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Mohamed Oukka

Researcher at University of Washington

Publications -  97
Citations -  33795

Mohamed Oukka is an academic researcher from University of Washington. The author has contributed to research in topics: FOXP3 & T cell. The author has an hindex of 50, co-authored 91 publications receiving 31464 citations. Previous affiliations of Mohamed Oukka include Harvard University & Seattle Children's Research Institute.

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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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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.
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Small intestine lamina propria dendritic cells promote de novo generation of Foxp3 T reg cells via retinoic acid

TL;DR: It is shown that peripheral conversion of CD4+ T cells to T reg cells occurs primarily in gut-associated lymphoid tissue (GALT) after oral exposure to antigen and in a lymphopenic environment, and that the intestinal immune system has evolved a self-contained strategy to promote T reg cell neoconversion.