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It has been recently hypothesized that septic microangio-\udpathy is caused or at least promoted by the interaction between endo-\udthelial surface receptor CD40 and its ligand CD40L, expressed by activated \udplatelets. This interaction produces procoagulative changes in endothelial \udcells,   endothelial   apoptosis,   subendothelial   matrix   exposition   and microthrombi formation. Since virtually all septic patients show a certain degree  of  coagulation abnormalities,  we  hypothesized  that  low  platelet count is associated with a diff erent degree of CD40L expression and that this could correlate with the severity of disease.\udMethods To determine the infl uence of sepsis on levels of platelet-derived \udCD40L expression, we performed a prospective observational study in a \udpolyvalent university hospital ICU. Eighteen consecutively septic patients \udwere enrolled in the study, independently of the platelet count and the severity of disease (SOFA score). Flow cytometry of fresh blood from septic \udpatients  (n  =  18)  and  age-matched  controls  (n  =  8)  was  performed  for membrane-bound CD40L and CD62P on circulating platelets.\udResults  Flow  cytometry  demonstrated  low  levels  of  CD62P  in  controls \udwhile the levels in patients were high. CD40L+ platelets were selectively \udfound  from  patients  with  thrombocytopenia  (platelet  count  ≤60,000/mm3).  Furthermore  a  direct  correlation  between  CD40L  expression  and the SOFA score was found in patients with sepsis and thrombocytopenia compared to patients with sepsis without thrombocytopenia.\udConclusions These results suggest that CD40L expression on platelets is \udsomehow related to the degree of thrombocytopenia and possibly can \udbe a marker of the severity of sepsis. Although the role of endothelial-\udderived CD40/platelet-derived CD40L interaction is not fully understood \udduring sepsis, the expression of CD40L on platelets could be related to \udthe severity of organ disease due to the possible bursting of endothelial \uddamage  through  this  pathway.  Further  investigation  is  needed  to \uddetermine  whether  platelets  CD40L  contributes  to  endothelial  and \udsubsequent   organ   damage,   its   role   in   thrombocytopenia   and   its correlation with the outcome of sepsis. The microvascular injury seems to  be  a  central  event  in  sepsis,  so  understanding  the  mechanisms \udunderlying its development is crucial for the individuation of new and \udspecifi c therapeutic strategies

CD40L is selectively expressed on platelets from thrombocytopenic septic patients