SummaryIn quinine- and quinidine-induced thrombocytopenic purpura IgG antibodies are known to react in a drug-dependent manner with different combinations of surface glycoproteins (GP) Ib , IIb, IIIa and IX. Because endothelial cells share a number of properties of platelets, including the presence of GP Ilia and GPIb-like proteins, we have compared these two cell types for their quinine-dependent IgG binding abilities. By immunoblotting of endothelial cells, quinine-dependent IgG binding from four patient sera was observed only to a 93 kDa component corresponding to GP Ilia. Strong IgG binding independent of the drug was found at 170–180 kDa. Thus endothelial cells express the GP Ilia quinine-dependent epitope on platelet GP IIIa , but not those on other platelet glycoproteins.
26Plasmodium falciparum malaria causes half a million deaths per year, with up to 27 9% of this mortality caused by cerebral malaria (CM). One of the major processes 28 contributing to the development of CM is an excess of host inflammatory 29 cytokines. Recently K+ signaling has emerged as an important mediator of the 30 inflammatory response to infection; we therefore investigated whether mice 31 carrying an ENU--induced activation of the electroneutral K+ channel KCC1 had 32 an altered response to Plasmodium berghei. Here we show that Kcc1 M935K/M935K 33 mice are protected from the development of experimental cerebral malaria, and 34 that this protection is associated with an attenuated INF--ɣ response. This is the 35 first description of a K+ channel affecting the development of cerebral malaria. 36 37
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