Monocytes/macrophages play a double role by phagocyting platelets recognized by autoantibodies and by maintaining the autoimmune response via their function as antigen presenting cells. The functions of macrophages are partially regulated by binding with Immunoglobulin G at their receptors (FcγR) which could be inhibiting, FcγRIIb, or activating (FcγRI, FcγRIIa, FcγRIII). Therefore, a disequilibrium in the FcγRIIa/FcγRIIb ration could be implicated in ITP, as already reported for other autoimmune diseases like rheumatoid arthritis (RA) and systemic lupus erythematous (SLE) The aim of this project is to compare the expression of FcγR in patients with ITP who have been treated with rituximab with that in matched healthy subjects. A correlation between relative expression of these different FcγR (FcγRIIa/FcγRIIb ratio) and the response to splenectomy and to rituximab will be studied.