Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production. - Wikidata - wikimedia - TriplyDB

Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production.

Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production.

http://www.wikidata.org/entity/Q36219326

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DOCK8 deficiency impairs CD8 T cell survival and function in humans and mice DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation Dynamics of the actin cytoskeleton mediates receptor cross talk: An emerging concept in tuning receptor signaling Human Immunodeficiencies Related to Defective APC/T Cell Interaction S1PR2 links germinal center confinement and growth regulation The multiple faces of leukocyte interstitial migration Dissecting immunity by germline mutagenesis Actin cytoskeletal defects in immunodeficiency Molecular mechanisms and functional implications of polarized actin remodeling at the T cell immunological synapse DOCK8 is a Cdc42 activator critical for interstitial dendritic cell migration during immune responses.The Hyper-IgE Syndromes: Lessons in Nature, From Bench to Bedside DOCK8 is essential for T-cell survival and the maintenance of CD8+ T-cell memory ATP11C is critical for the internalization of phosphatidylserine and differentiation of B lymphocytes DOCK8 regulates lymphocyte shape integrity for skin antiviral immunity Cdc42 is a key regulator of B cell differentiation and is required for antiviral humoral immunity.A DOCK8-WIP-WASp complex links T cell receptors to the actin cytoskeleton.The transcription factor EPAS1 links DOCK8 deficiency to atopic skin inflammation via IL-31 induction LRCH1 interferes with DOCK8-Cdc42-induced T cell migration and ameliorates experimental autoimmune encephalomyelitis.DOCK8 regulates signal transduction events to control immunity IL-21 acts directly on B cells to regulate Bcl-6 expression and germinal center responses.ASCT2 (SLC1A5)-Deficient Mice Have Normal B-Cell Development, Proliferation, and Antibody Production.Recurrent and Sustained Viral Infections in Primary Immunodeficiencies.Redemption of autoantibodies on anergic B cells by variable-region glycosylation and mutation away from self-reactivity.Somatic reversion in dedicator of cytokinesis 8 immunodeficiency modulates disease phenotype.DOCK8 regulates protective immunity by controlling the function and survival of RORγt+ ILCs Dedicator of cytokinesis 8 (DOCK8) deficiency The emerging role of guanine nucleotide exchange factors in ALS and other neurodegenerative diseases.How B cells capture, process and present antigens: a crucial role for cell polarity.Deficient T Cell Receptor Excision Circles (TRECs) in autosomal recessive hyper IgE syndrome caused by DOCK8 mutation: implications for pathogenesis and potential detection by newborn screening.Growth-factor receptor-bound protein-2 (Grb2) signaling in B cells controls lymphoid follicle organization and germinal center reaction.Coincidental loss of DOCK8 function in NLRP10-deficient and C3H/HeJ mice results in defective dendritic cell migration.Zinc finger protein Zfp335 is required for the formation of the naïve T cell compartment.Dynamics of B cells in germinal centres.Silencing of RhoA nucleotide exchange factor, ARHGEF3, reveals its unexpected role in iron uptake.Sequential class switching is required for the generation of high affinity IgE antibodies.Hyperimmunoglobulin E syndromes in pediatrics.Delayed control of herpes simplex virus infection and impaired CD4(+) T-cell migration to the skin in mouse models of DOCK8 deficiency The extended clinical phenotype of 64 patients with dedicator of cytokinesis 8 deficiency.Maintaining intestinal health: the genetics and immunology of very early onset inflammatory bowel disease.Comparison of predicted and actual consequences of missense mutations.

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P2860

Dock8 mutations cripple B cell immunological synapses, germinal centers and long-lived antibody production.

http://www.wikidata.org/entity/Q36219326

description

2009 nî lūn-bûn

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2009年の論文

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2009年論文

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2009年論文

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2009年论文

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2009年论文

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2009年论文

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Dock8 mutations cripple B cell ...... ong-lived antibody production.

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Nature Immunology

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Dock8 mutations cripple B cell ...... long-lived antibody production

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Andy L Johnson

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Bebhinn Treanor

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Belinda Whittle

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Carola G Vinuesa

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Duncan Alston

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Edyta Kucharska

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Facundo D Batista

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Heather Domaschenz

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Jason G Cyster

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Katrina L Randall

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P2860

Combined immunodeficiency associated with DOCK8 mutations

GEF what? Dock180 and related proteins help Rac to polarize cells in new ways

X-ray snapshots of the maturation of an antibody response to a protein antigen

Activation of Rho GTPases by DOCK exchange factors is mediated by a nucleotide sensor

Structure of an antibody-antigen complex: crystal structure of the HyHEL-10 Fab-lysozyme complex

A crucial role for the p110delta subunit of phosphatidylinositol 3-kinase in B cell development and activation

Balanced responsiveness to chemoattractants from adjacent zones determines B-cell position

Homozygous loss of ICOS is associated with adult-onset common variable immunodeficiency

Impaired B and T cell antigen receptor signaling in p110delta PI 3-kinase mutant mice

An antibody-deficiency syndrome due to mutations in the CD19 gene

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1283-1291

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10.1038/NI.1820

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12

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10

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Elissa K. Deenick

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Christopher C. Goodnow

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2009-11-08T00:00:00Z

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38075387

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19898472

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3437189

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