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Comment on Gros et al , page 1017 Platelet GPVI repairs its own damage

In 2008, the laboratory of Denisa Wagner demonstrated an unexpected role for platelets in prevention of bleeding at sites of inflammation using dermatitis, lung, and stroke models. In their seminal paper, Goerge et al demonstrated that bleeding is only seen on inflammatory challengewhen the platelet count is reduced by over 95%. Not only was the presence of hemorrhaging surprising, but it was also not seen in mice lacking the major glycoprotein receptors,GPIIbIIIa,GPIba, and GPVI–Fc receptor (FcR) g-chain complex, or the regulator of platelet activation, CALDAGGEFI, indicating that it was independent of hemostasis. A breakthrough in the understanding of this unexpected role of platelets subsequently came from the laboratory of Wolfgang Bergmeier. Using a novel adoptive transfer approach to introduce genetically or chemically modified platelets into thrombocytopenic mice, Boulaftali et al reported that hemorrhaging in lung and skin models was not rescued by platelets deficient in GPVI or CLEC-2, whereas recovery was seen on introduction of platelets with a combined deficiency of the major G-protein–coupled receptors for thrombin, adenosine 59-diphosphate, and thromboxane A2. 3 This study establishes a unique role for the 2 immunoreceptor tyrosine-based activation motif (ITAM) receptors, which