TIMP1 and malaria: Collectively, the present data show phagocytosis of nHZ by human monocytes induces inflammation-mediated expression and release of TIMP-1 through p38 MAPK- and NF-κB-dependent mechanisms, suggesting that in vivo nHZ-fed human monocytes may be a source for the high TIMP-1 serum levels found by Dietmann and colleagues in malaria patients [21].