BAFF and MyD88 signals promote a lupuslike disease independent of T cells. - Wikidata - wikimedia - TriplyDB

BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

http://www.wikidata.org/entity/Q36229560

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The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88 Toll-Like Receptors in the Pathogenesis of Autoimmune Diseases Anergic B Cells: Precarious On-Call Warriors at the Nexus of Autoimmunity and False-Flagged Pathogens Defects in Germinal Center Selection in SLE Linking susceptibility genes and pathogenesis mechanisms using mouse models of systemic lupus erythematosus The rationale for BAFF inhibition in systemic lupus erythematosus Role of type I interferons in the activation of autoreactive B cells Effect of TACI signaling on humoral immunity and autoimmune diseases B cells take the front seat: dysregulated B cell signals orchestrate loss of tolerance and autoantibody production The effect of targeted rheumatoid arthritis therapies on anti-citrullinated protein autoantibody levels and B cell responses Autoantibodies in systemic autoimmune diseases: specificity and pathogenicity Mechanisms of autoantibody production in systemic lupus erythematosus The Deubiquitinase OTULIN Is an Essential Negative Regulator of Inflammation and Autoimmunity Elevated pretransplantation soluble BAFF is associated with an increased risk of acute antibody-mediated rejection Prevention of murine antiphospholipid syndrome by BAFF blockade Pathway of Toll-like receptor 7/B cell activating factor/B cell activating factor receptor plays a role in immune thrombocytopenia in vivo.Critical role for mouse marginal zone B cells in PF4/heparin antibody production.Critical role of CD4 T cells in PF4/heparin antibody production in mice Investigations of a rabbit (Oryctolagus cuniculus) model of systemic lupus erythematosus (SLE), BAFF and its receptors.Restoring the balance: immunotherapeutic combinations for autoimmune disease TLR4 signaling augments B lymphocyte migration and overcomes the restriction that limits access to germinal center dark zones.Interleukin-10 mediated autoregulation of murine B-1 B-cells and its role in Borrelia hermsii infection.B cell activating factor (BAFF) and T cells cooperate to breach B cell tolerance in lupus-prone New Zealand Black (NZB) mice The function of BAFF on T helper cells in autoimmunity Effect of long-term belimumab treatment on B cells in systemic lupus erythematosus: extension of a phase II, double-blind, placebo-controlled, dose-ranging study.Requirement for MyD88 signaling in B cells and dendritic cells for germinal center anti-nuclear antibody production in Lyn-deficient mice Altered B cell signalling in autoimmunity.B-cell activating factor-receptor specific activation of tumor necrosis factor receptor associated factor 6 and the phosphatidyl inositol 3-kinase pathway in lymphoma B cells Interferon regulatory factor-5 deficiency ameliorates disease severity in the MRL/lpr mouse model of lupus in the absence of a mutation in DOCK2.Lupus nephritis: lessons from murine models Modulation of in vitro murine B-lymphocyte response by curcumin Modulation of adaptive immunity with Toll-like receptors Immunoglobulin responses at the mucosal interface.CD4+ T cells and CD40 participate in selection and homeostasis of peripheral B cells.BAFF and innate immunity: new therapeutic targets for systemic lupus erythematosus.TLR tolerance reduces IFN-alpha production despite plasmacytoid dendritic cell expansion and anti-nuclear antibodies in NZB bicongenic mice.Systemic autoimmunity in BAFF-R-mutant A/WySnJ strain mice Marginal zone B cells: virtues of innate-like antibody-producing lymphocytes.B cell-intrinsic TLR7 signaling is essential for the development of spontaneous germinal centers.Interferon-α accelerates murine systemic lupus erythematosus in a T cell-dependent manner.

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P2860

BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

http://www.wikidata.org/entity/Q36229560

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2007年论文

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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BAFF and MyD88 signals promote a lupuslike disease independent of T cells.

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Carrie A Fletcher

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Mathew J Sweet

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Sally V Watt

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Shane T Grey

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Stacey N Walters

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P2860

BAFF, a novel ligand of the tumor necrosis factor family, stimulates B cell growth

IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines

Adjuvant-enhanced antibody responses in the absence of toll-like receptor signaling

DCs induce CD40-independent immunoglobulin class switching through BLyS and APRIL

A RING-type ubiquitin ligase family member required to repress follicular helper T cells and autoimmunity

T-bet regulates IgG class switching and pathogenic autoantibody production

B cell-activating factor belonging to the TNF family (BAFF)-R is the principal BAFF receptor facilitating BAFF costimulation of circulating T and B cells

Targeted disruption of the MyD88 gene results in loss of IL-1- and IL-18-mediated function

Role of anti-DNA antibodies in the pathogenesis of lupus nephritis.

B cell abnormalities in systemic lupus erythematosus

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Charles R. Mackay

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