WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity. - Wikidata - wikimedia - TriplyDB

WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

http://www.wikidata.org/entity/Q35237494

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Anergic B Cells: Precarious On-Call Warriors at the Nexus of Autoimmunity and False-Flagged Pathogens WIP remodeling actin behind the scenes: how WIP reshapes immune and other functions B cells take the front seat: dysregulated B cell signals orchestrate loss of tolerance and autoantibody production Actin cytoskeletal defects in immunodeficiency WIP regulates persistence of cell migration and ruffle formation in both mesenchymal and amoeboid modes of motility Wiskott-Aldrich syndrome protein (WASP) and N-WASP are critical for peripheral B-cell development and function Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity.Toll-like receptor ligands sensitize B-cell receptor signalling by reducing actin-dependent spatial confinement of the receptor.Germinal center B cells recognize antigen through a specialized immune synapse architecture.In Vivo Chronic Stimulation Unveils Autoreactive Potential of Wiskott-Aldrich Syndrome Protein-Deficient B Cells.Development of IgA nephropathy-like glomerulonephritis associated with Wiskott-Aldrich syndrome protein deficiency.Wiskott-Aldrich syndrome: a comprehensive review.Comparison of insulators and promoters for expression of the Wiskott-Aldrich syndrome protein using lentiviral vectors.Current and emerging treatment options for Wiskott-Aldrich syndrome.N-WASP is required for B-cell-mediated autoimmunity in Wiskott-Aldrich syndrome.Actin-binding protein 1 links B-cell antigen receptors to negative signaling pathways Altered B cell signalling in autoimmunity.Nuclear role of WASp in gene transcription is uncoupled from its ARP2/3-dependent cytoplasmic role in actin polymerization.CD4+ T cells and CD40 participate in selection and homeostasis of peripheral B cells.Exacerbated experimental arthritis in Wiskott-Aldrich syndrome protein deficiency: modulatory role of regulatory B cells N-wasp is essential for the negative regulation of B cell receptor signaling.The Rho GTPase Cdc42 Is Essential for the Activation and Function of Mature B Cells.B cell-intrinsic deficiency of the Wiskott-Aldrich syndrome protein (WASp) causes severe abnormalities of the peripheral B-cell compartment in mice.Ubiquitous high-level gene expression in hematopoietic lineages provides effective lentiviral gene therapy of murine Wiskott-Aldrich syndrome.Maintaining intestinal health: the genetics and immunology of very early onset inflammatory bowel disease.Altered BCR and TLR signals promote enhanced positive selection of autoreactive transitional B cells in Wiskott-Aldrich syndrome.Autoimmunity in wiskott-Aldrich syndrome: an unsolved enigma.Lentiviral-mediated gene therapy restores B cell tolerance in Wiskott-Aldrich syndrome patients.Actin engine in immunological synapse B-cell intrinsic TLR7 signals promote depletion of the marginal zone in a murine model of Wiskott-Aldrich syndrome.BCR and co-receptor crosstalk facilitate the positive selection of self-reactive transitional B cells.Wiskott-Aldrich syndrome protein-mediated actin dynamics control type-I interferon production in plasmacytoid dendritic cells.A disease-associated PTPN22 variant promotes systemic autoimmunity in murine models.B cell IFN-γ receptor signaling promotes autoimmune germinal centers via cell-intrinsic induction of BCL-6.Deletion of Wiskott-Aldrich syndrome protein triggers Rac2 activity and increased cross-presentation by dendritic cells.Molecular and phenotypic abnormalities of B lymphocytes in patients with Wiskott-Aldrich syndrome.TLR signaling in B-cell development and activation.Using the emerging Collaborative Cross to probe the immune system.Integration of B cell responses through Toll-like receptors and antigen receptors.Primary antibody deficiencies.

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

http://www.wikidata.org/entity/Q35237494

description

2011 nî lūn-bûn

@nan

2011 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2011 թվականի օգոստոսին հրատարակված գիտական հոդված

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2011年の論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年論文

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2011年论文

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name

WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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type

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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prefLabel

WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

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Journal of Experimental Medicine

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WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.

@en

P2093

Almut Meyer-Bahlburg

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

Blythe D Sather

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

Chaohong Liu

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Charles E Alpers

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David J Rawlings

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Denny Liggitt

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Gregg J Silverman

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Kelly L Hudkins

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Marc A Schwartz

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Shaun W Jackson

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P2860

The transmembrane activator TACI triggers immunoglobulin class switching by activating B cells through the adaptor MyD88

WIP deficiency reveals a differential role for WIP and the actin cytoskeleton in T and B cell activation

Polygenic autoimmune traits: Lyn, CD22, and SHP-1 are limiting elements of a biochemical pathway regulating BCR signaling and selection

Autoimmunity in Wiskott-Aldrich syndrome: risk factors, clinical features, and outcome in a single-center cohort of 55 patients.

Clinical course of patients with WASP gene mutations.

A multiinstitutional survey of the Wiskott-Aldrich syndrome.

Btk regulates B cell receptor-mediated antigen processing and presentation by controlling actin cytoskeleton dynamics in B cells.

Systemic autoimmunity and defective Fas ligand secretion in the absence of the Wiskott-Aldrich syndrome protein

Development of self-reactive germinal center B cells and plasma cells in autoimmune Fc gammaRIIB-deficient mice.

WASp in immune-system organization and function.

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2033-2042

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10.1084/JEM.20110200

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10

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208

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2011-08-29T00:00:00Z

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51603890

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21875954

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3182055

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