title: Helicobacter pylori eradication shifts monocyte Fcgamma receptor balance toward inhibitory FcgammaRIIB in immune thrombocytopenic purpura patients.
abstract: Immune thrombocytopenia purpura (ITP) is a bleeding disorder in which platelet-specific autoantibodies cause a loss of platelets. In a subset of patients with ITP and infected with Helicobacter pylori, the number of platelets recovers after eradication of H. pylori. To examine the role of H. pylori infection in the pathogenesis of ITP, the response of 34 ITP patients to treatment with a standard H. pylori eradication regimen, irrespective of whether they were infected with H. pylori, was evaluated. Eradication of H. pylori was achieved in all H. pylori-positive patients, and a significant increase in platelets was observed in 61% of these patients. By contrast, none of the H. pylori-negative patients showed increased platelets. At baseline, monocytes from the H. pylori-positive patients exhibited an enhanced phagocytic capacity and low levels of the inhibitory Fcgamma receptor IIB (FcgammaRIIB). One week after starting the H. pylori eradication regimen, this activated monocyte phenotype was suppressed and improvements in autoimmune and platelet kinetic parameters followed. Modulation of monocyte FcgammaR balance was also found in association with H. pylori infection in individuals who did not have ITP and in mice. Our findings strongly suggest that the recovery in platelet numbers observed in ITP patients after H. pylori eradication is mediated through a change in FcgammaR balance toward the inhibitory FcgammaRIIB.
authors.affiliation: Division of Rheumatology, Department of Internal Medicine, and Institute for Advanced Medical Research, Keio University School of Medicine, Tokyo, Japan.
authors.forename: Atsuko
authors.initials: A
authors.lastname: Asahi
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Nishimoto
authors.forename: Yuka
authors.initials: Y
authors.lastname: Okazaki
authors.forename: Hidekazu
authors.initials: H
authors.lastname: Suzuki
authors.forename: Tatsuhiro
authors.initials: T
authors.lastname: Masaoka
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kawakami
authors.forename: Yasuo
authors.initials: Y
authors.lastname: Ikeda
authors.forename: Masataka
authors.initials: M
authors.lastname: Kuwana
mesh_terms: D000368:Aged; D001792:Blood Platelets / Q000276:immunology; D001944:Breath Tests; D015331:Cohort Studies; D003613:Danazol / Q000627:therapeutic use; D005260:Female; D005938:Glucocorticoids / Q000627:therapeutic use; D016481:Helicobacter Infections / Q000188:drug therapy; D016480:Helicobacter pylori; D006801:Humans; D007700:Kinetics; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D010976:Platelet Count; D011239:Prednisolone / Q000627:therapeutic use; D011446:Prospective Studies; D016553:Purpura, Thrombocytopenic, Idiopathic / Q000276:immunology*; D017452:Receptors, IgG / Q000037:antagonists & inhibitors / Q000235:genetics / Q000276:immunology*; D014508:Urea / Q000032:analysis
chemical_list: C499173:FCGR2B protein, human; D005938:Glucocorticoids; D017452:Receptors, IgG; D014508:Urea; D011239:Prednisolone; D003613:Danazol