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It is well known that platelets interact with cells of the innate immune system to promote tissue repair. In contrast, it is less clear whether these links extend to cells of the adaptive immune system, such as T cells. In this issue of the JCI, Morrell and colleagues provide compelling evidence that platelets are required to limit CD4+ Th17 differentiation through the actions of the chemokine platelet factor 4 (PF4). Absence of PF4 in the host leads to exaggerated Th17 differentiation after transplantation and rapid graft rejection. The authors' findings argue that platelets are not bit part players, but rather fully fledged, critical members of the adaptive immune system.

Original publication

DOI

10.1172/JCI74231

Type

Journal article

Journal

J Clin Invest

Publication Date

02/2014

Volume

124

Pages

480 - 482

Keywords

Animals, Graft Rejection, Heart Transplantation, Humans, Platelet Factor 4, Th17 Cells