Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
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Characterization of SH2D1A missense mutations identified in X-linked lymphoproliferative disease patientsThe X-linked lymphoproliferative disease gene product SAP associates with PAK-interacting exchange factor and participates in T cell activationResponses to Microbial Challenges by SLAMF ReceptorsFine specificity and molecular competition in SLAM family receptor signallingDual functional roles for the X-linked lymphoproliferative syndrome gene product SAP/SH2D1A in signaling through the signaling lymphocyte activation molecule (SLAM) family of immune receptorsA spectrum of mutations in SH2D1A that causes X-linked lymphoproliferative disease and other Epstein-Barr virus-associated illnessesAssociation of the X-linked lymphoproliferative disease gene product SAP/SH2D1A with 2B4, a natural killer cell-activating molecule, is dependent on phosphoinositide 3-kinaseEssential function for SAP family adaptors in the surveillance of hematopoietic cells by natural killer cellsHigh expression of CD244 and SAP regulated CD8 T cell responses of patients with HTLV-I associated neurologic diseaseOn guard--activating NK cell receptors.TGF-β1 down-regulation of NKG2D/DAP10 and 2B4/SAP expression on human NK cells contributes to HBV persistenceAn Epstein-Barr virus encoded inhibitor of Colony Stimulating Factor-1 signaling is an important determinant for acute and persistent EBV infection.X-linked lymphoproliferative disease: genetic lesions and clinical consequences.X-linked lymphoproliferative disease: clinical, diagnostic and molecular perspective.Molecular and immunological basis of X-linked lymphoproliferative disease.Exploiting the interplay between innate and adaptive immunity to improve immunotherapeutic strategies for Epstein-Barr-virus-driven disordersSLAM Family Receptors Regulate Immunity with and without SAP-related AdaptorsMolecular and cellular pathogenesis of X-linked lymphoproliferative disease.Altered lymphocyte responses and cytokine production in mice deficient in the X-linked lymphoproliferative disease gene SH2D1A/DSHP/SAPNatural killer cell inhibitory receptors block actin cytoskeleton-dependent recruitment of 2B4 (CD244) to lipid rafts.2B4 acts as a non-major histocompatibility complex binding inhibitory receptor on mouse natural killer cells.Immune regulation by SLAM family receptors and SAP-related adaptors.NK cell regulation by SLAM family receptors and SAP-related adapters.Dissecting natural killer cell activation pathways through analysis of genetic mutations in human and mouse.Antiviral NK cell responses in HIV infection: I. NK cell receptor genes as determinants of HIV resistance and progression to AIDS.X-linked lymphoproliferative disease (XLP): a model of impaired anti-viral, anti-tumor and humoral immune responses.Signal transduction during activation and inhibition of natural killer cells.Human natural killer receptors, co-receptors, and their ligands.X-linked lymphoproliferative syndrome: a genetic condition typified by the triad of infection, immunodeficiency and lymphoma.Familial hemophagocytic lymphohistiocytosis: a model for understanding the human machinery of cellular cytotoxicity.Mice deficient in the X-linked lymphoproliferative disease gene sap exhibit increased susceptibility to murine gammaherpesvirus-68 and hypo-gammaglobulinemia.Protein kinase C is involved in 2B4 (CD244)-mediated cytotoxicity and AP-1 activation in natural killer cells.SH2D1A expression in Burkitt lymphoma cells is restricted to EBV positive group I lines and is downregulated in parallel with immunoblastic transformation.Clinical evidence implicating gamma-delta T cells in EBV control following cord blood transplantation.
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Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
description
im Oktober 2000 veröffentlichter wissenschaftlicher Artikel
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wetenschappelijk artikel
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наукова стаття, опублікована в жовтні 2000
@uk
name
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
@en
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
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type
label
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
@en
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
@nl
prefLabel
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
@en
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
@nl
P2093
P1476
Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease
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P2093
P304
P356
10.4049/JIMMUNOL.165.7.3549
P407
P50
P577
2000-10-01T00:00:00Z