TF and infection: The results show here that, on one hand, microbes possibly beneficially up-regulate host transferrin as a negative regulator of PRRs signaling to counteract immune-mediated iron withdrawal upon infections, but on the other hand, given its function as a clotting regulator in our recent reports [29,68], transferrin up-regulation in host possibly evokes immunothrombosis to defend invading pathogens, demonstrating an important role of transferrin in mediating reciprocal interactions among iron homeostasis, infection, and immunity.