The role of Fcγ receptors in murine autoimmune thrombocytopenia

Abstract

International audienceImmune thrombocytopenia (ITP) can become a life-threatening condition that requires immediate medical attention. The loss in platelet numbers during ITP can be induced by a variety of triggers. Anti-platelet antibodies of several isotypes and subclasses are a major cause for ITP and are a hallmark of many complex autoimmune diseases such as systemic lupus erythematosus. Mouse models have been important to understand the effector pathways involved in antibody-mediated platelet depletion. Therapeutic interventions based on these results have been proven successful in treating human ITP, thus validating the use of these model systems. One major problem that remains to be answered is which cell populations are crucial for platelet removal. Targeting these cells directly might be a novel therapeutic strategy and will also be important to understand the underlying biological mechanisms

Monocyte Subsets Responsible for Immunoglobulin G-Dependent Effector Functions In Vivo

“…In chronic human ITP, removal of the spleen can stabilize platelet counts in about 60%-70% of patients, which has been used as indirect evidence that splenic-resident macrophages might be involved in autoantibody-mediated platelet phagocytosis (Biburger et al, 2010;Cines and McMillan, 2005;Mizutani et al, 1992). Moreover, liver-resident macrophages (Kupffer cells) are suggested to be involved in removal of opsonized platelets and do express the relevant activating FcgRIV ( Figure 1B; Coetzee et al, 2000;Heyns et al, 1980;Schmidt and Rasmussen, 1985;Stratton et al, 1989).…”