Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now? - Wikidata - awgldk - TriplyDB

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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Induction of Tolerogenic Dendritic Cells by Endogenous Biomolecules: An Update Tryptophan and arginine catabolic enzymes and regulatory cytokines in clinically isolated syndrome and multiple sclerosis

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Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

http://www.wikidata.org/entity/Q47157913

description

2017 nî lūn-bûn

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2017年の論文

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2017年学术文章

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2017年学术文章

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2017年学术文章

@zh-cn

2017年学术文章

@zh-hans

2017年学术文章

@zh-my

2017年学术文章

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2017年學術文章

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2017年學術文章

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name

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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type

label

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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prefLabel

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

@en

Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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FIMMU.2017.01360

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Frontiers in Immunology

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Indoleamine 2,3-Dioxygenase and Tolerance: Where Are We Now?

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P2093

Andrew L Mellor

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Henrique Lemos

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P2860

Prevention of allogeneic fetal rejection by tryptophan catabolism

Indoleamine 2,3-dioxygenase is a signaling protein in long-term tolerance by dendritic cells

Indoleamine 2,3-dioxygenase in lung dendritic cells promotes Th2 responses and allergic inflammation

Activation of the STING adaptor attenuates experimental autoimmune encephalitis.

Anti-CTLA-4 treatment induces IL-10-producing ICOS+ regulatory T cells displaying IDO-dependent anti-inflammatory properties in a mouse model of colitis.

Indoleamine 2,3 dioxygenase and metabolic control of immune responses.

IDO in the Tumor Microenvironment: Inflammation, Counter-Regulation, and Tolerance

Leishmania major attenuates host immunity by stimulating local indoleamine 2,3-dioxygenase expression.

Induction and role of indoleamine 2,3 dioxygenase in mouse models of influenza a virus infection

Activation of Gpr109a, receptor for niacin and the commensal metabolite butyrate, suppresses colonic inflammation and carcinogenesis.

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1360

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scholarly article

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10.3389/FIMMU.2017.01360

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8

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2017-10-27T00:00:00Z

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