TLR-mediated cell signaling by malaria GPIs.
Proinflammatory responses to malaria have crucial roles in controlling parasite growth and disease pathogenesis. The glycosylphosphatidylinositol (GPI) of Plasmodium falciparum is thought to be an important factor in the induction of proinflammatory responses. The GPI induces host cellular responses mainly through Toll-like receptor (TLR)2/MyD88-mediated signaling. Knowledge of the parasite-host factors involved in activating and regulating innate immune responses and of the associated signaling mechanisms is likely to provide insights into the modulation of parasite-specific adaptive immunity and offer targets for the development of novel therapeutics or a vaccine for malaria. This article focuses on the malaria GPI-mediated cell-signaling mechanisms.
Gowda
D Channe
DC
Department of Biochemistry and Molecular Biology, Pennsylvania State University College of Medicine, Hershey, PA 17033, USA. gowda@psu.edu
D000818:Animals; D017261:Glycosylphosphatidylinositols / Q000737:chemistry / Q000276:immunology*; D006790:Host-Parasite Interactions / Q000276:immunology* / Q000502:physiology; D006801:Humans; D007113:Immunity, Innate; D007249:Inflammation; D017780:Malaria Vaccines; D053594:Myeloid Differentiation Factor 88; D010963:Plasmodium falciparum / Q000378:metabolism*; D011956:Receptors, Cell Surface / Q000378:metabolism; D011971:Receptors, Immunologic / Q000378:metabolism; D015398:Signal Transduction; D051193:Toll-Like Receptors / Q000378:metabolism*
D017261:Glycosylphosphatidylinositols; D017780:Malaria Vaccines; D053594:Myeloid Differentiation Factor 88; D011956:Receptors, Cell Surface; D011971:Receptors, Immunologic; D051193:Toll-Like Receptors