Editing Platelet (section)

===Immunothrombosis===
As hemostasis is a basic function of thrombocytes in mammals, it also has its uses in possible infection confinement.<ref name=":0"/> In case of injury, platelets, together with the coagulation cascade, provide the first line of defense by forming a blood clot. Hemostasis and host defense were thus intertwined in evolution. For example, in the [[Atlantic horseshoe crab]] (estimated to be over 400&nbsp;million years old), the only blood cell type, the [[amebocyte]], facilitates both the hemostatic function and immune functions, including encapsulation, phagocytosis of [[pathogen]]s, and [[exocytosis]] of intracellular granules containing [[bactericide|bactericidal]] defense molecules. Blood clotting supports immune function by trapping the bacteria.<ref>{{citation |last=Levin |first=Jack |name-list-style=vanc |title=Platelets |chapter=The Evolution of Mammalian Platelets |date=2007 |pages=3–22 |publisher=Elsevier |isbn=978-0-12-369367-9 |doi=10.1016/B978-012369367-9/50763-1 }}</ref>

Thrombosis (blood coagulation in intact blood vessels) is usually viewed as a pathological immune response, leading to obturation of lumen of blood vessel and subsequent hypoxic tissue damage. In some cases, however, directed thrombosis (or ''immunothrombosis)'' can locally control the spread of an infection. The thrombosis is directed in concordance with platelets, [[neutrophil]]s and [[monocyte]]s. The process is initiated either by immune cells by activating their pattern recognition receptors (PRRs), or by platelet-bacterial binding. Platelets can bind to bacteria either directly through thrombocytic PRRs<ref name=":1"/> and bacterial surface proteins, or via plasma proteins that bind both to platelets and bacteria.<ref>{{cite journal |vauthors=Cox D, Kerrigan SW, Watson SP |title=Platelets and the innate immune system: mechanisms of bacterial-induced platelet activation |journal=Journal of Thrombosis and Haemostasis |volume=9 |issue=6 |pages=1097–1107 |date=June 2011 |pmid=21435167 |doi=10.1111/j.1538-7836.2011.04264.x |url=https://epubs.rcsi.ie/cgi/viewcontent.cgi?article=1041&context=mctart |doi-access=free}}</ref> Monocytes respond to bacterial [[pathogen-associated molecular pattern]]s (PAMPs), or [[damage-associated molecular pattern]]s (DAMPs) by activating the extrinsic pathway of coagulation. Neutrophils facilitate the blood coagulation by [[Neutrophil extracellular traps|NETosis]], while platelets facilitate neutrophils' NETosis. NETs bind tissue factor, binding the coagulation centers to the location of infection. They also activate the intrinsic coagulation pathway by providing a negatively charged surface for factor XII. Other neutrophil secretions, such as proteolytic enzymes which cleave coagulation inhibitors, also bolster the process.<ref name=":0"/>

In case of imbalance in the regulation of immunothrombosis, this process can become aberrant. Regulatory defects in immunothrombosis are suspected to be a major factor in pathological thrombosis in forms such as [[disseminated intravascular coagulation]] (DIC) or [[deep vein thrombosis]]. DIC in sepsis is a prime example of both the dysregulated coagulation process and an undue systemic inflammatory response. It results in a multitude of microthrombi. These are similar in composition to the thrombi produced in native immunothrombosis — they are made up of fibrin, platelets, neutrophils and NETs.<ref name=":0"/>