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Alexander Y. Rudensky

Researcher at Memorial Sloan Kettering Cancer Center

Publications -  284
Citations -  75131

Alexander Y. Rudensky is an academic researcher from Memorial Sloan Kettering Cancer Center. The author has contributed to research in topics: FOXP3 & Immune system. The author has an hindex of 116, co-authored 268 publications receiving 66717 citations. Previous affiliations of Alexander Y. Rudensky include University of Washington & Yale University.

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Foxp3 programs the development and function of CD4 + CD25 + regulatory T cells

TL;DR: It is reported that the forkhead transcription factor Foxp3 is specifically expressed in CD4+CD25+ regulatory T cells and is required for their development and function and ectopic expression ofFoxp3 confers suppressor function on peripheral CD4-CD25− T cells.
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Metabolites produced by commensal bacteria promote peripheral regulatory T-cell generation

TL;DR: The results suggest that bacterial metabolites mediate communication between the commensal microbiota and the immune system, affecting the balance between pro- and anti-inflammatory mechanisms.
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Regulatory T Cells: Mechanisms of Differentiation and Function

TL;DR: Cellular and molecular mechanisms in the differentiation and function of regulatory T cells and their role in autoimmune and autoinflammatory disorders, allergy, acute and chronic infections, cancer, and metabolic inflammation are discussed.
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Regulatory T Cell Lineage Specification by the Forkhead Transcription Factor Foxp3

TL;DR: Analysis of Foxp3 expression during thymic development suggests that this mechanism is not hard-wired but is dependent on TCR/MHC ligand interactions, and it is shown that expression ofFoxp3 is highly restricted to the subset alphabeta of T cells and, irrespective of CD25 expression, correlates with suppressor activity.
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A function for interleukin 2 in Foxp3-expressing regulatory T cells

TL;DR: Gene expression analysis showed that IL-2 signaling was required for maintenance of the expression of genes involved in the regulation of cell growth and metabolism, which seems to be critically required for maintaining the homeostasis and competitive fitness of Treg cells in vivo.