In this study we R788 show that LPS induces apoptosis of bone marrow-derived dendritic cells (DCs) and modulates phenotypes of DCs. LPS treatment up-regulates expression of tolerance-associated molecules such as CD205 and galectin-1,

but down-regulates expression of Gr-1 and B220 on CD11c+ DCs. Moreover, LPS treatment regulates the numbers of CD11c+CD8+, CD11c+CD11blow and CD11c+CD11bhi DCs, which perform different immune functions in vivo. Our data also demonstrated that intravenous transfer of LPS-treated DCs blocks experimental autoimmune encephalomyelitis (EAE) development and down-regulates expression of retinoic acid-related orphan receptor gamma t (ROR-γt), interleukin (IL)-17A, IL-17F, www.selleckchem.com/products/Temsirolimus.html IL-21, IL-22 and interferon (IFN)-γ in myelin oligodendrocyte glycoprotein (MOG)-primed CD4+ T cells in the

peripheral environment. These results suggest that LPS-induced apoptotic DCs may lead to generation of tolerogenic DCs and suppress the activity of MOG-stimulated effector CD4+ T cells, thus inhibiting the development of EAE in vivo. Our results imply a potential mechanism of LPS-induced tolerance mediated by DCs and the possible use of LPS-induced apoptotic DCs to treat autoimmune diseases such as multiple sclerosis. “
“Complement is the central host defense system that clears invading microbes and balances homeostasis. Pathogenic microbes such as Candida albicans have to breach this efficient and important immune defense layer in order to propagate within

the host and to establish an infection. Knowing exactly how the activated complement cascade responds to and attacks microbial invaders is central to understanding the immune battle and the infection process. This also allows a better understanding of how Candida counteracts the individual steps of host innate immunity. Ultimately this knowledge will allow the design of appropriate PIK3C2G therapeutic molecules. In this issue Cheng et al. [Eur. J. Immunol. 2012. 42: 993-1004] identify a new cellular effect of the activated human complement system in the defense against the fungal pathogen C. albicans. The authors show that the complement activation fragment C5a, which is formed in response to Candida infection, induces the cellular release of the inflammatory cytokines IL-6 and IL-1β. In this issue of the European Journal of Immunology, Cheng et al. [1] show that Candida activates complement and that the newly formed activation peptide C5a activates human peripheral blood mononuclear cells (PBMCs) and induces the release of the inflammatory cytokines IL-6 and IL-1β. Thereby, the authors identify a new C5a-mediated cytokine response by the activated complement system. Fungal pathogens such as Candida albicans and Aspergillus fumigatus activate the human complement system [[2-4]], which in turn generates damaging effector molecules that normally attack and eliminate the invading microorganism [[5]].