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Autoimmune manifestations in the transforming growth factor-beta 1 knockout
mouse
L Yaswen, AB Kulkarni, T Fredrickson, B Mittleman, R Schiffman, S Payne, G Longenecker, E Mozes and S Karlsson
Molecular and Medical Genetics Section, National Institute of Neurological
Disorders and Stroke, National Cancer Institute, National Institutes of
Health, Bethesda, MD 20892, USA.
Targeted disruption of the transforming growth factor-beta 1 (TGF-beta 1)
gene in mice results in the development of a massive multifocal
inflammatory disease in many tissues. Because no detectable pathogen was
identified, we examined whether autoimmune mechanisms played a role in
initiating or maintaining the inflammatory disease. The serum of TGF- beta
1 knockout mice contained elevated titers of antibodies to nuclear antigens
(ssDNA, dsDNA, Sm, and RNP) as well as reactivity against the 16/6 idiotype
(16/6 Id). In addition, Ig deposits were detected in renal glomeruli of
TGF- beta 1 knockout mice. Transplantation of TGF- beta 1 knockout
hematopoietic cells into normal irradiated recipients resulted in a similar
profile of autoantibody production as well as in the induction of
inflammatory lesions. Our results describe autoimmune activity that ensues
when the TGF-beta 1 cytokine is absent.
Volume 87,
Issue 4,
pp. 1439-1445,
02/15/1996
Copyright © 1996 by The American Society of Hematology
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