Jurnal Internasional Patroli monosit mencari sel darah sabit endotelial-adherent: sebuah mekanisme baru penghambatan vaso-oklusi di SCD
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Abstract  Painful vaso-occlusive crisis (VOC) is the most common complication of sickle cell disease (SCD). More and more evidence shows that vaso-occlusion is initiated by increased compliance with sickle red blood cells (RBC) to endothelial blood vessels. Thus, the mechanism that removes red blood cells attached to the endothelium from microvasculature is expected to be very important for optimal blood flow and VOC prevention in SCD. We hypothesize that patrol monocytes (PMos), which protect against vascular damage by cleaning cellular debris, can eliminate endothelial-adherent sickle RBCs and improve VOC in SCD. We detected RBC (GPA + ) – materials that float in PMos circulating in patients with SCD, and their frequency increases during an acute crisis. The absorption of red blood cells by PMos is specific to sickles attached to the endothelium, but does not control, red blood cells and occurs mostly through ICAM-1, CD11a, and CD18. Induction of Heme oxygenase 1, by neutralizing the cytotoxic effects of red blood cell damage products, increases the viability of PMo. In addition, transfusion, by decreasing sickle RBC uptake, increases PMo survival. Selective depletion of PMos in Townes sickle mice worsens vascular stasis and tissue damage, while treatment with muramyl dipeptide (NOD2 ligand), which increases PMo mass, reduces stasis and SCD-related organ damage. Overall, these data indicate a new mechanism for removing red blood cells attached to endothelial mediated by PMos that can protect against the pathogenesis of VOCs, further supporting PMos as a promising therapeutic target in VOC SCD.
- Submitted February 14, 2019 .  Received May 2, 2019.
- © 2019 by The American Society of Hematology