Induction of the CD23/nitric oxide pathway in endothelial cells downregulates ICAM-1 expression and decreases cytoadherence of Plasmodium falciparum-infected erythrocytes.

摘要: Summary Cytoadherence of parasitized red blood cells (PRBCs) to postcapillary venules and cytokine production are clearly involved in the pathogenesis cerebral malaria. Nitric oxide TNF- a have been proposed as major effector molecules both protective physiopathological processes during malaria infec- tions. has shown be induced by engagement CD23 antigen. This study aimed investigate potential role CD23/ nitric pathway control cytoadher- ence PRBCs on human endothelial cells. We dem- onstrate that normal lung (HLECs) able express low affinity receptor for IgE (Fc Œ RII/CD23), following cell incubation with interleukin 4 or PRBCs. Ligation antigen specific anti-CD23 monoclonal antibody at surface HLECs was found induce iNOS mRNA protein expression, NO release P. falciparum killing. In addition, CD23-engagement these also significant decrease ICAM-1 an adhesion molecule implicated cytoadherence. These data not only described first time expression but suggest possible new regulatory mechanisms via CD23/NO infection.