Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP. - Wikidata - awgldk - TriplyDB

Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP.

Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP.

http://www.wikidata.org/entity/Q34070452

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Mg2+ regulates cytotoxic functions of NK and CD8 T cells in chronic EBV infection through NKG2D Responses to Microbial Challenges by SLAMF Receptors Severe infectious diseases of childhood as monogenic inborn errors of immunity Cytotoxic granule secretion by lymphocytes and its link to immune homeostasis Infectious Mononucleosis Immune regulation of human herpesviruses and its implications for human transplantation NK Cell Influence on the Outcome of Primary Epstein-Barr Virus Infection Infectious mononucleosis.Expansion of murine gammaherpesvirus latently infected B cells requires T follicular help.Signaling lymphocytic activation molecule (SLAM)/SLAM-associated protein pathway regulates human B-cell tolerance.Dominant-activating germline mutations in the gene encoding the PI(3)K catalytic subunit p110δ result in T cell senescence and human immunodeficiency XMEN disease: a new primary immunodeficiency affecting Mg2+ regulation of immunity against Epstein-Barr virus.Expansion of somatically reverted memory CD8+ T cells in patients with X-linked lymphoproliferative disease caused by selective pressure from Epstein-Barr virus.CRISPR-Mediated Slamf1Δ/Δ Slamf5Δ/Δ Slamf6Δ/Δ Triple Gene Disruption Reveals NKT Cell Defects but Not T Follicular Helper Cell Defects CRISPR-Mediated Triple Knockout of SLAMF1, SLAMF5 and SLAMF6 Supports Positive Signaling Roles in NKT Cell Development.Positive and negative signaling through SLAM receptors regulate synapse organization and thresholds of cytolysis.The receptor Ly108 functions as a SAP adaptor-dependent on-off switch for T cell help to B cells and NKT cell development.Recent advances in the diagnosis and treatment of hemophagocytic lymphohistiocytosis.Evolving role of 2B4/CD244 in T and NK cell responses during virus infection.The adaptor molecule SAP plays essential roles during invariant NKT cell cytotoxicity and lytic synapse formation.Interleukin-21 overexpression dominates T cell response to Epstein-Barr virus in a fatal case of X-linked lymphoproliferative syndrome type 1 Roles of CD48 in regulating immunity and tolerance.Stepwise phosphorylation of p65 promotes NF-κB activation and NK cell responses during target cell recognition.Intronic SH2D1A mutation with impaired SAP expression and agammaglobulinemia.Inherited human OX40 deficiency underlying classic Kaposi sarcoma of childhood.Simultaneous TCR and CD244 signals induce dynamic downmodulation of CD244 on human antiviral T cells.Innate immune responses against Epstein Barr virus infection Inherited CD70 deficiency in humans reveals a critical role for the CD70-CD27 pathway in immunity to Epstein-Barr virus infection.Combined immunodeficiency and Epstein-Barr virus-induced B cell malignancy in humans with inherited CD70 deficiency EAT-2, a SAP-like adaptor, controls NK cell activation through phospholipase Cγ, Ca++, and Erk, leading to granule polarization.Familial hemophagocytic lymphohistiocytosis: when rare diseases shed light on immune system functioning.T cell-B cell interactions in primary immunodeficiencies.Diagnostic evaluation of patients with suspected haemophagocytic lymphohistiocytosis.XLP: clinical features and molecular etiology due to mutations in SH2D1A encoding SAP.Human Genetic Determinants of Viral Diseases.Advances in the pathogenesis of primary and secondary haemophagocytic lymphohistiocytosis: differences and similarities.Human immunity against EBV-lessons from the clinic.Asymptomatic primary infection with Epstein-Barr virus: observations on young adult cases.Inhibitory 2B4 contributes to NK cell education and immunological derangements in XLP1 patients.2B4-SAP signaling is required for the priming of naive CD8+ T cells by antigen-expressing B cells and B lymphoma cells.

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Molecular pathogenesis of EBV susceptibility in XLP as revealed by analysis of female carriers with heterozygous expression of SAP.

http://www.wikidata.org/entity/Q34070452

description

2011 nî lūn-bûn

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2011 թուականի Նոյեմբերին հրատարակուած գիտական յօդուած

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2011 թվականի նոյեմբերին 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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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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JOURNAL.PBIO.1001187

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Molecular pathogenesis of EBV ...... eterozygous expression of SAP.

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Alan B Rickinson

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Alessandro Moretta

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Andrew D Hislop

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Anna Chan

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Carol Low

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Claire Booth

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D Sean Riminton

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Edwin Ho

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Elissa Deenick

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Frank Alvaro

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P2860

The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM

Activation of NK cell-mediated cytotoxicity by a SAP-independent receptor of the CD2 family

Molecular analysis of NTB-A signaling: a role for EAT-2 in NTB-A-mediated activation of human NK cells

Identification of a novel signal transduction surface molecule on human cytotoxic lymphocytes

Early expression of triggering receptors and regulatory role of 2B4 in human natural killer cell precursors undergoing in vitro differentiation.

Selective generation of functional somatically mutated IgM+CD27+, but not Ig isotype-switched, memory B cells in X-linked lymphoproliferative disease

Inactivating mutations in an SH2 domain-encoding gene in X-linked lymphoproliferative syndrome

NTB-A [correction of GNTB-A], a novel SH2D1A-associated surface molecule contributing to the inability of natural killer cells to kill Epstein-Barr virus-infected B cells in X-linked lymphoproliferative disease

X-linked lymphoproliferative disease. 2B4 molecules displaying inhibitory rather than activating function are responsible for the inability of natural killer cells to kill Epstein-Barr virus-infected cells

X-linked lymphoproliferative syndromes: brothers or distant cousins?

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