The circulating blood cells bind to neutrophils, prompting inflammation-related activity in these immune cell partners.
During a local inflammatory response, white blood cells called neutrophils bind to the sides of blood vessels and crawl along them. This allows neutrophils to migrate toward infection: the cells find favorable locations to exit the blood vessels and migrate into infected tissues, where they engulf pathogens. Initiating this process requires that activated platelets bind to a protein called PSGL-1 that neutrophils project into the blood stream like antennae, according to a paper published today (December 4) in Science. When neutrophils are unable to bind to platelets, they fail to migrate normally, and inflammation is reduced.
“It’s a very interesting concept that platelets would be so important in inflammation and in regulating neutrophil biology,” said Paul Kubes, an immunologist at the University of Calgary in Canada who was not involved in the study. “I think people are starting to appreciate that platelets are becoming more and more important in immunity.”
Study coauthor Andrés Hidalgo, an immunologist at the Spanish National Center for Cardiovascular Research (CNIC), refers to the interaction between neutrophils and platelets as a checkpoint: it confirms to the neutrophils that there has been an insult to the body. Inflammatory cytokines spur the lining of the blood vessels to become activated and the neutrophils to bind them, but this alone is not sufficient to activate the full inflammatory response. The presence of activated platelets indicates a vascular injury. “It’s not only that . . . the vessel gets activated in this local place were you get the injury,” said Hidalgo. “You need the circulation to tell you something is really wrong.”