Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function. - Wikidata - awgldk - TriplyDB

Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function.

Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function.

http://www.wikidata.org/entity/Q34044929

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CD1d- and MR1-Restricted T Cells in Sepsis Targeting the programmed cell death 1: programmed cell death ligand 1 pathway reverses T cell exhaustion in patients with sepsis Effect of PD-1: PD-L1 in Invariant Natural Killer T-Cell Emigration and Chemotaxis Following Sepsis.Lymphocyte integrin expression differences between SIRS and sepsis patients.Cl-Amidine Prevents Histone 3 Citrullination and Neutrophil Extracellular Trap Formation, and Improves Survival in a Murine Sepsis Model.Program Cell Death Receptor-1-Mediated Invariant Natural Killer T-Cell Control of Peritoneal Macrophage Modulates Survival in Neonatal Sepsis.

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Inflammatory mechanisms in sepsis: elevated invariant natural killer T-cell numbers in mouse and their modulatory effect on macrophage function.

http://www.wikidata.org/entity/Q34044929

description

2013 nî lūn-bûn

@nan

2013 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2013 թվականի օգոստոսին հրատարակված գիտական հոդված

@hy

2013年の論文

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年学术文章

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2013年學術文章

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name

Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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type

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Inflammatory mechanisms in sep ...... effect on macrophage function.

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Chun-Shiang Chung

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Daithi S Heffernan

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Mai L Tran

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Rajan K Thakkar

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Sean F Monaghan

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Stephen H Gregory

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William G Cioffi

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P2860

Intravascular immune surveillance by CXCR6+ NKT cells patrolling liver sinusoids

Phase I study of single-agent anti-programmed death-1 (MDX-1106) in refractory solid tumors: safety, clinical activity, pharmacodynamics, and immunologic correlates

Tumor necrosis factor-alpha is required in the protective immune response against Mycobacterium tuberculosis in mice

An intravascular immune response to Borrelia burgdorferi involves Kupffer cells and iNKT cells.

PD-1/PD-L blockade prevents anergy induction and enhances the anti-tumor activities of glycolipid-activated invariant NKT cells

Innate invariant NKT cells recognize Mycobacterium tuberculosis-infected macrophages, produce interferon-gamma, and kill intracellular bacteria.

Alpha-galactosylceramide promotes killing of Listeria monocytogenes within the macrophage phagosome through invariant NKT-cell activation

PD-1 expression by macrophages plays a pathologic role in altering microbial clearance and the innate inflammatory response to sepsis

Programmed death-1 levels correlate with increased mortality, nosocomial infection and immune dysfunctions in septic shock patients.

Upregulation of programmed death-1 on T cells and programmed death ligand-1 on monocytes in septic shock patients.

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122-128

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