Aspirin exerts a broad spectrum of pharmacological actions, including inhibition of activation of the transcription factor NF-κB and other molecular pathways of inflammation. In June 15 Journal of Immunology Holger Hackstein and colleagues from the Thomas E. Starzl Transplantation Institute at the University of Pittsburgh show that aspirin targets the dendritic cells responsible for triggering transplanted organ rejection.

Hackstein et al showed that aspirin profoundly inhibited the expression of CD40, CD80, CD86, and MHC class II molecules on stimulated murine myeloid dendritic cells (DC). The inhibitory action was dose dependent and was evident at physiological concentrations higher than those necessary to inhibit prostaglandin synthesis. In addition, they showed that aspirin inhibited the maturation of myeloid DC in a dose-dependent manner, without impairing the differentiation of progenitor cells into CD11c+ DC. The drug effects were COX independent and involved primarily the suppression of NF-κB p50 activation (J Immunol 2001,...

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