Abstract
Introduction: Platelets contribute to pathological inflammation during myocardial infarction (MI) and can mediate this response by interacting with neutrophils, which, when activated, can also contribute to myocardial inflammation. Both cells can regulate inflammation by expression of Toll-like receptors (TLRs), but the extent to which platelets modulate neutrophil activation in response to TLR stimulation is currently not understood.
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