Phenotypes associated with this allele

• Allele Symbol: Retnla^tm1Mer
• Allele Name: targeted mutation 1, Marc E Rothenberg
• Allele ID: MGI:3832583
• Summary: 3 genotypes

Jump to	Allelic Composition	Genetic Background	Genotype ID
hm1	Retnla^tm1Mer/Retnla^tm1Mer	C.B6-Retnla^tm1Mer	MGI:3832585
hm2	Retnla^tm1Mer/Retnla^tm1Mer	C57BL/6-Retnla^tm1Mer	MGI:3832584
hm3	Retnla^tm1Mer/Retnla^tm1Mer	involves: C57BL/6	MGI:3845085

Genotype
MGI:3832585

hm1

• Allelic Composition: Retnla^tm1Mer/Retnla^tm1Mer
• Genetic Background: C.B6-Retnla^tm1Mer

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

immune system

decreased susceptibility to induced colitis ( J:144784 , J:144927 )

• DSS-induced colitis is less severe in these mice as demonstrated by reduced scores in the disease activity index and in histology scores (J:144784)

• colons from DSS-treated mice had decreased edema formation, less epithelial cell damage and decreased leukocyte formation than in controls (J:144784)

• mice are resistant to colitis induced by dextran sulfate sodium (DSS) administration to the drinking water (J:144927)

• after DSS administration, mice have delayed development of diarrhea, less rectal bleeding, and less weight loss (J:144927)

• there was less shortening of the colon after DSS administration than in controls (J:144927)

• less mice die from DSS- induced colitis than controls with all mice alive after 10 days of DSS administration compared to only 20% of controls (J:144927)

• histology reveals less epithelial erosion and decreased submucosal inflammation resulting from DSS administration (J:144927)

homeostasis/metabolism

improved glucose tolerance ( J:144784 )

• mice in an inflammatory state from DSS-induced colitis are resistant to hyperglycemia when challenged with glucose compared to controls

digestive/alimentary system

decreased susceptibility to induced colitis ( J:144784 , J:144927 )

• DSS-induced colitis is less severe in these mice as demonstrated by reduced scores in the disease activity index and in histology scores (J:144784)

• colons from DSS-treated mice had decreased edema formation, less epithelial cell damage and decreased leukocyte formation than in controls (J:144784)

• mice are resistant to colitis induced by dextran sulfate sodium (DSS) administration to the drinking water (J:144927)

• after DSS administration, mice have delayed development of diarrhea, less rectal bleeding, and less weight loss (J:144927)

• there was less shortening of the colon after DSS administration than in controls (J:144927)

• less mice die from DSS- induced colitis than controls with all mice alive after 10 days of DSS administration compared to only 20% of controls (J:144927)

• histology reveals less epithelial erosion and decreased submucosal inflammation resulting from DSS administration (J:144927)

Genotype
MGI:3832584

hm2

• Allelic Composition: Retnla^tm1Mer/Retnla^tm1Mer
• Genetic Background: C57BL/6-Retnla^tm1Mer

immune system

decreased susceptibility to induced colitis ( J:144784 , J:144927 )

• DSS-induced colitis is less severe in these mice as demonstrated by reduced scores in the disease activity index and in histology scores (J:144784)

• colons from DSS-treated mice had decreased edema formation, less epithelial cell damage and decreased leukocyte formation than in controls (J:144784)

• the number of eosoniphils that infiltrate the colon after 6 days of DSS treatment is about half that of wild-type controls (J:144784)

• colonic biopsies from mice treated with DSS produce less IL-5, CCL11 and CCL5 when cultured (J:144784)

• mice are resistant to colitis induced by dextran sulfate sodium (DSS) administration to the drinking water (J:144927)

• after DSS administration, mice have delayed development of diarrhea, less rectal bleeding, and less weight loss (J:144927)

• there was less shortening of the colon after DSS administration than in controls (J:144927)

• less mice die from DSS- induced colitis than controls with all mice alive after 10 days of DSS administration compared to only 20% of controls (J:144927)

• histology reveals less epithelial erosion and decreased submucosal inflammation resulting from DSS administration (J:144927)

impaired eosinophil recruitment ( J:144784 )

• colonic biopsies from mice treated with DSS produce less IL-5 when cultured

• the number of eosoniphils that infiltrate the colon after 6 days of DSS treatment is about half that of wild-type controls

• colonic biopsies from mice treated with DSS produce CCL11 and CCL5 when cultured

• mice in an inflammatory state from DSS-induced colitis are resistant to hyperglycemia from glucose challenged compared to wild-type mice in the DSS-colitis model

abnormal chemokine secretion ( J:144784 )

• colonic biopsies from mice treated with DSS produce CCL11 and CCL5 when cultured

increased interleukin-10 secretion ( J:144927 )

• more IL-10 is secreted in culture by colon biopsy specimens collected from mice treated with DSS than in controls

decreased interleukin-5 secretion ( J:144784 )

• colonic biopsies from mice treated with DSS produce less IL-5 when cultured

decreased interleukin-6 secretion ( J:144927 )

• less IL-6 is secreted in culture by colon biopsy specimens collected from mice treated with DSS than in controls

digestive/alimentary system

decreased susceptibility to induced colitis ( J:144784 , J:144927 )

• DSS-induced colitis is less severe in these mice as demonstrated by reduced scores in the disease activity index and in histology scores (J:144784)

• colons from DSS-treated mice had decreased edema formation, less epithelial cell damage and decreased leukocyte formation than in controls (J:144784)

• the number of eosoniphils that infiltrate the colon after 6 days of DSS treatment is about half that of wild-type controls (J:144784)

• colonic biopsies from mice treated with DSS produce less IL-5, CCL11 and CCL5 when cultured (J:144784)

• mice are resistant to colitis induced by dextran sulfate sodium (DSS) administration to the drinking water (J:144927)

• after DSS administration, mice have delayed development of diarrhea, less rectal bleeding, and less weight loss (J:144927)

• there was less shortening of the colon after DSS administration than in controls (J:144927)

• less mice die from DSS- induced colitis than controls with all mice alive after 10 days of DSS administration compared to only 20% of controls (J:144927)

• histology reveals less epithelial erosion and decreased submucosal inflammation resulting from DSS administration (J:144927)

homeostasis/metabolism

decreased circulating leptin level ( J:144784 )

• leptin circulating levels in the sera of fasted mice is almost two-thirds less than in controls

improved glucose tolerance ( J:144784 )

• mice in an inflammatory state from DSS-induced colitis are resistant to hyperglycemia when challenged with glucose compared to controls

hematopoietic system

impaired eosinophil recruitment ( J:144784 )

• the number of eosoniphils that infiltrate the colon after 6 days of DSS treatment is about half that of wild-type controls

• colonic biopsies from mice treated with DSS produce less IL-5 when cultured

• colonic biopsies from mice treated with DSS produce CCL11 and CCL5 when cultured

• mice in an inflammatory state from DSS-induced colitis are resistant to hyperglycemia from glucose challenged compared to wild-type mice in the DSS-colitis model

Genotype
MGI:3845085

hm3

• Allelic Composition: Retnla^tm1Mer/Retnla^tm1Mer
• Genetic Background: involves: C57BL/6

Retnla^tm1Mer/Retnla^tm1Mer mice exhibit exacerbated Schistosoma mansoni egg-induced pulmonary inflammation

immune system

increased IgE level ( J:147863 )

• mean IgE titers after Schistosoma mansoni (Sm) egg challenge are about 4-fold higher than controls

increased IgG1 level ( J:147863 )

• IgG1 titers specific to Sm antigen are 3-fold higher than controls

abnormal T-helper 2 physiology ( J:147863 )

• about double the numbers of CD4⁺ T cells expressing IL-13 are found in mediastinal LN cells after Sm egg challenge compared to controls

• mediastinal LN cells restimulated with Sm eggs produce much higher levels of IL-4, IL-13 and IL-5 than in controls

• mutant mice develop exacerbated pulmonary inflammation and fibrosis after exposure to Sm eggs

• mice exhibit exacerbated pulmonary inflammation characterized by increased cellularity within the arterial lumen, hypertrophy of the endothelium, and the accumulation of lymphocytes, eosinophils, and activated macrophages around the vessel wall

• granuloma size is about twice that of controls

• after sensitization and challenge of wild-type mice with Sm eggs, eggs are transported to the lungs where they become trapped within the lung parenchyma by the formation of Th2 cytokine-dependent granulomas

abnormal macrophage physiology ( J:147863 )

• alternatively-activated macrophages (AAMacs) have increased activity after Schistosoma mansoni (Sm) egg challenge as evidenced by increased deposition of collagen in the lung

• in vitro derived AAMacs from mutant mice enhance development of Th2 CD4⁺ T cells

• threefold increase in IL-4 secretion and a 10-fold increase in IL-5 secretion when OT-II T cells were cocultured with OVA-pulsed mutant AAMacs

increased interleukin-13 secretion ( J:147863 )

• mediastinal LN cells from mice infected with Sm eggs produce 5-fold more IL-13 than controls when restimulated with Sm antigen

increased interleukin-4 secretion ( J:147863 )

• mediastinal LN cells from mice infected with Sm eggs produce 5-fold more IL-4 than controls when restimulated with Sm antigen

increased interleukin-5 secretion ( J:147863 )

• mediastinal LN cells from mice infected with Sm eggs produce 2-fold more IL-5 than controls when restimulated with Sm antigen

hematopoietic system

increased IgE level ( J:147863 )

• mean IgE titers after Schistosoma mansoni (Sm) egg challenge are about 4-fold higher than controls

increased IgG1 level ( J:147863 )

• IgG1 titers specific to Sm antigen are 3-fold higher than controls

abnormal T-helper 2 physiology ( J:147863 )

• about double the numbers of CD4⁺ T cells expressing IL-13 are found in mediastinal LN cells after Sm egg challenge compared to controls

• mediastinal LN cells restimulated with Sm eggs produce much higher levels of IL-4, IL-13 and IL-5 than in controls

• mutant mice develop exacerbated pulmonary inflammation and fibrosis after exposure to Sm eggs

• mice exhibit exacerbated pulmonary inflammation characterized by increased cellularity within the arterial lumen, hypertrophy of the endothelium, and the accumulation of lymphocytes, eosinophils, and activated macrophages around the vessel wall

• granuloma size is about twice that of controls

• after sensitization and challenge of wild-type mice with Sm eggs, eggs are transported to the lungs where they become trapped within the lung parenchyma by the formation of Th2 cytokine-dependent granulomas

abnormal macrophage physiology ( J:147863 )

• alternatively-activated macrophages (AAMacs) have increased activity after Schistosoma mansoni (Sm) egg challenge as evidenced by increased deposition of collagen in the lung

• in vitro derived AAMacs from mutant mice enhance development of Th2 CD4⁺ T cells

• threefold increase in IL-4 secretion and a 10-fold increase in IL-5 secretion when OT-II T cells were cocultured with OVA-pulsed mutant AAMacs