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. 2011 Nov;3(11):a005017. doi: 10.1101/cshperspect.a005017

Table 2.

Comparison of phenotypes of mice with TGF-β gene mutations and mice lacking integrin activators of TGF-β

Mouse Phenotype
Tgfb1–/– Variable (strain-dependent) embryonic lethality because of vasculogenesis failure; lethal multiorgan lymphocyte-mediated inflammation and lack of Langerhans cells in remainder.
Tgfb1RGE/RGE Identical to Tgfb1–/–, reduced fibrosis in heterozygotes.
Tgfb2–/– Embryonic lethality with defects in multiple organ systems.
Tgfb3–/– Cleft palate caused by failure of fusion of palatal shelves; mild, variable delayed lung development.
Itgav–/– ∼80% embryonic lethality because of vasculogenesis failure; brain hemorrhage and cleft palate in remainder. Note that these mice lack αvβ1, αvβ3, αvβ5, αvβ6, and αvβ8 integrins.
Itgb6–/– Lymphocyte-predominant lung inflammation, reduced Langerhans cells, late-onset lung emphysema because of increased MMP-12, reduced fibrosis.
Itgb8–/– Variable embryonic lethality because of vasculogenesis failure, CNS hemorrhage, cleft palate (∼10%); conditional KO in dendritic cells causes mild inflammation.
Itgb6–/–Itgb8–/– Individual phenotypes plus high incidence of cleft palate causing early postnatal death.
Itgb8–/– treated perinatally with anti-αvβ6 Lethal multiorgan lymphocyte-mediated inflammation, lack of Langerhans cells.

See text for references.