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Thrombosis as an intravascular effector of innate immunity: a review


B. E. Echonwere-Uwikor
S.U. Ken-Ezihuo
A. I. Jackreece

Abstract

Background: Thrombosis is the pathological creation of blood clots in the circulatory system; it is a significant worldwide health burden that increases morbidity and mortality, especially in cardiovascular illnesses such as myocardial infarction, stroke, and venous thromboembolism. The discovery of immunothrombosis, a condition in which the innate immune system participates in the development of clots as a defense mechanism against infections, better our understanding of thrombosis.
Aim: This review aimed to present a thorough analysis of the molecular mechanisms underpinning immunothrombosis, with a particular emphasis on thrombosis as an intravascular effector of innate  mmunity.
Methodology: In this review 36 primary studies from various electronic databases such as Google scholar, Semantic scholar, Research Gate and PubMed were obtained on the basis that they were focused on Platelets and immune responses during thromboinflammation, innate immunity signaling and immunothrombosis, as the molecular processes of immunothrombosis, with emphasis on the release of Neutrophil Extracellular Traps (NETs), which act as clot formation scaffolds, by immune cells like neutrophils. This was made possible by the use of Boolean function.
Result: Coagulation process is promoted by platelets, endothelial cells, and inflammatory cytokines such as Tumor necrotic factor alpha (TNF-α) and Interleukin 6 (IL-6). Immunothrombosis is necessary for ensnaring and neutralizing pathogens, but when it is dysregulated, it can lead to pathological states like pulmonary embolism, disseminated intravascular coagulation (DIC), and deep vein thrombosis (DVT). This is especially true in systemic inflammatory conditions like autoimmune disorders and sepsis. The interaction of the complement system and the coagulation cascade, which further connects immune activation and thrombosis, was also covered in this review. Treatments for thromboinflammatory disorders may benefit from novel therapeutic approaches that modify immunothrombosis. Examples of these approaches include focusing on NET formation, inflammatory cytokines, and platelet-immune interactions.
Conclusion: However, to avoid excessive clotting and preserve the body's defense mechanisms, these strategies need to be carefully balanced. Comprehending the dual character of immunothrombosis provides essential knowledge for formulating tactics to alleviate thrombotic consequences while maintaining immunological integrity.


Journal Identifiers


eISSN: 2635-3792
print ISSN: 2545-5672