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In autoimmune disease, Fc receptors (FcRs) form the interface between immune effector cells and their antibody-coated targets, and as such are attractive targets for immunomodulatory therapy. In this issue of the JCI, two highly novel studies of Fc-FcR interactions provide new insights into the role of FcRs in immune thrombocytopenia. Asahi et al. utilized a comprehensive platform of immunological assays to examine the mechanism underlying Helicobacter pylori-associated immune thrombocytopenic purpura, and Ghevaert et al. describe a specially designed antibody that saturates binding sites on fetal platelets without initiating FcgammaR-mediated platelet phagocytosis, preventing the binding of pathological maternal anti-HLA antibodies that cause fetomaternal alloimmune thrombocytopenia (see the related articles beginning on pages 2939 and 2929, respectively). These reports illustrate how a remarkably detailed molecular understanding of the FcR network may translate into new therapeutic strategies with high clinical impact.

Original publication

DOI

10.1172/JCI36451

Type

Journal article

Journal

J Clin Invest

Publication Date

08/2008

Volume

118

Pages

2677 - 2681

Keywords

Female, Humans, Infant, Newborn, Models, Immunological, Pregnancy, Purpura, Thrombocytopenic, Idiopathic, Receptors, Fc, Thrombocytopenia, Neonatal Alloimmune