Delayed wound healing in immunodeficient TGF-beta 1 knockout mice

Previous studies showed that full-thickness wounds in transforming growth f actor-beta 1-deficient mice initially heal normally. Unfortunately, transfo rming growth factor-beta 1 deficiency leads to a multifocal inflammatory di sease affecting most organs of the body, which ultimately interferes with l ater stages of wound healing in these mice. As this inflammatory disease is eliminated in transforming growth factor-beta 1-deficient mice lacking T a nd B cells (Tgfb1(-/-) Scid(-/-) mice), we hypothesized that wound repair i n the latter would proceed normally, even at later stages of healing. Unexp ectedly, Tgfb1(-/-) Scid(-/-) mice demonstrate a major delay of approximate ly 1 wk in each of the major phases of wound healing: inflammation, prolife ration, and maturation. Immunodeficient Scid(-/-) mice that have the wild-t ype Tgfb1 allele do not experience this delay in wound healing. One interpr etation of these findings is that lymphocytes and transforming growth facto r-beta 1 affect compensatory pathways in wound healing. An alternative inte rpretation is that the delayed expression of Tgfb2 and Tgfb3 that occurs in the absence of transforming growth factor-beta 1 results in the delayed wo und healing, suggesting that transforming growth factor-beta 2 and/or trans forming growth factor-beta 3 play important parts in wound healing.