The ectoenzyme CD73 is a potent producer of extracellular adenosine as it dephosphorylates adenosine monophosphate (AMP). While CD73 can exert enzymatic-independent effects such as promoting angiogenesis, many of its functions are related to this enzymatic activity. This activity cannot only play a role in lymphocyte migration, but it can also be involved in downregulation of antitumour immunity, as the produced adenosine is highly anti-inflammatory. Due to the influence of CD73 on inflammation, its overexpression in several cancer types and its effect on cell trafficking, CD73 is an important player in the immune system.

While research on several aspects of the immune system concerning CD73 has been carried out, macrophages have so far not been studied very intensively. Macrophages can be separated into a pro-  and an anti-inflammatory phenotype, also called M1 and M2. As both CD73 and macrophages are involved in (anti)-inflammatory processes, our aim was to find and characterize a connection between them. We therefore were focusing to determine whether CD73 is differently expressed on M1 and M2 macrophages and to analyse whether CD73 is required for macrophage polarization towards either phenotype. In order to answer these questions, human macrophages were cultured and polarized towards M1 or M2 in vitro .In addition, mouse macrophages were polarized towards  he same phenotype in vivo . After a successful polarization, the macrophage populations were compared by applying different techniques such as flow cytometry, qPCR and multiplex. We could clearly detect the expression of CD73 on in vitro M1 polarized human monocytes/macrophages, while no expression on unpolarized or M2 macrophages could be found. Furthermore, we could neither detect any difference in the CD73 expression of polarized mouse macrophages nor could we see any effect of CD73 on the polarization ability of those cells.