The pathogenesis of malaria is characterized by vascular inflammation exacerbated by immune cells that travel to areas where red blood cells infected with parasites stick to the endothelium lining the blood vessels. The molecules that mediate this process are not well-understood, yet such knowledge may lead to therapeutic targets that block vascular inflammation due to malaria.
The Lamb lab has made significant discoveries demonstrating a key role for receptor tyrosine kinase family Eph receptors in malaria pathogenesis. They have identified EphB2 as a critical mediator of malaria-induced liver fibrosis and EphA2 as a molecule essential for the integrity of the blood-brain barrier in cerebral malaria. The malaria studies were carried out as part of the Utah Global Health Initiative with the Pasteur Institute in Cameroon, Central Africa.
Tracey Lamb, Ph.D. with Lawrence Ayong, Ph.D. and team at Centre Pasteur du Cameroun in Yaoundeé, Cameroon.
The receptor tyrosine kinase EphB2 promotes hepatic fibrosis in mice. Mimche PN, Brady LM, Bray CF, Lee CM, Thapa M, King TP, Quicke K, McDermott CD, Mimche SM, Grakoui A, Morgan ET, Lamb TJ. Hepatology. 2015 Sep;62(3):900.
EphB2 receptor tyrosine kinase promotes hepatic fibrogenesis in mice via activation of hepatic stellate cells. Mimche PN, Lee CM, Mimche SM, Thapa M, Grakoui A, Henkemeyer M, Lamb TJ. Sci Rep. 2018 Feb;8(1):2532.
Press Releases and Media:
University of Utah Health: “Discovery Paves Path Forward in the Fight Against the Deadliest Form of Malaria”