ArticleCellular immunology
Elimination of both CD4+ and CD8+ T cells but not B cells eliminates inflammation and prolongs the survival of TGFbeta1-deficient mice.
Article in Cellular immunology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
11 citing papers in PubMed, 23 citations in OpenAlex.
- Review
- LncRNA-Dependent Mechanisms of Transforming Growth Factor-β: From Tissue Fibrosis to Cancer Progression.Non-coding RNA · 2022Review
- Preoperative CD52 Level Predicts Graft Survival following Kidney Transplantation.BioMed research international · 2022Article
- Unchaining the beast; insights from structural and evolutionary studies on TGFβ secretion, sequestration, and activation.Cytokine & growth factor reviews · 2013Review
- TGF-β signaling to T cells inhibits autoimmunity during lymphopenia-driven proliferation.Nature immunology · 2012Article
- Prostaglandin E2 and SOCS1 have a role in intestinal immune tolerance.Nature communications · 2011Article
- Cellular and molecular basis for the regulation of inflammation by TGF-beta.Journal of biochemistry · 2010Review
- Calcineurin deficiency decreases inflammatory lesions in transforming growth factor beta1-deficient mice.Clinical and experimental immunology · 2009Article
- TGFbeta1 and Treg cells: alliance for tolerance.Trends in molecular medicine · 2007Review
- Self-antigen recognition by TGF beta1-deficient T cells causes their activation and systemic inflammation.Laboratory investigation; a journal of technical methods and pathology · 2006Article
- Increase of CD4(+)CD25(+) T cells in Smad3(-/-) mice.World journal of gastroenterology · 2006Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Transforming growth factor beta1 (TGFbeta1) is a potent negative immunoregulatory molecule. We have previously shown that the autoimmune-mediated weaning-age lethality of Tgfb1-/- mice is reversed upon genetic combination with Scid or Rag null alleles. Here, we show that elimination of T but not B cells is sufficient for the reversal, but elimination of either CD4+ or CD8+ cells is not. Although elimination of B cells does not rescue TGFbeta1-deficient animals from autoimmunity, B cells are hyperresponsive to LPS in the absence of TGFbeta1. TGFbeta1 deficiency leads to activation of CD8+ T cells as suggested by down-modulation of CD8 even in the absence of CD4+ T cells. This study provides evidence that both CD4+ and CD8+ T cells, but not B cells, have the ability to cause inflammation in the absence of TGFbeta1. However, though TGFbeta1-deficient B cells are hyperresponsive to stimulation, alone they are not sufficient to cause inflammation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.