Editing Platelet (section)

===Inflammation===
Platelets rapidly deploy to sites of injury or infection. There, they are thought to modulate inflammatory processes ''via'' interactions with [[leukocyte]]s and secretion of [[cytokine]]s, [[chemokine]]s, and other inflammatory mediators.<ref>{{cite journal |vauthors=Weyrich AS, Zimmerman GA |title=Platelets: signaling cells in the immune continuum |journal=Trends in Immunology |volume=25 |issue=9 |pages=489–495 |date=September 2004 |pmid=15324742 |doi=10.1016/j.it.2004.07.003}}</ref><ref name="pmid14500287">{{cite journal |vauthors=Wagner DD, Burger PC |title=Platelets in inflammation and thrombosis |journal=Arteriosclerosis, Thrombosis, and Vascular Biology |volume=23 |issue=12 |pages=2131–7 |date=December 2003 |pmid=14500287 |doi=10.1161/01.ATV.0000095974.95122.EC |doi-access=free}}</ref><ref name="pmid8662511">{{cite journal |vauthors=Diacovo TG, Puri KD, Warnock RA, Springer TA, von Andrian UH |title=Platelet-mediated lymphocyte delivery to high endothelial venules |journal=Science |volume=273 |issue=5272 |pages=252–5 |date=July 1996 |pmid=8662511 |doi=10.1126/science.273.5272.252 |bibcode=1996Sci...273..252D |s2cid=21334521}}</ref><ref name="pmid16258538">{{cite journal |vauthors=Iannacone M, Sitia G, Isogawa M, Marchese P, Castro MG, Lowenstein PR, Chisari FV, Ruggeri ZM, Guidotti LG |title=Platelets mediate cytotoxic T lymphocyte-induced liver damage |journal=Nature Medicine |volume=11 |issue=11 |pages=1167–9 |date=November 2005 |pmid=16258538 |pmc=2908083 |doi=10.1038/nm1317}}</ref><ref>{{cite journal |last1=Oehlers |first1=Stefan H. |last2=Tobin |first2=David M. |last3=Britton |first3=Warwick J. |last4=Shavit |first4=Jordan A. |last5=Nguyen |first5=Tuong |last6=Johansen |first6=Matt D. |last7=Johnson |first7=Khelsey E. |last8=Hortle |first8=Elinor |title=Thrombocyte inhibition restores protective immunity to mycobacterial infection in zebrafish |url= |journal=The Journal of Infectious Diseases |volume=220 |issue=3 |pages=524–534 |language=en |doi=10.1093/infdis/jiz110 |pmid=30877311 |pmc=6603966 |year=2019}}</ref> Platelets also secrete [[platelet-derived growth factor]] (PDGF).

Platelets modulate neutrophils by forming platelet-leukocyte aggregates (PLAs). These formations induce upregulated production of the [[complement receptor]] αmβ2 ([[integrin alpha M|Mac-1]]) integrin in neutrophils. Interaction with PLAs also induces degranulation and increased phagocytosis in neutrophils.

Platelets are the largest source of soluble [[CD40L|CD40L (CD154)]] which induces production of [[reactive oxygen species]] (ROS) and upregulates expression of adhesion molecules (such as [[E-selectin]], [[ICAM-1]], and [[VCAM-1]]) in neutrophils. CD40L also activates macrophages and activates cytotoxic response in [[T lymphocyte|T]] and [[B lymphocytes]].<ref name=":1" />

Mammalian platelets lacking nucleus are able to conduct autonomous locomotion.<ref>{{cite journal |vauthors=Gaertner F, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa-Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher RT, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y, Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt M, Massberg S |title=Migrating Platelets Are Mechano-scavengers that Collect and Bundle Bacteria |journal=Cell |volume=171 |issue=6 |pages=1368–82 |date=November 2017 |pmid=29195076 |doi=10.1016/j.cell.2017.11.001 |doi-access=free}}</ref> Platelets are active scavengers, scaling walls of blood vessels and reorganising the thrombus. They are able to recognize and adhere to many surfaces, including bacteria, and can envelop them in their open canalicular system (OCP), leading to a proposal to name the process as ''covercytosis'' (OCS) rather than phagocytosis, as OCS is merely an invagination of outer plasma membrane. These platelet-bacteria bundles provide an interaction platform for neutrophils that destroy bacteria using [[Neutrophil extracellular traps|NETs]] and phagocytosis.

Platelets also participate in chronic inflammatory disease, such as [[synovitis]] or [[rheumatoid arthritis]].<ref>{{cite journal |vauthors=Boilard E, Nigrovic PA, Larabee K, Watts GF, Coblyn JS, Weinblatt ME, Massarotti EM, Remold-O'Donnell E, Farndale RW, Ware J, Lee DM |title=Platelets amplify inflammation in arthritis via collagen-dependent microparticle production |journal=Science |volume=327 |issue=5965 |pages=580–3 |date=January 2010 |pmid=20110505 |pmc=2927861 |doi=10.1126/science.1181928 |bibcode=2010Sci...327..580B}}</ref> Platelets are activated by collagen receptor [[GPVI|glycoprotein IV]] (GPVI). Proinflammatory platelet microvesicles trigger constant cytokine secretion from neighboring [[fibroblast-like synoviocyte]]s, most prominently [[interleukin 6|Il-6]] and [[interleukin 8|Il-8]]. Inflammatory damage to the surrounding extracellular matrix continuously reveals more collagen, binding receptors on platelets and maintaining microvesicle production.