Regulatory T Cells and Foxp3
By Alexander Y. Rudensky. Immunological Reviews, 2011
814 citations recorded by the source corpus.
Summary: Regulatory T (Treg) cells play central role in regulation of immune responses to self‐antigens, allergens, and commensal microbiota as well as immune responses to infectious agents and tumors. Transcriptional factor Foxp3 serves as a lineage specification factor of Treg cells. Paucity of Treg cells due to loss‐of‐function mutations of the Foxp3 gene is responsible for highly aggressive, fatal, systemic immune‐mediated inflammatory lesions in mice and humans. Recent studies of Foxp3 expression and function provided critical novel insights into biology of Treg cells and into cellular mechanisms of the immune homeostasis.
Subfields: Immunology
View Paper: https://www.semanticscholar.org/paper/1eb31231f66a840f35468c18aa38039fbf3a7fe2
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In Immunology
Citations in the corpus
- Regulatory B cells: origin, phenotype, and function. (2015, result): “Thus, as a result of the heterogeneity of Breg cell subsets, a principal challenge of Breg cell research has been the identification of a Breg-cell-specific transcription factor, similar to Foxp3 in Treg cells (Rudensky, 2011).”
- Vitamin D and Immune Function (2013, background): “Tregs act to suppress proinflammatory responses by other immune cells and aim to prevent exaggerated or autoimmune responses [88].”
- Dictionary learning for integrative, multimodal, and massively scalable single-cell analysis (2022, neutral): “P values were calculated by Fisher’s exact test and were adjusted by the Benjamini–Hochberg test. g , Expression distributions of top transcriptional markers recovered from single-cell differential expression analysis (red) or pseudobulk analysis (blue).”
- Development and maintenance of regulatory T cells. (2013, background): “…CD25+CD4+ regulatory T (Treg) cells, which constitutively express the transcription factor Foxp3, are indispensable for the maintenance of immune self-tolerance and homeostasis by suppressing aberrant or excessive immune responses harmful to the host (Rudensky, 2011; Sakaguchi et al., 2008).”