Abstract

The traditional view of platelets is often limited to anuclear cells that only function in hemostasis. That view is outmoded: platelets have clear roles in antimicrobial host defense, immune modulation, and wound healing. Platelets have explicit structures and functions of host defense effector cells, including recently specified toll-like and other receptors that enable detection of microbial threats. Platelets engage microorganisms directly and indirectly through multiple molecular and cellular mechanisms. In so doing platelets mediate temporally- and mechanisticially-orchestrated responses that coordinate with complementary immune defenses to optimally protect the host. Platelets respond to infection via opsonophagocytosis, degranulation of an array of microbicidal polypeptides, and convergence of synergistic molecular and cellular host defenses. Thus, platelets serve as key immune effector cells that bridge innate and adaptive immunity. Consistent with these perspectives, deficiencies in platelet quantity or quality are recognized to increase clinical risk and severity of infection. Likewise, certain pathogens may subvert platelet-mediated host defenses to exploit platelets as adhesive surfaces. Collectively, platelet immunobiology is rapidly evolving to shed new light on platelet roles in host-pathogen relationships and antimicrobial host defense.

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