Transforming growth factor beta-1 null mutation in mice causes excessive inflammatory response and early death

Transgenic mouse lines harboring null mutations in the transforming growth factor-beta-1 (TGF-beta-1) locus were generated to elucidate the physiological role of this isoform of TGF-beta. The homozygous mutants exhibited high intrauterine lethality and the surviving mice had widespread inflammatory reactions in various organs causing death at around three to four weeks. The results indicate that TGF-beta-1 is involved in processes such as inflammation, tissue repair, autoimmune disease and allograftrejection.