 This study demonstrated that a monoclonal antibody against beta-2-glycoprotein IWB6 when injected into normal BALB-C mice caused thrombosis in the skin after exposure to a pulse laser. The thrombosis was significantly reduced by pretreatment with a nonsteroidal anti-inflammatory drug and said indicating that the thrombosis was mediated by inflammation. Furthermore, this effect was almost completely reversed by administration of a NF-KappaB specific inhibitor demonstrating that the NF-KappaB pathway plays a key role in the pathophysiology of thrombosis in this model. These findings suggest that the NF-KappaB pathway may be a potential target for the development of new treatments for antifospholipid syndrome. This article was authored by Mizzato Nishimura, Tachikoni, Gulls in Trimova, and others.