Acute rejection of a transplanted organ by the recipient is mediated by an inflammatory immune response.
Despite current immunosuppressive therapies, organ rejection remains problematic.
In this issue of the Journal of Clinical Investigation, Craig Morrell and colleagues of the University of Rochester discovered that mice lacking the chemokine, platelet factor 4 (PF4), had an enhanced immune response to heart transplant that was associated with an increase in Th17 cells.
The authors found that PF4 was essential for limiting the differentiation of naive T cells into the Th17 subtype.
In a companion Commentary, Ronjon Chakraverty of University College London discusses this exciting new role for platelets in limiting transplant rejection.
TITLE: Platelet factor 4 limits Th17 differentiation and cardiac allograft rejection ACCOMPANYING COMMENTARY