Table 1.

Summary of major platelet mechanisms that modulate inflammation

Pathogen Reduction

Carrying pathogens (viruses, bacteria and parasites) [11, 16–18]

Elimination of viruses and bacteria [19–22]

Inhibiting growth of S. aureus via β-defensins and NETs induction [23–26]

Growth inhibition of plasmodia via PF 4- and Duffy Ag-dependent manner [11]

Platelet TLRs

Pathogen detection [1]

TLR4: LPS-induced platelet-neutrophil aggregation [35, 36], bacterial trapping via NETs in sepsis [13], possible role in thrombopoiesis [29]

TLR2: producing ROS which may act directly on bacteria [39]

Platelet CD40L (CD154)

Inflammatory reactions via interaction with CD40 of endothelial cells: release of adhesion molecules [42]

Secreting soluble CD40L, and promoting thrombosis [42]

Binding of DCs: inhibiting DC differentiation, suppressing the proinflammatory cytokines

IL-12p70 and TNF-α, promoting IL-10 secretion [47]

Triggering of T cell responses and migration to inflammatory areas [48, 49]

Promoting B cell differentiation and Ab class switching [50]

Platelet MHC class I

Interference with T cell-mediated cytotoxicity responses [53–55]

Intracellular MHC class I connection with α granules [56]

Platelet cytokines/chemokines

Carrying abundant chemokines and cytokines involved in pro/anti-inflammatory pathways [57]

PF4: promoting monocytes and neutrophils migration [62], inducing leukocyte pro-inflammatory cytokine release, phagocytosis, chemotaxis, generation of ROS [64]

RANTES (CCL5): promoting monocytes and macrophages chemotaxis and recruitment to the endothelium [65–70]

IL-1β: central to pro-inflammatory cytokine cascade [73], possible role in dengue virus replication in platelets [74, 75]