Basophil FcɛRI histamine release parallels expression of Src-homology 2–containing inositol phosphatases in chronic idiopathic urticaria

[1]  Suephy C. Chen,et al.  Basophil histamine release activity and disease severity in chronic idiopathic urticaria. , 2008, Annals of allergy, asthma & immunology : official publication of the American College of Allergy, Asthma, & Immunology.

[2]  S. Saini,et al.  Evidence of in vivo basophil activation in chronic idiopathic urticaria , 2006 .

[3]  Suephy C. Chen,et al.  Basophil Histamine Release (HR) Activity and Disease Severity in Chronic Idiopathic Urticaria (CIU) , 2006 .

[4]  Yijie Wang,et al.  The inositol phosphatase SHIP-2 down-regulates FcgammaR-mediated phagocytosis in murine macrophages independently of SHIP-1. , 2006, Blood.

[5]  K. Chichester,et al.  Regulation of Rat Basophilic Leukemia-2H3 Mast Cell Secretion by a Constitutive Lyn Kinase Interaction with the High Affinity IgE Receptor (FcεRI)1 , 2005, The Journal of Immunology.

[6]  A. Kaplan,et al.  Functional assessment of pathogenic IgG subclasses in chronic autoimmune urticaria. , 2005, The Journal of allergy and clinical immunology.

[7]  M. Manfredi,et al.  Chronic idiopathic urticaria: infiltrating cells and related cytokines in autologous serum-induced wheals. , 2005, Clinical immunology.

[8]  A. Kaplan Chronic urticaria: pathogenesis and treatment. , 2004, The Journal of allergy and clinical immunology.

[9]  G. Krystal,et al.  LPS-induced upregulation of SHIP is essential for endotoxin tolerance. , 2004, Immunity.

[10]  S. Saini,et al.  Relationship between Syk protein and degranulation in basophils from chronic urticaria donors , 2004 .

[11]  G. Krystal,et al.  SHIP, SHIP2, and PTEN activities are regulated in vivo by modulation of their protein levels: SHIP is up-regulated in macrophages and mast cells by lipopolysaccharide. , 2003, Experimental hematology.

[12]  C. Marsh,et al.  SHIP-2 Inositol Phosphatase Is Inducibly Expressed in Human Monocytes and Serves to Regulate Fcγ Receptor-mediated Signaling* , 2003, Journal of Biological Chemistry.

[13]  G. Mills,et al.  Targeting PI3K-AKT pathway for cancer therapy. , 2003, Reviews in clinical and experimental hematology.

[14]  G. Krystal,et al.  Activin/TGF-β induce apoptosis through Smad-dependent expression of the lipid phosphatase SHIP , 2002, Nature Cell Biology.

[15]  E. Fiebiger,et al.  Classification of anti-FcepsilonRI and anti-IgE autoantibodies in chronic idiopathic urticaria and correlation with disease severity. , 2002, The Journal of allergy and clinical immunology.

[16]  G. Krystal,et al.  Of mice and men: elucidating the role of SH2-containing inositol 5-phosphatase (SHIP) in human disease. , 2002, Clinical and investigative medicine. Medecine clinique et experimentale.

[17]  A. Kay,et al.  TH1/TH2 cytokines and inflammatory cells in skin biopsy specimens from patients with chronic idiopathic urticaria: comparison with the allergen-induced late-phase cutaneous reaction. , 2002, The Journal of allergy and clinical immunology.

[18]  D. MacGlashan,et al.  Localizing a Control Region in the Pathway to Leukotriene C4 Secretion Following Stimulation of Human Basophils with Anti-IgE Antibody1 , 2001, The Journal of Immunology.

[19]  J. Langdon,et al.  Src homology 2 domain-containing inositol 5' phosphatase is negatively associated with histamine release to human recombinant histamine-releasing factor in human basophils. , 2001, The Journal of allergy and clinical immunology.

[20]  C. Grattan Basophils in chronic urticaria. , 2001, The journal of investigative dermatology. Symposium proceedings.

[21]  A. Kaplan,et al.  Mechanisms of autoimmune activation of basophils in chronic urticaria. , 2001, The Journal of allergy and clinical immunology.

[22]  C. Wofsy,et al.  Expression and modulation of Fc?RIa and Fc?RI in human blood basophils , 2001 .

[23]  D. MacGlashan,et al.  The tyrosine kinases p53/56lyn and p72syk are differentially expressed at the protein level but not at the messenger RNA level in nonreleasing human basophils. , 2000, American journal of respiratory cell and molecular biology.

[24]  D. Lucas,et al.  Structure, function, and biology of SHIP proteins. , 2000, Genes & development.

[25]  J. Oliver,et al.  Syk deficiency in nonreleaser basophils. , 1999, The Journal of allergy and clinical immunology.

[26]  B. Goldstein,et al.  One lyn molecule is sufficient to initiate phosphorylation of aggregated high-affinity IgE receptors. , 1999, Proceedings of the National Academy of Sciences of the United States of America.

[27]  M. Black,et al.  Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: comparison of patients with and without anti-FcepsilonRI or anti-IgE autoantibodies. , 1999, The Journal of allergy and clinical immunology.

[28]  A. Black,et al.  Anti-FcϵRI autoantibodies and basophil histamine releasability in chronic idiopathic urticaria☆☆☆★★★♢ , 1998 .

[29]  M. Huber,et al.  The src homology 2-containing inositol phosphatase (SHIP) is the gatekeeper of mast cell degranulation. , 1998, Proceedings of the National Academy of Sciences of the United States of America.

[30]  J. Kinet,et al.  Comparative studies of functional and binding assays for IgG anti-FcϵRIα (α-subunit) in chronic urticaria ☆ ☆☆ ★ ★★ , 1998 .

[31]  C. Grattan,et al.  Flow cytometric analysis of basophil numbers in chronic urticaria: basopenia is related to serum histamine releasing activity , 1997, Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology.

[32]  A. Togias,et al.  Down-regulation of Fc(epsilon)RI expression on human basophils during in vivo treatment of atopic patients with anti-IgE antibody. , 1997, Journal of immunology.

[33]  T. Rafnar,et al.  Molecular identification of an IgE-dependent histamine-releasing factor. , 1995, Science.

[34]  J. Kochan,et al.  Autoantibodies against the high-affinity IgE receptor as a cause of histamine release in chronic urticaria. , 1993, The New England journal of medicine.

[35]  D. MacGlashan Releasability of human basophils: cellular sensitivity and maximal histamine release are independent variables. , 1993, The Journal of allergy and clinical immunology.

[36]  A. Kaplan,et al.  Prevalence and functional role of anti-IgE autoantibodies in urticarial syndromes. , 1988, The Journal of investigative dermatology.

[37]  L. Lichtenstein,et al.  Defective histamine release in chronic urticaria. , 1976, The Journal of clinical investigation.

[38]  H. Gilbert,et al.  Basophil counting with a new staining method using alcian blue. , 1975, Blood.

[39]  R. Siraganian Refinements in the automated fluorometric histamine analysis system. , 1975, Journal of immunological methods.

[40]  A. Kaplan,et al.  A role for C5a in augmenting IgG-dependent histamine release from basophils in chronic urticaria. , 2002, The Journal of allergy and clinical immunology.

[41]  S. Miescher,et al.  Natural anti-FcεRIα autoantibodies isolated from healthy donors and chronic idiopathic urticaria patients reveal a restricted repertoire and autoreactivity on human basophils , 2001 .

[42]  E. Fiebiger,et al.  Anti-FcepsilonRIalpha autoantibodies in autoimmune-mediated disorders. Identification of a structure-function relationship. , 1998, The Journal of clinical investigation.