Helicobacter pylori eradication shifts monocyte Fcγ receptor balance toward inhibitory FcγRIIB in immune thrombocytopenic purpura patients

Atsuko Asahi, Tetsuya Nishimoto, Yuka Okazaki, Hidekazu Suzuki, Tatsuhiro Masaoka, Yutaka Kawakami, Yasuo Ikeda, Masataka Kuwana

研究成果: Article

87 引用 (Scopus)

抄録

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 Fcγ receptor IIB (FcγRIIB). 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 FcγR 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 FcγR balance toward the inhibitory FcγRIIB.

元の言語English
ページ(範囲)2939-2949
ページ数11
ジャーナルJournal of Clinical Investigation
118
発行部数8
DOI
出版物ステータスPublished - 2008 8 1

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Idiopathic Thrombocytopenic Purpura
Fc Receptors
Helicobacter pylori
Monocytes
Purpura
Blood Platelets
Helicobacter Infections
Platelet Count
Autoantibodies

ASJC Scopus subject areas

  • Medicine(all)

これを引用

Helicobacter pylori eradication shifts monocyte Fcγ receptor balance toward inhibitory FcγRIIB in immune thrombocytopenic purpura patients. / Asahi, Atsuko; Nishimoto, Tetsuya; Okazaki, Yuka; Suzuki, Hidekazu; Masaoka, Tatsuhiro; Kawakami, Yutaka; Ikeda, Yasuo; Kuwana, Masataka.

:: Journal of Clinical Investigation, 巻 118, 番号 8, 01.08.2008, p. 2939-2949.

研究成果: Article

Asahi, Atsuko ; Nishimoto, Tetsuya ; Okazaki, Yuka ; Suzuki, Hidekazu ; Masaoka, Tatsuhiro ; Kawakami, Yutaka ; Ikeda, Yasuo ; Kuwana, Masataka. / Helicobacter pylori eradication shifts monocyte Fcγ receptor balance toward inhibitory FcγRIIB in immune thrombocytopenic purpura patients. :: Journal of Clinical Investigation. 2008 ; 巻 118, 番号 8. pp. 2939-2949.
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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 Fcγ receptor IIB (FcγRIIB). 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 FcγR 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 FcγR balance toward the inhibitory FcγRIIB.",
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