Transforming growth factor-beta regulation of immune responses.

By Ming O. Li, Y. Wan, Shomyseh Sanjabi, A. Robertson, R. Flavell. Annual Review of Immunology, 2006

2,303 citations recorded by the source corpus.

Subfields: Immunology and Allergy, Molecular Biology, Oncology

View Paper: https://www.semanticscholar.org/paper/6cdf3dfad59b69a966e805b0b50448b81214617b

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Immunology and Allergy

1. Werner Müller
2. R. Flavell
3. Jeremy S. Duffield

In Molecular Biology

1. J. Massagué
2. D. Sheppard
3. R. Flavell
4. H. Moses
5. Shomyseh Sanjabi
6. S. Friedman
7. TA Wynn
8. V. Bronte

In Oncology

1. J. Massagué
2. D. Sheppard
3. R. Flavell
4. Laura M. McLane
5. Mohamed S. Abdel-Hakeem
6. H. Moses
7. Shomyseh Sanjabi
8. V. Bronte

Citations in the corpus

• TGF-β inhibits the activation and functions of NK cells by repressing the mTOR pathway (2016, background): “This occurs because of the essential role of TGF-b in the control of T cell tolerance in part by promoting the development of the natural regulatory T (Treg) cell lineage and inducing the differentiation of peripherally induced Tregs, and also by directly restraining the activation and differentiati”
• Foxp3 transcription-factor-dependent and -independent regulation of the regulatory T cell transcriptional signature. (2007, background): “TGF-b is intimately associated with the survival and function of Treg cells (Li et al., 2006) and can induce Foxp3 as well as a sizable component of the Treg signature; some of this induction occurs independently of Foxp3 because it is also observed in TGF-b-treated CD8, or Foxp3 CD4, cells.”
• Heterogeneity of Microglial Activation in the Innate Immune Response in the Brain (2009, background): “2002) while TGF-β signaling is mediated by both Smaddependent and Smad-independent pathways (Li et al. 2006).”
• Tumor‐induced tolerance and immune suppression by myeloid derived suppressor cells (2008, background): “For example, transforming growth factor-b (TGF-b) inhibits the proliferation, differentiation, and activation of T lymphocytes (16), and, in association with interleukin-10 (IL-10), can induce the maturation of different subsets of T-regulatory (Treg) lymphocytes (17).”
• Cellular and molecular mechanisms of fibrosis (2008, background): “During this period, lymphocytes and other cells become activated and begin secreting profibrotic cytokines and growth factors, such as TGFβ, IL-13 and PDGF [6–8], which further activate the macrophages and fibroblasts.”
• Therapy for Fibrotic Diseases: Nearing the Starting Line (2013, background): “Nevertheless, TGFb has important normal homeostatic activities, including immune regulation and tumor suppression (194, 195).”
• Differential Roles of Macrophages in Diverse Phases of Skin Repair (2010, background): “Furthermore, withdrawal of TGF-b1, a potent immunosuppressive mediator (45), might be responsible for the increased influx of neutrophils into the macrophage-depleted granulation tissue.”
• Effects of Rehmannia glutinosa on growth performance, immunological parameters and disease resistance to Aeromonas hydrophila in common carp (Cyprinus carpio L.) (2015, background): “The pivotal function of TGF-β was its potent regulatory effect on awide variety of cells, including cell proliferation, differentiation, migration and apoptosis, under physiological and pathological conditions (Jacobsen et al., 1991; Li et al., 2006).”
• CD8 T Cell Exhaustion During Chronic Viral Infection and Cancer. (2019, background): “During acute infection, TGF-β acts as a negative regulator of effector function (154) through the repression of T-bet (T-box expressed in T cells) (155) and results in the upregulation of the proapoptotic factor Bim (156).”