The interaction of platelets with bacteria-activated platelets and formatted immune thrombosis to prevent a spreading bacterium and, meanwhile, pro-inflammatory mediator released by platelets could play a significant role in bacterial infections immunity.[31] For instance, streptococcus purulent is first snared by fibrinogen and then combined with GPIIb/IIIa signals from platelets, thus activating platelets.[4] When platelets act, platelet volume expansion induces the aggregation of platelets, leading to the capture of bacteria. Here, ITGA2B is linked to bacterial infectious disease.