Wiskott-Aldrich syndrome protein deficiency in B cells results in impaired peripheral homeostasis. - Wikidata - wikimedia - TriplyDB

Wiskott-Aldrich syndrome protein deficiency in B cells results in impaired peripheral homeostasis.

Wiskott-Aldrich syndrome protein deficiency in B cells results in impaired peripheral homeostasis.

http://www.wikidata.org/entity/Q36969829

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Actin cytoskeletal defects in immunodeficiency WIP regulates persistence of cell migration and ruffle formation in both mesenchymal and amoeboid modes of motility DOCK8 is essential for T-cell survival and the maintenance of CD8+ T-cell memory Wiskott-Aldrich syndrome protein (WASP) and N-WASP are critical for peripheral B-cell development and function A balance of Bruton's tyrosine kinase and SHIP activation regulates B cell receptor cluster formation by controlling actin remodeling.The tumor promoter and NF-κB modulator Bcl-3 regulates splenic B cell development.Hematopoietic cell transplantation for Wiskott-Aldrich syndrome: advances in biology and future directions for treatment.Long-term outcome and lineage-specific chimerism in 194 patients with Wiskott-Aldrich syndrome treated by hematopoietic cell transplantation in the period 1980-2009: an international collaborative study Foamy virus vector-mediated gene correction of a mouse model of Wiskott-Aldrich syndrome.Wiskott-Aldrich syndrome protein is required for homeostasis and function of invariant NKT cells.How B cells capture, process and present antigens: a crucial role for cell polarity.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.Defective inhibition of B-cell proliferation by Wiskott-Aldrich syndrome protein-deficient regulatory T cells WASp-deficient B cells play a critical, cell-intrinsic role in triggering autoimmunity.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.Dendritic cell functional improvement in a preclinical model of lentiviral-mediated gene therapy for Wiskott-Aldrich syndrome Autoimmunity in wiskott-Aldrich syndrome: an unsolved enigma.B-cell intrinsic TLR7 signals promote depletion of the marginal zone in a murine model of Wiskott-Aldrich syndrome.Wiskott-Aldrich syndrome protein-mediated actin dynamics control type-I interferon production in plasmacytoid dendritic cells.Wiskott-Aldrich Syndrome at the nexus of autoimmune and primary immunodeficiency diseases.Reduced type I interferon production by dendritic cells and weakened antiviral immunity in patients with Wiskott-Aldrich syndrome protein deficiency Wiskott-Aldrich Syndrome: Immunodeficiency resulting from defective cell migration and impaired immunostimulatory activation Signal Integration during T Lymphocyte Activation and Function: Lessons from the Wiskott-Aldrich Syndrome.B cell subsets are modulated during allergic airway inflammation but are not required for the development of respiratory tolerance in a murine model.A Chemoattractant-Guided Walk Through Lymphopoiesis: From Hematopoietic Stem Cells to Mature B Lymphocytes.Cytoskeletal control of B cell responses to antigens.Validation of a mutated PRE sequence allowing high and sustained transgene expression while abrogating WHV-X protein synthesis: application to the gene therapy of WAS.Spontaneous germinal centers and autoimmunity.The early activation of memory B cells from Wiskott-Aldrich syndrome patients is suppressed by CD19 downregulation.Gene therapy for Wiskott-Aldrich syndrome in a severely affected adult.Autonomous role of Wiskott-Aldrich Syndrome platelet deficiency in inducing autoimmunity and inflammation.Distinct Roles for Bruton's Tyrosine Kinase in B Cell Immune Synapse Formation

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P2860

Wiskott-Aldrich syndrome protein deficiency in B cells results in impaired peripheral homeostasis.

http://www.wikidata.org/entity/Q36969829

description

2008 nî lūn-bûn

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2008年の論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年論文

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2008年论文

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2008年论文

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2008年论文

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name

Wiskott-Aldrich syndrome prote ...... paired peripheral homeostasis.

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type

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Wiskott-Aldrich syndrome prote ...... paired peripheral homeostasis.

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Wiskott-Aldrich syndrome prote ...... paired peripheral homeostasis.

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Wiskott-Aldrich syndrome prote ...... paired peripheral homeostasis.

@en

P2093

Almut Meyer-Bahlburg

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David J Rawlings

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Facundo D Batista

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Shirly Becker-Herman

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Socheath Khim

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Stephanie Humblet-Baron

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P2860

Human immunoglobulin M memory B cells controlling Streptococcus pneumoniae infections are generated in the spleen

Impaired integrin-dependent function in Wiskott-Aldrich syndrome protein-deficient murine and human neutrophils.

B-1a and B-1b cells exhibit distinct developmental requirements and have unique functional roles in innate and adaptive immunity to S. pneumoniae

Absence of marginal zone B cells in Pyk-2-deficient mice defines their role in the humoral response

Spontaneous apoptosis in lymphocytes from patients with Wiskott-Aldrich syndrome: correlation of accelerated cell death and attenuated bcl-2 expression.

Actin cytoskeletal function is spared, but apoptosis is increased, in WAS patient hematopoietic cells.

WASP deficiency leads to global defects of directed leukocyte migration in vitro and in vivo.

A multiinstitutional survey of the Wiskott-Aldrich syndrome.

T cells of patients with the Wiskott-Aldrich syndrome have a restricted defect in proliferative responses.

Defective actin polymerization in EBV-transformed B-cell lines from patients with the Wiskott-Aldrich syndrome.

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4158-4169

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10.1182/BLOOD-2008-02-140814

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10

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112

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Adrian J Thrasher

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2008-08-07T00:00:00Z

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23156784

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18687984

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2582000

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