CCL23 and autoimmune thrombocytopenic purpura: Among these predicted molecular interactions, TNFSF/TNFRSF, whose overactivation had been reported to be associated with the pathogenesis of various autoimmune diseases, was significantly activated in ITP.33 In addition, chemokine signaling (CCL3_IDE, CCR10_CCL28, and IDE_CCL23) and integrin-mediated cell adhesion and migration (e.g., COL9A2_a2b1 complex and ICAM2_aLb2 complex) were enhanced in ITP.