Review Article Open Access
Volume 2 | Issue 1 | DOI: https://doi.org/10.33696/immunology.2.012

Is Platelet Desialylation a Novel Biomarker and Therapeutic Target in Immune Thrombocytopenia?

  • 1Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada
  • 2Toronto Platelet Immunobiology Group, University of Toronto, Toronto, Canada
  • 3Department of Laboratory Medicine, Keenan Research Centre for Biomedical Science, St. Michael’s Hospital, Toronto, Can
  • 4Canadian Blood Services Centre for Innovation, Toronto, Canada
  • 5Department of Physiology, University of Toronto, Toronto, Canada
  • 6Department of Medicine, University of Toronto, Toronto, Canada
+ Affiliations - Affiliations

Corresponding Author

Heyu Ni, heyu.ni@unityhealth.to

Received Date: December 03, 2019

Accepted Date: December 20, 2019


Immune thrombocytopenia is an autoimmune disease predominantly caused by autoantibody mediated platelet and megakaryocyte destruction and or dysfunction, which leads to low platelet counts and risk of bleeding. Currently prognostic biomarkers are underdeveloped and there lacks a gold-standard for therapeutics, which leaves an inexplicable refractory subset of patients which are clinically challenging. Autoantibodies in ITP predominantly target the two most abundantly expressed platelet surface antigens integrin GPIIbIIIa and GPIb-IX. We and others have reported antibodies against GPIbα tend to exhibit more refractoriness to common ITP therapies such as steroids and intravenous IgG (IVIG). Here we discuss the mechanisms which could contribute to the increased resistance, including our recent finding of anti-GPIbα-, and some anti-GPIIbIIIa- mediated platelet activation and desialylation, leading to Fc-independent platelet clearance. Furthermore, we discuss the emerging clinical investigations of utilizing desialylation as a biomarker/prognostic tool in identifying the refractory subset, as well as the therapeutic benefits of targeting desialylation with sialidase inhibitors.


Immune thrombocytopenia, Autoantibodies, Platelets, GPIbα, Integrin

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