Analysis of SH2D1A mutations in patients with severe Epstein-Barr virus infections, Burkitt's lymphoma, and Hodgkin's lymphoma

[1]  O. Haas,et al.  Differential methylation pattern of the X-linked lymphoproliferative (XLP) disease gene SH2D1A correlates with the cell lineage-specific transcription , 2003, Immunogenetics.

[2]  O. Silander,et al.  Alterations of the X-linked lymphoproliferative disease gene SH2D1A in common variable immunodeficiency syndrome. , 2001, Blood.

[3]  J. Jung,et al.  Abnormal T Cell Receptor Signal Transduction of CD4 Th Cells in X-Linked Lymphoproliferative Syndrome1 , 2001, The Journal of Immunology.

[4]  H. Kanegane,et al.  SH2D1A mutations in Japanese males with severe Epstein-Barr virus--associated illnesses. , 2001, Blood.

[5]  B. van der Holt,et al.  Epstein-Barr virus (EBV) reactivation is a frequent event after allogeneic stem cell transplantation (SCT) and quantitatively predicts EBV-lymphoproliferative disease following T-cell--depleted SCT. , 2001, Blood.

[6]  L. Notarangelo,et al.  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. , 2001, The Journal of experimental medicine.

[7]  H. Kanegane,et al.  Clinical and virologic characteristics of chronic active Epstein-Barr virus infection. , 2001, Blood.

[8]  P. Engel,et al.  Cell surface receptors Ly-9 and CD84 recruit the X-linked lymphoproliferative disease gene product SAP. , 2001, Blood.

[9]  A. Sher,et al.  Altered lymphocyte responses and cytokine production in mice deficient in the X-linked lymphoproliferative disease gene SH2D1A/DSHP/SAP , 2001, Proceedings of the National Academy of Sciences of the United States of America.

[10]  P. Borrow,et al.  SAP controls T cell responses to virus and terminal differentiation of TH2 cells , 2001, Nature Immunology.

[11]  R. Clementi,et al.  Hemophagocytic lymphohistiocytosis due to germline mutations in SH2D1A, the X-linked lymphoproliferative disease gene. , 2001, Blood.

[12]  J. Schatzle,et al.  Potential pathways for regulation of NK and T cell responses: differential X-linked lymphoproliferative syndrome gene product SAP interactions with SLAM and 2B4. , 2000, International immunology.

[13]  M. Colonna,et al.  Patients with X‐linked lymphoproliferative disease have a defect in 2B4 receptor‐mediated NK cell cytotoxicity , 2000, European journal of immunology.

[14]  G. Klein,et al.  Correlation of mutations of the SH2D1A gene and epstein-barr virus infection with clinical phenotype and outcome in X-linked lymphoproliferative disease. , 2000, Blood.

[15]  L. Szekely,et al.  SH2D1A and slam protein expression in human lymphocytes and derived cell lines , 2000 .

[16]  P. Murray,et al.  Hodgkin's disease and the Epstein-Barr virus , 2000, Molecular pathology : MP.

[17]  H. Pabst,et al.  Cutting Edge: Defective NK Cell Activation in X-Linked Lymphoproliferative Disease1 , 2000, The Journal of Immunology.

[18]  L. Notarangelo,et al.  X-Linked Lymphoproliferative Disease , 2000, The Journal of experimental medicine.

[19]  S. Tangye,et al.  2B4-mediated activation of human natural killer cells. , 2000, Molecular immunology.

[20]  K. Nichols,et al.  Diagnosis of X‐linked lymphoproliferative disease by analysis of SLAM‐associated protein expression , 2000, European journal of immunology.

[21]  Meindl,et al.  Recurrent B‐cell non‐Hodgkin's lymphoma in two brothers with X‐linked lymphoproliferative disease without evidence for Epstein–Barr virus infection , 2000, British journal of haematology.

[22]  W. Friedrich,et al.  Epstein-Barr virus-negative boys with non-Hodgkin lymphoma are mutated in the SH2D1A gene, as are patients with X-linked lymphoproliferative disease (XLP). , 1999, Human molecular genetics.

[23]  D. Hayoz,et al.  SH2D1A mutation analysis for diagnosis of XLP in typical and atypical patients , 1999, Human Genetics.

[24]  S. Tangye,et al.  Cutting edge: human 2B4, an activating NK cell receptor, recruits the protein tyrosine phosphatase SHP-2 and the adaptor signaling protein SAP. , 1999, Journal of immunology.

[25]  L. M. Shlapatska,et al.  CDw150 associates with src-homology 2-containing inositol phosphatase and modulates CD95-mediated apoptosis. , 1999, Journal of immunology.

[26]  G. Konjević,et al.  The difference in NK‐cell activity between patients with non‐Hodgkin's lymphomas and Hodgkin's disease , 1999, British journal of haematology.

[27]  D. Allen,et al.  The X-linked lymphoproliferative-disease gene product SAP regulates signals induced through the co-receptor SLAM , 1998, Nature.

[28]  Jack R. Davis,et al.  Host response to EBV infection in X-linked lymphoproliferative disease results from mutations in an SH2-domain encoding gene , 1998, Nature Genetics.

[29]  M. Cazzola,et al.  X-linked Wiskott-Aldrich syndrome in a girl. , 1998, The New England journal of medicine.

[30]  O. Parolini,et al.  High prevalence of nonsense, frame shift, and splice-site mutations in 16 patients with full-blown Wiskott-Aldrich syndrome. , 1995, Blood.

[31]  Jack R. Davis,et al.  X-Linked Lymphoproliferative Disease: Twenty-Five Years after the Discovery , 1995, Pediatric Research.

[32]  A. Carbone,et al.  Local suppression of Epstein-Barr virus (EBV)-specific cytotoxicity in biopsies of EBV-positive Hodgkin's disease. , 1995, Blood.

[33]  A Gloghini,et al.  Identification and characterization of an Epstein-Barr virus-specific T-cell response in the pathologic tissue of a patient with Hodgkin's disease. , 1995, Cancer research.

[34]  M. Pauza,et al.  Immunoglobulin class and subclass deficiencies prior to Epstein-Barr virus infection in males with X-linked lymphoproliferative disease. , 1991, American journal of medical genetics.

[35]  U. Nater,et al.  Epstein-Barr virus. , 1991, The Journal of family practice.

[36]  D. Weisenburger,et al.  Fatal infectious mononucleosis and virus-associated hemophagocytic syndrome. , 1987, Archives of pathology & laboratory medicine.

[37]  P. Engel,et al.  X-linked lymphoproliferative disease: a progressive immunodeficiency. , 2001, Annual review of immunology.

[38]  M. Colonna,et al.  2B4: an NK cell activating receptor with unique specificity and signal transduction mechanism. , 2000, Human immunology.

[39]  D. Purtilo,et al.  X-linked lymphoproliferative syndrome provides clues to the pathogenesis of Epstein-Barr virus-induced lymphomagenesis. , 1987, Princess Takamatsu symposia.