Anti-GPIb mediated thrombocytopenia: implications for IVIG and other therapies

Platelets are small blood cells important for bleeding arrest. When vessel injury occurs, platelets aggregate to form a plug and support coagulation. Immune thrombocytopenia (ITP) is a disease where one’s immune system mistakenly attacks and produces autoantibodies that destroy one’s own platelets, leading to increased bleeding risk. The autoantibodies mainly target two platelet surface proteins GPIIbIIIa and GPIb. Currently, our lab has demonstrated that antibodies against GPIIbIIIa and GPIb cause ITP by different mechanisms. However, it is unclear why antibodies targeting the same proteins of platelets can be dramatically diverse in response to IVIG therapy, or whether some patients have more severe bleeding than others due to the specific type of antibodies in their blood. We propose to investigate why antibodies against different regions of GPIb act differently by affecting platelet generation, where and how the platelets are destroyed and how patients respond to current therapies like IVIG. This study will focus directly on the antibodies resistant to IVIG therapy and the mechanisms, and provide insights into development of new diagnostic/therapeutic methods in aims to effectively control this disease.

NI, Heyu

St. Michael's Hospital

Graduate Fellowship Program

Ontario

$52,000