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Vijay K. Kuchroo

Researcher at Brigham and Women's Hospital

Publications -  555
Citations -  98090

Vijay K. Kuchroo is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: T cell & Immune system. The author has an hindex of 144, co-authored 525 publications receiving 86936 citations. Previous affiliations of Vijay K. Kuchroo include Science for Life Laboratory & King Abdulaziz University.

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Reciprocal developmental pathways for the generation of pathogenic effector TH17 and regulatory T cells.

TL;DR: It is shown that IL-6, an acute phase protein induced during inflammation, completely inhibits the generation of Foxp3+ Treg cells induced by TGF-β, and the data demonstrate a dichotomy in thegeneration of pathogenic (TH17) T cells that induce autoimmunity and regulatory (Foxp3+) T Cells that inhibit autoimmune tissue injury.
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IL-17 and Th17 Cells.

TL;DR: The investigation of the differentiation, effector function, and regulation of Th17 cells has opened up a new framework for understanding T cell differentiation and now appreciate the importance of Th 17 cells in clearing pathogens during host defense reactions and in inducing tissue inflammation in autoimmune disease.
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Adenosine generation catalyzed by CD39 and CD73 expressed on regulatory T cells mediates immune suppression

TL;DR: It is concluded that CD39 and CD73 are surface markers of T reg cells that impart a specific biochemical signature characterized by adenosine generation that has functional relevance for cellular immunoregulation.
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Regulatory T cell clones induced by oral tolerance: suppression of autoimmune encephalomyelitis

TL;DR: Mucosally derived TH2-like clones induced by oral antigen can actively regulate immune responses in vivo and may represent a different subset of T cells.
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IL-21 initiates an alternative pathway to induce proinflammatory T H 17 cells

TL;DR: It is shown that IL-6-deficient (Il6-/-) mice do not develop a TH17 response and their peripheral repertoire is dominated by Foxp3+ Treg cells, suggesting an additional pathway by which TH17 cells might be generated in vivo.