American Society of Hematology

Stasi Figure 1 (pp 206–211).

$Stasi Figure 1 (pp 206–211). Potential mechanisms of Helicobacter pylori–induced thrombocytopenia. A) H pylori could induce antibody production in response to antigens, such as CagA, that crossreact against various platelet glycoprotein antigens. B) Platelets may be activated by binding of first-generation H pylori antibodies to platelet FcγRIIA or through an interaction between H pylori–bound von Willebrand factor (VWF) and platelet glycoprotein IB (gpIB). Activation may promote platelet clearance and antigen presentation, which augments production of antibacterial antibodies. C) In the presence of antiplatelet antibodies, the LPS of Gram-negative bacteria can significantly enhance Fc-dependent platelet phagocytosis. D) Epitope spreading and somatic mutation may lead to the development of second- and third-generation antibodies that either recognize bacterially derived factors or crossreact with platelet antigens. The production of these antibodies is no longer dependent upon the stimulation of bacterial antigens, thereby leading to the development of chronic thrombocytopenia refractory to eradication of H pylori infection. / Abbreviations: APC, antigen-presenting cell; P, platelet.$

Potential mechanisms ofHelicobacter pylori–induced thrombocytopenia. A) H pylori could induce antibody production in response to antigens, such as CagA, that crossreact against various platelet glycoprotein antigens. B) Platelets may be activated by binding of first-generation H pylori antibodies to platelet FcγRIIA or through an interaction between H pylori–bound von Willebrand factor (VWF) and platelet glycoprotein IB (gpIB). Activation may promote platelet clearance and antigen presentation, which augments production of antibacterial antibodies. C) In the presence of antiplatelet antibodies, the LPS of Gram-negative bacteria can significantly enhance Fc-dependent platelet phagocytosis. D) Epitope spreading and somatic mutation may lead to the development of second- and third-generation antibodies that either recognize bacterially derived factors or crossreact with platelet antigens. The production of these antibodies is no longer dependent upon the stimulation of bacterial antigens, thereby leading to the development of chronic thrombocytopenia refractory to eradication of H pylori infection.

Abbreviations: APC, antigen-presenting cell; P, platelet.

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