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Cited by 2,985TGF-β signaling in diseasesT-cell and B-cell ImmunologyTransplantation: Methods and Outcomes

Targeted disruption of the mouse transforming growth factor-β1 gene results in multifocal inflammatory disease

Open access
Shull, Marcia M., Ormsby, Ilona, Kier, Ann B., Pawlowski, Sharon, Diebold, Ronald J., Yin, Moying, Allen, Ruth, Sidman, Charles +4 more·1992·Nature
DOI 10.1038/359693a0PMC PMC3889166
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Abstract

Transforming growth factor-beta 1 (TGF-beta 1) is a multifunctional growth factor that has profound regulatory effects on many developmental and physiological processes. Disruption of the TGF-beta 1 gene by homologous recombination in murine embryonic stem cells enables mice to be generated that carry the disrupted allele. Animals homozygous for the mutated TGF-beta 1 allele show no gross developmental abnormalities, but about 20 days after birth they succumb to a wasting syndrome accompanied by a multifocal, mixed inflammatory cell response and tissue necrosis, leading to organ failure and death. TGF-beta 1-deficient mice may be valuable models for human immune and inflammatory disorders, including autoimmune diseases, transplant rejection and graft versus host reactions.

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  • TGF-β1−/− mice develop a lethal autoinflammatory syndrome shortly after birth linked to a T-cell specific deficiency of TGF-β.

    “TGF-β1−/− mice develop a lethal autoinflammatory syndrome shortly after birth29,30 which is linked to a T-cell specific deficiency of TGF-β31.”

    From Identification of a unique TGF-β–dependent molecular and functional signature in microglia (2014) · cites this paper as [30]

  • Tgfb1−/− animals die at 3 weeks of age of a severe multifocal autoinflammatory disorder.

    “Tgfb1−/− animals die at 3 weeks of age of a severe multifocal autoinflammatory disorder30 and it has been reported that the loss of TGF-β1 in these mice leads to increased neuronal cell death and microgliosis in the brain47.”

    From Identification of a unique TGF-β–dependent molecular and functional signature in microglia (2014) · cites this paper as [30]

  • TGF-β signaling suppresses processes that lead to CD8+ T cell activation and maturation, including, in APCs, expression of components of the antigen processing and presentation machinery, such as HLA/MHC.

    “TGF-β signaling suppresses processes that lead to CD8+ T cell activation and maturation, including, in APCs, expression of components of the antigen processing and presentation machinery, such as HLA/MHC175,183,202.”

    From TGFβ biology in cancer progression and immunotherapy (2021) · cites this paper as [202]

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Authors
Shull, M. M., Ormsby, I., Kier, A. B., Pawlowski, S., Diebold, R. J., Yin, M., Allen, R., Sidman, C., Proetzel, G., Calvin, D., Annunziata, N., & Doetschman, T.
Affiliations
University of Cincinnati (US)
ORCID
Proetzel, Gabriele
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1992-10
Volume
359
Issue
6397
Pages
693-699
ISSN
  • 0028-0836 (ISSN-L)
  • 1476-4687
DOI
10.1038/359693a0
PMC
PMC3889166
OpenAlex
W2044069347
Cited by
2,985
References
55
Citations by year
2026: 28 · 2025: 24 · 2024: 43 · 2023: 53 · 2022: 54 · 2021: 67 · 2020: 66 · 2019: 56 · 2018: 73 · 2017: 76 · 2016: 82 · 2015: 79 · 2014: 77 · 2013: 95 · 2012: 105
FWCI
34.28
Type
journal article
Language
en
Open access
Licence
www.springer.com/tdm (tdm)
Locations
  • Nature (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
Eunice Kennedy Shriver National Institute of Child Health and Human Development (R01HD026471)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › TGF-β signaling in diseases
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
Keywords
TGF-β1, gene disruption, cachexia, tissue necrosis, organ failure, autoimmune disease, graft rejection, graft-versus-host disease
MeSH terms
Animals, Base Sequence, Genes, Homozygote, Inflammation, Leukocyte Count, Mice, Transgenic, Molecular Sequence Data, Necrosis, Oligodeoxyribonucleotides, RNA, Messenger, Restriction Mapping, Gene Expression, Polymerase Chain Reaction, Cytokines, Transforming Growth Factor beta, Mutagenesis, Insertional, Mice

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