Even in the steady state some DC populations can arise from monocytes [44]. In unique, as reported by Jakubzick et al., 2008 [45], in the absence of inflammation CD103+ and CD11bhi pulmonary DCs can, respectively, originate from two different monocyte populations characterized by the higher or low expression of Ly-6. Nevertheless, certain DC populations are generated below inflammatory situations. For instance, it has been shown that a DC subset specialized in producing higher levels of TNF and upregulating nitric oxide synthase II is originated from monocytes through bacterial infections [40]. These TNF/iNOS-producing (Tip) DCs are recruited for the spleen via CCR2 signaling and have already been shown to mediate the innate immune response against Listeria EAI045 monocytogenes, an intracellular bacterial pathogen [38]. The generation of specific DC populations has also been observed in pathological circumstances for example cancer. For instance, a DC subset with cytotoxic activity has been described inside the final years. This subset, named killer4 DC, is characterized by coexpression of B220 and NK1.1 receptors and is able to kill tumor cells, as a result stopping tumor growth when used in adoptive therapies [46?9]. These B220+ CD11c+ NK1.1+ DCs make large amounts of interferon (IFN) and are named IFN-producing killer DCs (IKDCs). In vitro research employing fusokines (molecules generated by fusing different chemokines) have shown that murine monocytes may be transformed into inducible killer DCs using the capability of inducing apoptosis of tumor cells without losing their antigen presenting capabilities [50]. Furthermore, treatment of bone marrow precursors with MHC-I peptides within the context of a ligand epitope antigen presentation technique (LEAPS) is able to create yet a further DC population characterized by expression of levels of IL12, therefore getting in a position to promote and steer immunity towards a ajhp.120120-QUAN-57 particular T helper-1 (Th1) response [51, 52]. Yet another subset of DCs described in tumor settings is restricted to the spleen, express CD19, and suppresses T cells responses through indoleamine two,3-dioxygenase (IDO) expression [53?6]. The expression of IDO in these cells is triggered upon CTLA4-mediated ligation of CD80 or CD86 molecules [53]. Adding to the complexity of DC subsets, it has been shown that some DC populations can alter their phenotype under pathological settings. As an example, pDCs could obtain cDC qualities below the influence of viral infection [57]. This DC plasticity was evidenced by pioneering function showing that CD8- DCs can give rise to other splenic DC subpopulations [58].Journal of Biomedicine and Biotechnology Three diverse DC subsets have already been described in human skin characterized by expression of CD1ahigh CD14- HLA-DR+ , CD1adim CD14- HLA- DR+ DCs, and CD1a- CD14+ HLA-DR+ DCs [64]. CD1ahigh CD14- HLA-DR+ Langerhans cells reside within the epidermis, while the other subsets reside in the dermis but contrary to what happens in the mouse they do not express langerin [64]. Not too long ago, two skin-derived and 2 resident human cDC subsets had been described in skin-draining lymph nodes characterized by the expression of CD1a+ CD11cint langerin+ Ecadherin+ (skin Langerhans cells); CD1a+ CD11chi and variable expression of langerin fnhum.2014.00074 contrary to what was described above (dermal Langerhans cells); CD14- BDCA3/CD141hi CD103- and CD14+ BDCA3lo CD103+ [65].