Fc receptors in immune thrombocytopenias: a target for immunomodulation? uri icon

Overview

abstract

  • 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.

publication date

  • August 1, 2008

Research

keywords

  • Purpura, Thrombocytopenic, Idiopathic
  • Receptors, Fc
  • Thrombocytopenia, Neonatal Alloimmune

Identity

PubMed Central ID

  • PMC2483687

Scopus Document Identifier

  • 48749101490

Digital Object Identifier (DOI)

  • 10.1002/(SICI)1521-4141(199908)29:08<2613::AID-IMMU2613>3.0.CO;2-J

PubMed ID

  • 18654670

Additional Document Info

volume

  • 118

issue

  • 8