Regulatory T Cells: Mechanisms of Differentiation and Function
By Steven Z. Josefowicz, Li-Fan Lu, Alexander Y. Rudensky. Annual Review of Immunology, 2012
2,797 citations recorded by the source corpus.
The immune system has evolved to mount an effective defense against pathogens and to minimize deleterious immune-mediated inflammation caused by commensal microorganisms, immune responses against self and environmental antigens, and metabolic inflammatory disorders. Regulatory T (Treg) cell–mediated suppression serves as a vital mechanism of negative regulation of immune-mediated inflammation and features prominently in autoimmune and autoinflammatory disorders, allergy, acute and chronic infections, cancer, and metabolic inflammation. The discovery that Foxp3 is the transcription factor that specifies the Treg cell lineage facilitated recent progress in understanding the biology of regulatory T cells. In this review, we discuss cellular and molecular mechanisms in the differentiation and function of these cells.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/5b2265345608fb496909695a8f0a4e906272f0de
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In Immunology
- Alexander Y. Rudensky
- C. Iadecola
- D. Mathis
- C. Benoist
- Jongsoon Lee
- F. Quintana
- M. Feuerer
- Byung-Cheol Lee
Citations in the corpus
- TGF-β Activation and Function in Immunity (2013, background): “Tregs are a subset of CD4+ T cells that are crucial in suppression of self-harmful T cell responses (52).”
- Zinc as a Gatekeeper of Immune Function (2017, background): “Treg secreted high amounts of anti-inflammatory cytokines such as IL-10 and transforming growth factor (TGF)-β1 [278], constraining immunological anti-tumor defense.”
- Fusobacterium nucleatum potentiates intestinal tumorigenesis and modulates the tumor immune microenvironment (2013, background): “These cells play a role in the regulation of immune responses by promoting the expansion of Foxp3 regulatory T cells, a CD4 T cell subset that suppresses cytotoxic and effector T cells, and thus dampen antitumor immunity (Coombes et al., 2007; Josefowicz et al., 2012).”
- PPARγ is a major driver of the accumulation and phenotype of adipose-tissue Treg cells (2012, positive): “…notion that the Foxp3 + CD4 + T reg compartment includes a number of sub-types with distinct phenotypes, localizations and effector functions 15 has evoked the exciting possibility of developing strategies to precisely expand or contract disease-relevant T regs , leaving the bulk of the…”
- Defining dysbiosis and its influence on host immunity and disease (2014, background): “Tolerance to self tissue and resident commensals is, in part, governed by a specialized subset of T lymphocytes termed T regulatory cells (Tregs) (Josefowicz et al., 2012).”
- Tolerogenic dendritic cells (2016, background): “Regulatory T cells (Tregs) are crucial in the maintenance of peripheral tolerance in mice and humans [1].”
- Transcriptional Landscape of Human Tissue Lymphocytes Unveils Uniqueness of Tumor-Infiltrating T Regulatory Cells (2016, background): “Treg cells, which are physiologically engaged in the maintenance of immunological self-tolerance and immune homeostasis (Josefowicz et al., 2012; Sakaguchi et al., 2008), are potent suppressors of effector cells and are found at high frequencies in various types of cancers (Fridman et al., 2012;…”
- Commensal microbiota affects ischemic stroke outcome by regulating intestinal γδT cells (2016, positive): “This is to be expected, because IL-10 is only one of the possible mechanism by which T reg suppress T cell proliferation 31 .”
- Regulatory T cells exhibit distinct features in human breast cancer (2016, positive): “Graphical abstract Introduction Regulatory T (Treg) cells expressing the transcription factor Foxp3 play an essential role in controlling autoimmunity and maintain immunological tolerance in mouse and man (Josefowicz et al., 2012).”
- Cellular and Molecular Players in Adipose Tissue Inflammation in the Development of Obesity-induced Insulin Resistance (2013, positive): “Tregs play an important role in the suppression of inflammation [88].”