How microorganisms tip the balance between interleukin-12 family members. - Wikidata - awgldk - TriplyDB

How microorganisms tip the balance between interleukin-12 family members.

How microorganisms tip the balance between interleukin-12 family members.

http://www.wikidata.org/entity/Q37033837

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Primary biliary cirrhosis associated with HLA, IL12A, and IL12RB2 variants Interleukin-23: as a drug target for autoimmune inflammatory diseases Toll-like Receptor 7 Mitigates Lethal West Nile Encephalitis via Interleukin 23-Dependent Immune Cell Infiltration and Homing Interleukin 12 a key immunoregulatory cytokine in infection applications Frailty in old age is associated with decreased interleukin-12/23 production in response to toll-like receptor ligation Complement: a key system for immune surveillance and homeostasis Toll-like receptor 2 (TLR2)-TLR9 crosstalk dictates IL-12 family cytokine production in microglia.The adenosine a2a receptor inhibits matrix-induced inflammation in a novel fashion Microbial manipulation of receptor crosstalk in innate immunity Helicobacter pylori stimulates dendritic cells to induce interleukin-17 expression from CD4+ T lymphocytes.Trypanosomiasis-induced Th17-like immune responses in carp.Delineation of the innate and adaptive T-cell immune outcome in the human host in response to Campylobacter jejuni infection.Immunomodulatory effects of dsRNA and its potential as vaccine adjuvant.Toll-like receptors, tissue injury, and tumourigenesis IL-17 and Th17 cells in tuberculosis Impaired blood dendritic cell numbers and functions after aneurysmal subarachnoid hemorrhage Epstein Barr virus-induced 3 (EBI3) together with IL-12 negatively regulates T helper 17-mediated immunity to Listeria monocytogenes infection.IL-12 promotes myeloid-derived suppressor cell recruitment and bacterial persistence during Staphylococcus aureus orthopedic implant infection Interplay between innate and adaptive immunity in the development of non-infectious uveitis Neonatal innate TLR-mediated responses are distinct from those of adults.The FomA porin from Fusobacterium nucleatum is a Toll-like receptor 2 agonist with immune adjuvant activity TRAF3: a novel tumor suppressor gene in macrophages.Innate immune function by Toll-like receptors: distinct responses in newborns and the elderly.The pathogenic Th17 cell response to major schistosome egg antigen is sequentially dependent on IL-23 and IL-1β Production of interleukin-27 by human neutrophils regulates their function during bacterial infection.IL-27 Induced by Select Candida spp. via TLR7/NOD2 Signaling and IFN-β Production Inhibits Fungal Clearance.Acute exercise decreases airway inflammation, but not responsiveness, in an allergic asthma model.Yersinia pestis evades TLR4-dependent induction of IL-12(p40)2 by dendritic cells and subsequent cell migration Tristetraprolin regulation of interleukin 23 mRNA stability prevents a spontaneous inflammatory disease A new inflammatory cytokine on the block: re-thinking periodontal disease and the Th1/Th2 paradigm in the context of Th17 cells and IL-17.HDAC inhibition by LBH589 affects the phenotype and function of human myeloid dendritic cells.Toll gates to periodontal host modulation and vaccine therapy Complementary Tolls in the periodontium: how periodontal bacteria modify complement and Toll-like receptor responses to prevail in the host.Interleukin 27: a double-edged sword for offense and defense.Analysis of the common genetic component of large-vessel vasculitides through a meta-Immunochip strategy.Crosstalk pathways between Toll-like receptors and the complement system.Spirulina lipopolysaccharides inhibit tumor growth in a Toll-like receptor 4-dependent manner by altering the cytokine milieu from interleukin-17/interleukin-23 to interferon-γ.Interactions between Type 1 Interferons and the Th17 Response in Tuberculosis: Lessons Learned from Autoimmune Diseases.New interleukin-23 pathway inhibitors in dermatology: ustekinumab, briakinumab, and secukinumab.A controversial role for IL-12 in immune response and bone resorption at apical periodontal sites.

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How microorganisms tip the balance between interleukin-12 family members.

http://www.wikidata.org/entity/Q37033837

description

article científic

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article scientifique

@fr

articolo scientifico

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artigo científico

@pt

bilimsel makale

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scientific article published on January 2008

@en

vedecký článok

@sk

vetenskaplig artikel

@sv

videnskabelig artikel

@da

vědecký článek

@cs

name

How microorganisms tip the balance between interleukin-12 family members.

@en

How microorganisms tip the balance between interleukin-12 family members.

@nl

type

label

How microorganisms tip the balance between interleukin-12 family members.

@en

How microorganisms tip the balance between interleukin-12 family members.

@nl

prefLabel

How microorganisms tip the balance between interleukin-12 family members.

@en

How microorganisms tip the balance between interleukin-12 family members.

@nl

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Nature Reviews Immunology

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How microorganisms tip the balance between interleukin-12 family members.

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Markus F Neurath

http://www.w3.org/2001/XMLSchema#string

Michel Goldman

http://www.w3.org/2001/XMLSchema#string

Stanislas Goriely

http://www.w3.org/2001/XMLSchema#string

P2860

Infections and autoimmunity--good or bad?

T cell-independent, TLR-induced IL-12p70 production in primary human monocytes.

A role for IL-27 in early regulation of Th1 differentiation.

EBV-induced gene 3 transcription is induced by TLR signaling in primary dendritic cells via NF-kappa B activation.

C/EBP beta gene inactivation causes both impaired and enhanced gene expression and inverse regulation of IL-12 p40 and p35 mRNAs in macrophages.

An IFN-gamma-inducible transcription factor, IFN consensus sequence binding protein (ICSBP), stimulates IL-12 p40 expression in macrophages.

Microbial recognition via Toll-like receptor-dependent and -independent pathways determines the cytokine response of murine dendritic cell subsets to CD40 triggering.

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81-86

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scholarly article

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10.1038/NRI2225

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1

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8

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2008-01-01T00:00:00Z

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1000035607

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18084185

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