Relb mutation (32 available)
phenotype observed in females
phenotype observed in males
N normal phenotype
hematopoietic system
• homozygotes exhibit a 9-fold increase in the number of eosinophils in blood
• eosinophils are a major component of the inflammatory infiltrate in the lung, dermis and epidermis of homozygotes with pulmonary inflammation and skin lesions

immune system
• homozygotes exhibit a 9-fold increase in the number of eosinophils in blood
• eosinophils are a major component of the inflammatory infiltrate in the lung, dermis and epidermis of homozygotes with pulmonary inflammation and skin lesions
• eosinophils are a major component of the inflammatory infiltrate in the lung
• homozygotes with moderate to marked skin lesions exhibit features of allergic pulmonary inflammation, including accumulation of inflammatory cells around the blood vessels and airways of lungs, and increased collagen deposition at sites of severe inflammation
• between 4 and 10 weeks of age, ~70-80% of homozygotes develop an itching dermatitis of variable severity
• this dermatitis affects the trunk and head but occasionally involves the ears and footpads; its severity does not increase significantly over time
• bacterial and fungal infections have been excluded as the infectious causes of observed dermatitis
• importantly, no dermatitis develops in the offspring of homozygous mutants crossed with Tg(Lck-Nr4a1)2Brv transgenic mice that lack peripheral T cells, establishing that these skin lesions are T cell-dependent

cardiovascular system
• homozygotes with skin lesions exhibit prominent blood vessels in the dermis, suggesting neovascularization

respiratory system
• homozygotes with moderate to marked skin lesions exhibit features of allergic pulmonary inflammation, including accumulation of inflammatory cells around the blood vessels and airways of lungs, and increased collagen deposition at sites of severe inflammation
• eosinophils are a major component of the inflammatory infiltrate in the lung
• homozygotes with moderate to marked skin lesions exhibit a significant increase of mucus-secreting goblet cells within the airways

integument
• between 4 and 10 weeks of age, ~70-80% of homozygotes develop an itching dermatitis of variable severity
• this dermatitis affects the trunk and head but occasionally involves the ears and footpads; its severity does not increase significantly over time
• bacterial and fungal infections have been excluded as the infectious causes of observed dermatitis
• importantly, no dermatitis develops in the offspring of homozygous mutants crossed with Tg(Lck-Nr4a1)2Brv transgenic mice that lack peripheral T cells, establishing that these skin lesions are T cell-dependent
• homozygotes with skin lesions exhibit significant accumulation of numerous CD4+ T cells and eosinophils mixed with lesser numbers of CD8+ T cells and neutrophils in the dermis
• a moderate increase of MHC class II-positive dermal dendritic cells and dermal mast cells is also observed
• homozygotes with skin lesions display occasional microabscesses in the stratum corneum and ulcerations, probably due to scratching
• intracorneal pustules are occasionally detected in the epidermis
• homozygotes exhibit hyperproliferation of keratinocytes in the basal layer and a marked up-regulation of K6 expression in acanthotic epidermis
• a number of homozygotes with skin lesions contain occasional apoptotic keratinocytes in the epidermis
• homozygotes exhibit hyperproliferation of keratinocytes in the basal layer

cellular
• a number of homozygotes with skin lesions contain occasional apoptotic keratinocytes in the epidermis
• homozygotes exhibit hyperproliferation of keratinocytes in the basal layer

Mouse Models of Human Disease
DO ID OMIM ID(s) Ref(s)
atopic dermatitis DOID:3310 OMIM:603165
OMIM:PS603165
J:63950


Contributing Projects:
Mouse Genome Database (MGD), Gene Expression Database (GXD), Mouse Models of Human Cancer database (MMHCdb) (formerly Mouse Tumor Biology (MTB)), Gene Ontology (GO)
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last database update
04/16/2024
MGI 6.23
The Jackson Laboratory