Editorial : The role of platelet activation in the pathophysiology of HIV, tuberculosis and pneumococcal disease

Abstract

Platelets, best known as essential effector cells in coagulation and hemostasis, are increasingly recognized as major inflammatory cells that play a role in the innate and adaptive arms of the immune system. The interaction of platelets with various cell types of the innate immune system, particularly neutrophils, as well as with structural cells of the vascular endothelium, induces the release of platelet-derived mediators, thus exerting a protective effect in the physiologic response to diseases and control of invading microorganisms (1). However, it is also known that contrary to this protective anti-infective role of a tightly controlled activation of platelets, aberrant platelet activation can lead to systemic inflammation, with organ dysfunction and thrombotic complications in both acute and chronic inflammatory disorders of infective origin. It is, therefore, pleasing that this Research Topic of Frontiers in Immunology contains a series of up-to-date articles on the role of platelet activation in the pathophysiology of three important host infections, namely the human immunodeficiency virus (HIV), Mycobacterium tuberculosis (TB) and Streptococcus pneumoniae (pneumococcus).