Next to that, BMDCs treated with parasitic antigens

(E/S products) displayed a reduction in the expression of intact MHC class II (I-a) molecules. Indeed, a weak signal of (I-a) molecules was detected by western blotting in membrane-associated proteins isolated from BMDCs treated with E/S products. Thus, E/S products may contain proteases that would alter see more the structure of MHC class II molecules (I-a) expressed by BMDCs. Such an additional proteolytic effect may explain the practical absence of (I-a) molecules on pe-DCs isolate at the late stage of AE-infection, as revealed by flow cytometry analysis. We expected that the high level of compounds released by the large parasite mass in vivo triggered a pronounced alteration of the already low level of (I-a) molecules expressed by pe-DCs. Nevertheless, our still preliminary respective data will require further investigations to experimentally prove such proteolytic activities of metabolites. We conclude that the intraperitoneal E. multilocularis metacestode tissue affected peritoneal DCs such as to remain in an immature or resting state, characterized by low expression of co-stimulatory molecules and MHC class II (I-a) molecules. Conclusively, we qualified AE-pe-DCs as tolerogenic cells. Moreover,

the high level of TGF-β expression classifies AE-pe-DCs within cells with suppressive features. In our future research, we will attempt to elucidate Trametinib order factor(s) released by E. multilocularis metacestodes that trigger and/or maintain the tolerogenic status of pe-DCs during infection. Better knowledge on these factors may be very useful in the design

of new treatment strategies, not only for echinococcosis but putatively also for organ transplantations and for autoimmune diseases. Norbert Mueller and Andrew Hemphill (Institute of Parasitology, University of Bern) are both acknowledged for their great support GBA3 and helpful comments and discussions. This work was supported by the Swiss National Science Foundation (grant no. 31-111780/1). “
“Acute graft-versus-host disease (GVHD) following allogeneic bone marrow transplantation (BMT) is initiated by donor T lymphocytes that recognize histocompatibility antigens presented by recipient dendritic cells (DCs). Current approaches to reduce GVHD are focused on suppressing donor T lymphocyte responses to alloantigens. However, these strategies may be inadequate in the setting of allogeneic transplants (particularly histoincompatible transplants), may increase the risk of tumour relapse and are associated with high rates of opportunistic infections. We hypothesized that inhibition of recipient DCs might suppress GVHD. We recently demonstrated in vitro that azithromycin, a macrolide antibiotic, also acts as a nuclear factor (NF)-κB inhibitor of murine DCs and inhibits their maturation and functions, including allogeneic responses.