Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome. - Wikidata - wikimedia - TriplyDB

Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome.

Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome.

http://www.wikidata.org/entity/Q36431053

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Mucosal-Associated Invariant T Cells in Multiple Sclerosis: The Jury is Still Out Inflammasomes: mechanism of action, role in disease, and therapeutics An Update on PYRIN Domain-Containing Pattern Recognition Receptors: From Immunity to Pathology NLRP3 inflammasome and its inhibitors: a review Activation and regulation of the inflammasomes NLRP3 inflammasome induces chemotactic immune cell migration to the CNS in experimental autoimmune encephalomyelitis.An interferon-β-resistant and NLRP3 inflammasome-independent subtype of EAE with neuronal damage Interferon-tau attenuates uptake of nanoparticles and secretion of interleukin-1β in macrophages Interleukin-1- and type I interferon-dependent enhanced immunogenicity of an NYVAC-HIV-1 Env-Gag-Pol-Nef vaccine vector with dual deletions of type I and type II interferon-binding proteins.Immune Complexes Indirectly Suppress the Generation of Th17 Responses In Vivo.Gene-Expression Profiling Suggests Impaired Signaling via the Interferon Pathway in Cstb-/- Microglia IL-1 family cytokines trigger sterile inflammatory disease.NLRP3 Inflammasome and MS/EAE.Expression of IL-1β in rhesus EAE and MS lesions is mainly induced in the CNS itself.Protein kinase Cβ as a therapeutic target stabilizing blood-brain barrier disruption in experimental autoimmune encephalomyelitis Unsolved Mysteries in NLR Biology.The nucleotide-binding leucine-rich repeat (NLR) family member NLRX1 mediates protection against experimental autoimmune encephalomyelitis and represses macrophage/microglia-induced inflammation.Inflammasomes in Myeloid Cells: Warriors Within.T cell-intrinsic ASC critically promotes T(H)17-mediated experimental autoimmune encephalomyelitis Subversion of inflammasome activation and pyroptosis by pathogenic bacteria.The role of interferon-β in the treatment of multiple sclerosis and experimental autoimmune encephalomyelitis - in the perspective of inflammasomes.Adaptive immune responses in CNS autoimmune disease: mechanisms and therapeutic opportunities.Innate immunity and neuroinflammation.Licensing Adaptive Immunity by NOD-Like Receptors.Interferons in the central nervous system: a few instruments play many tunes.Interferon regulatory factor 3 in adaptive immune responses.The pathogenic role of the inflammasome in neurodegenerative diseases.Lung inflammation stalls Th17-cell migration en route to the central nervous system during the development of experimental autoimmune encephalomyelitis.Opposing effects of Nrf2 and Nrf2-activating compounds on the NLRP3 inflammasome independent of Nrf2-mediated gene expression.Inflammasome activation in multiple sclerosis and experimental autoimmune encephalomyelitis (EAE).New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.IFN-β Facilitates Neuroantigen-Dependent Induction of CD25+ FOXP3+ Regulatory T Cells That Suppress Experimental Autoimmune Encephalomyelitis.Inflammasome activation has an important role in the development of spontaneous colitis.Comparative assessment of PDE 4 and 7 inhibitors as therapeutic agents in experimental autoimmune encephalomyelitis.Just say NO to NLRP3.Inflammatory cytokines at the summits of pathological signal cascades in brain diseases.Structure-activity studies of peptidomimetics based on kinase-inhibitory region of suppressors of cytokine signaling 1.The hygiene hypothesis in autoimmunity: the role of pathogens and commensals.Development and Characterization of a Hydroxyl-Sulfonamide Analogue, 5-Chloro-N-[2-(4-hydroxysulfamoyl-phenyl)-ethyl]-2-methoxy-benzamide, as a Novel NLRP3 Inflammasome Inhibitor for Potential Treatment of Multiple Sclerosis.NLR-Dependent Regulation of Inflammation in Multiple Sclerosis- Dependent Regulation of Inflammation in Multiple Sclerosis.

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P2860

Interferon-β therapy against EAE is effective only when development of the disease depends on the NLRP3 inflammasome.

http://www.wikidata.org/entity/Q36431053

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2012 nî lūn-bûn

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2012年の論文

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2012年学术文章

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Interferon-β therapy against E ...... nds on the NLRP3 inflammasome.

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Jayant V Rajan

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Kristi L Williams

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Makoto Inoue

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Mari L Shinohara

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Timothy Oliver

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P2860

Identification and characterization of CD39/vascular ATP diphosphohydrolase

A role for mitochondria in NLRP3 inflammasome activation

Gout-associated uric acid crystals activate the NALP3 inflammasome

Cryopyrin activates the inflammasome in response to toxins and ATP

Thioredoxin-interacting protein links oxidative stress to inflammasome activation

The NALP3 inflammasome is involved in the innate immune response to amyloid-beta

The inflammasomes: guardians of the body

NLRP3 inflammasome activation: The convergence of multiple signalling pathways on ROS production?

Differential regulation of central nervous system autoimmunity by T(H)1 and T(H)17 cells.

Rac1-mediated mitochondrial H2O2 generation regulates MMP-9 gene expression in macrophages via inhibition of SP-1 and AP-1

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