ArticleLaboratory investigation; a journal of technical methods and pathology2006
Self-antigen recognition by TGF beta1-deficient T cells causes their activation and systemic inflammation.
Article in Laboratory investigation; a journal of technical methods and pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 23 citations in OpenAlex.
- TGF-β, Bone Morphogenetic Protein, and Activin Signaling and the Tumor Microenvironment.Cold Spring Harbor perspectives in biology · 2017Review
- The roles of TGFβ in the tumour microenvironment.Nature reviews. Cancer · 2013Review
- The mRNA level of the transforming growth factor β1 gene, but not the amount of the gene product, can be considered as a potential prognostic parameter in inflammatory bowel diseases in children.International journal of colorectal disease · 2013Article
- TGF-β puts the brakes on homeostatic proliferation.Nature immunology · 2012Article
- Divergent effects of calcineurin Aβ on regulatory and conventional T-cell homeostasis.Clinical immunology (Orlando, Fla.) · 2011Article
- Calcineurin deficiency decreases inflammatory lesions in transforming growth factor beta1-deficient mice.Clinical and experimental immunology · 2009Article
- Kruppel-like factor KLF10 targets transforming growth factor-beta1 to regulate CD4(+)CD25(-) T cells and T regulatory cells.The Journal of biological chemistry · 2009Article
- Ligand-specific function of transforming growth factor beta in epithelial-mesenchymal transition in heart development.Developmental dynamics : an official publication of the American Association of Anatomists · 2009Article
- TGF-beta: a master of all T cell trades.Cell · 2008Review
- TGFbeta1 deficiency does not affect the generation and maintenance of CD4+CD25+FOXP3+ putative Treg cells, but causes their numerical inadequacy and loss of regulatory function.Clinical immunology (Orlando, Fla.) · 2008Article
- Dual roles of immunoregulatory cytokine TGF-beta in the pathogenesis of autoimmunity-mediated organ damage.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
- TGFbeta1 and Treg cells: alliance for tolerance.Trends in molecular medicine · 2007Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
To investigate whether the multifocal inflammatory disease in TGFbeta1-deficient mice is caused by self-antigen (self-Ag)-specific autoreactive T cells, or whether it is caused by antigen independent, spontaneous hyperactivation of T cells, we have generated Tgfb1(-/-) and Tgfb1(-/-) Rag1(-/-) mice expressing the chicken OVA-specific TCR transgene (DO11.10). On a Rag1-sufficient background, Tgfb1(-/-) DO11.10 mice develop a milder inflammation than do Tgfb1(-/-) mice, and their T cells display a less activated phenotype. The lower level of activation correlates with the expression of hybrid TCR (transgenic TCRbeta and endogenous TCRalpha), which could recognize self-Ag and undergo activation. In the complete absence of self-Ag recognition (Tgfb1(-/-) DO11.10 Rag1(-/-) mice) inflammation and T-cell activation are eliminated, demonstrating that self-Ag recognition is required for the hyper-responsiveness of TGFbeta1-deficient T cells. Thus, TGFbeta1 is required for the prevention of autoimmune disease through its ability to control the activation of autoreactive T cells to self-Ag.
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Registered trials
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