Abstract
Although the presence of autoantibodies is known to increase the risk of thrombosis in the antiphospholipid syndrome, the mechanism by which these antibodies exert their effects is poorly understood. Several studies suggest that autoantibody-mediated dysregulation of monocytes is one pathobiologic mechanism of this disease. Recent studies have focused on extra- and intracellular interactions involved in monocyte activation and expression of procoagulant activity. Agents specifically targeting monocyte activation and activity may provide a novel and efficacious approach that is safer than current antithrombotics.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
