Immunothrombosis epitomizes immunological platelet functions in co-operation with the innate and adaptive immune wing. Platelets express TLRs, complement and Fc?-receptors and are prompt and sensitive responders to immunological challenges arising from pathogenic intrusion during viral (e.g. SARS-CoV-2, dengue, influenza, HIV-1), bacterial (e.g. E. coli; S. aureus) and parasitic (e.g. malaria) infections as well as sepsis. Likewise, immunothrombosis can be inadvertently triggered by physiological immune defense mechanisms e.g. raising tires of antibodies in infections such as COVID-19. Platelets also succumb to autoimmune and alloimmune challenges in inherited (e.g. Immunethrombocytopenia-ITP), acquired (e.g. Vaccine induced thrombotic thrombocytopenia-VITT) or even sporadic (e.g. Antiphospholipid syndrome-APS) immune disorders. Such immunothrombotic anomalies affect circulatory platelet count and turnover. Further their functional attributes can result in life threatening consequences.
Immunothrombosis not only disrupts the delicate balance between physiological hemostasis, and pathological thrombosis, it creates an alarming immunological dysregulation in which physiological immune defense itself may turn into an adversity. Recently immunothrombotic complications have emerged as a prognostic determinant in COVID-19 and an unforeseen healthcare challenge in the management of VITT. Taking into consideration the enormous range of platelet-immune interactions, involving both innate and adaptive immune cells and the complement system, investigations directed at exploring molecular mediators and in devising novel therapeutics to tame the thrombosis-immune interface, are indisputably the need of the hour. Parallel advancements in experimental and clinical studies are expected to surmount this obstacle.
In this Research Topic ‘Molecular Drivers of Immunothrombosis’ we aim to engage your attention in a translational perspective on the multifaceted aspects of immunothrombosis. This will not only reveal novel therapeutic targets but also classify challenges in thromboprophylaxis. We are interested in a broad spectrum of themes (ITP, HIT, VITT, APS, bacterial, viral, parasitic infections, sepsis) encompassing the focus on Immunothrombosis, and inviting Review and Original Research articles.
We welcome submissions focusing on, but not limited to:
• The pathophysiological relevance of platelet-immune cell interaction
• The contribution of the immune system (neutrophils, monocytes, lymphocytes, complement system) in immunothrombosis
• The involvement of FcRs and TLRs as major drivers in aggravating thrombotic complications
• Platelet-associated inherited or acquired immune disorders which have a bearing on thrombotic adversity
Immunothrombosis epitomizes immunological platelet functions in co-operation with the innate and adaptive immune wing. Platelets express TLRs, complement and Fc?-receptors and are prompt and sensitive responders to immunological challenges arising from pathogenic intrusion during viral (e.g. SARS-CoV-2, dengue, influenza, HIV-1), bacterial (e.g. E. coli; S. aureus) and parasitic (e.g. malaria) infections as well as sepsis. Likewise, immunothrombosis can be inadvertently triggered by physiological immune defense mechanisms e.g. raising tires of antibodies in infections such as COVID-19. Platelets also succumb to autoimmune and alloimmune challenges in inherited (e.g. Immunethrombocytopenia-ITP), acquired (e.g. Vaccine induced thrombotic thrombocytopenia-VITT) or even sporadic (e.g. Antiphospholipid syndrome-APS) immune disorders. Such immunothrombotic anomalies affect circulatory platelet count and turnover. Further their functional attributes can result in life threatening consequences.
Immunothrombosis not only disrupts the delicate balance between physiological hemostasis, and pathological thrombosis, it creates an alarming immunological dysregulation in which physiological immune defense itself may turn into an adversity. Recently immunothrombotic complications have emerged as a prognostic determinant in COVID-19 and an unforeseen healthcare challenge in the management of VITT. Taking into consideration the enormous range of platelet-immune interactions, involving both innate and adaptive immune cells and the complement system, investigations directed at exploring molecular mediators and in devising novel therapeutics to tame the thrombosis-immune interface, are indisputably the need of the hour. Parallel advancements in experimental and clinical studies are expected to surmount this obstacle.
In this Research Topic ‘Molecular Drivers of Immunothrombosis’ we aim to engage your attention in a translational perspective on the multifaceted aspects of immunothrombosis. This will not only reveal novel therapeutic targets but also classify challenges in thromboprophylaxis. We are interested in a broad spectrum of themes (ITP, HIT, VITT, APS, bacterial, viral, parasitic infections, sepsis) encompassing the focus on Immunothrombosis, and inviting Review and Original Research articles.
We welcome submissions focusing on, but not limited to:
• The pathophysiological relevance of platelet-immune cell interaction
• The contribution of the immune system (neutrophils, monocytes, lymphocytes, complement system) in immunothrombosis
• The involvement of FcRs and TLRs as major drivers in aggravating thrombotic complications
• Platelet-associated inherited or acquired immune disorders which have a bearing on thrombotic adversity
