Proliferative lesions and metalloproteinase activity in murine lupus nephritis mediated by type I interferons and macrophages - Wikidata - wikimedia - TriplyDB

Proliferative lesions and metalloproteinase activity in murine lupus nephritis mediated by type I interferons and macrophages

Proliferative lesions and metalloproteinase activity in murine lupus nephritis mediated by type I interferons and macrophages

http://www.wikidata.org/entity/Q33733803

about

Overview of the biology of type I interferons Spatiotemporal Regulation of Hsp90-Ligand Complex Leads to Immune Activation Platelet-derived growth factors (PDGFs) in glomerular and tubulointerstitial fibrosis The regulation of inflammation by interferons and their STATs Intracellular nucleic acid sensors and autoimmunity Dendritic cells and macrophages in the kidney: a spectrum of good and evil Epidermal growth factor: a new therapeutic target in glomerular disease.Pathogenic and protective role of macrophages in kidney disease Type I interferon: friend or foe?Mechanisms of tissue injury in lupus nephritis Effects of Integrated Traditional Chinese and Western Medicine for the Treatment of Lupus Nephritis: A Meta-Analysis of Randomized Trials Demethylzeylasteral (T-96) Treatment Ameliorates Mice Lupus Nephritis Accompanied by Inhibiting Activation of NF-κB Pathway Amelioration of lupus nephritis by serum amyloid P component gene therapy with distinct mechanisms varied from different stage of the disease.Early Surgical Decompression Restores Neurovascular Blood Flow and Ischemic Parameters in an in Vivo Animal Model of Nerve Compression Injury Comparative effects of n-3, n-6 and n-9 unsaturated fatty acid-rich diet consumption on lupus nephritis, autoantibody production and CD4+ T cell-related gene responses in the autoimmune NZBWF1 mouse.Recent advances in the understanding of renal inflammation and fibrosis in lupus nephritis.Identification of Ceruloplasmin as a Gene that Affects Susceptibility to Glomerulonephritis Through Macrophage Function.Current status of lupus nephritis.Silencing of renal DNaseI in murine lupus nephritis imposes exposure of large chromatin fragments and activation of Toll like receptors and the Clec4e.Activation of type I interferon pathway in systemic lupus erythematosus: association with distinct clinical phenotypes.Interferon-α accelerates murine systemic lupus erythematosus in a T cell-dependent manner.Requirements for innate immune pathways in environmentally induced autoimmunity.Granulin exacerbates lupus nephritis via enhancing macrophage M2b polarization.Systemic lupus erythematosus and granulomatous lymphadenopathy STAT6 expression in multiple cell types mediates the cooperative development of allergic airway disease IFN-α confers resistance of systemic lupus erythematosus nephritis to therapy in NZB/W F1 mice A unique hybrid renal mononuclear phagocyte activation phenotype in murine systemic lupus erythematosus nephritis.Engraftment of peripheral blood mononuclear cells from systemic lupus erythematosus and antiphospholipid syndrome patient donors into BALB-RAG-2-/- IL-2Rγ-/- mice: a promising model for studying human disease.Epidermal growth factor receptor promotes glomerular injury and renal failure in rapidly progressive crescentic glomerulonephritis.Macrophage polarization in kidney diseases.Structure and function of renal macrophages and dendritic cells from lupus-prone mice Pristane-Accelerated Autoimmune Disease in (SWR X NZB) F1 Mice Leads to Prominent Tubulointerstitial Inflammation and Human Lupus Nephritis-Like Fibrosis.Epidermal injury promotes nephritis flare in lupus-prone mice.DNA-dependent activator of interferon-regulatory factors (DAI) promotes lupus nephritis by activating the calcium pathway.Plasma levels of osteopontin identify patients at risk for organ damage in systemic lupus erythematosus Deficiency of base excision repair enzyme NEIL3 drives increased predisposition to autoimmunity.Death receptor 5-targeted depletion of interleukin-23-producing macrophages, Th17, and Th1/17 associated with defective tyrosine phosphatase in mice and patients with rheumatoid arthritis.Btk-specific inhibition blocks pathogenic plasma cell signatures and myeloid cell-associated damage in IFNα-driven lupus nephritis.Cellular and molecular pathogenesis of systemic lupus erythematosus: lessons from animal models.Epidermal growth factor receptor mediates injury in rapidly progressive glomerular disease.

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Proliferative lesions and metalloproteinase activity in murine lupus nephritis mediated by type I interferons and macrophages

http://www.wikidata.org/entity/Q33733803

description

2010 nî lūn-bûn

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2010 թուականի Յունուարին հրատարակուած գիտական յօդուած

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2010 թվականի հունվարին հրատարակված գիտական հոդված

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2010年の論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年論文

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2010年论文

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name

Proliferative lesions and meta ...... I interferons and macrophages

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Proliferative lesions and meta ...... I interferons and macrophages

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Proliferative lesions and meta ...... I interferons and macrophages

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Proliferative lesions and meta ...... I interferons and macrophages

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PNAS.0914902107

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Proliferative lesions and meta ...... I interferons and macrophages

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P2093

Antigoni Triantafyllopoulou

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Claus-Werner Franzke

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Giorgio Perino

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Lionel B Ivashkiv

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Meera Ramanujam

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Surya V Seshan

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P2860

IL-33 amplifies the polarization of alternatively activated macrophages that contribute to airway inflammation

Exploring the full spectrum of macrophage activation

Stage-specific action of matrix metalloproteinases influences progressive hereditary kidney disease.

Alternative activation of macrophages

Interferon-inducible gene expression signature in peripheral blood cells of patients with severe lupus

Unique expression of suppressor of cytokine signaling 3 is essential for classical macrophage activation in rodents in vitro and in vivo

The healing myocardium sequentially mobilizes two monocyte subsets with divergent and complementary functions

Inflammatory monocytes recruited after skeletal muscle injury switch into antiinflammatory macrophages to support myogenesis

Interferon-alpha treatment of female (NZW x BXSB)F(1) mice mimics some but not all features associated with the Yaa mutation.

Type I interferons produced by resident renal cells may promote end-organ disease in autoantibody-mediated glomerulonephritis.

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7

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107

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George D. Kalliolias

Nico van Rooijen

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2010-01-26T00:00:00Z

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41408555

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20133703

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2840310

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