Fig. 1

The key roles of platelets in modulating inflammatory processes. (1) Platelets are activated by invading pathogens (or their products) that have already been targeted by IgG receptor FcγRIIA (via IgG production). (2) Platelets can carry and eliminate pathogens, and via the expression of TLRs they can bind bacterial LPS and activate neutrophils, inducing NETs formation. (3) Platelet CD40L expression allows them to interact with different immune cells and either activate (arrow) and/or suppress (T bar) them. Furthermore, CD40L may be cleaved into a soluble form (sCD40L) that enhances platelet activation, aggregation, and platelet-leukocyte conjugation. (4) Intact platelet MHC class I molecules are located intracellularly but upon activation are expressed and can activate antigen-specific CD8+ T cells. In contrast, the MHC class I molecules on the surface of resting platelets are denatured and lead to CD8+ T cell inhibition. (5) Platelets contain many proinflammatory and anti-inflammatory cytokines and chemokines and, upon activation, can release them to the extracellular space. The culmination of these events makes platelets a formidable immunomodulatory host