Their cytotoxic activity 
using concanamycin A, which is commonly used to inhibit the perforin/ granzyme B cytotoxic pathway. Intriguingly, we were unable to reveal expression of perforin in IL-15 DCs. This observation is in contrast to the study of Stary et al. in which TLR7/8-stimulated blood myeloid DCs were found to express both perforin and granzyme B, but is congruent with a recent report showing that mouse plasmacytoid DCs can kill in a granzyme B-dependent, perforin-independent fashion. Although puzzling at first sight, the discordant expression of perforin and granzyme B apparently does not preclude IL-15 DCs from inducing K562 cell death. This complements the notion that granzyme B-induced apoptosis can still occur in the absence of perforin, although not with the same efficiency or rapidity. The lack of perforin expression in IL-15 DCs may thus provide a plausible explanation for their differential lytic profile as compared to “classical” cytotoxic effector cells such as NK cells, which typically contain high levels of both perforin and granzyme B enabling them to induce rapid target cell death. In conclusion, we show here that IL-15 can drive the functional repertoire of human monocyte-derived DCs toward a killer DC profile. This study showcases the considerable potential for phenotypic and functional flexibility of human DCs and provides new converging evidence of the possibility that DCs can adopt a cytotoxic effector function. The observation that IL-15 DCs, in addition to being potent tumor antigen-presenting cells, are endowed with tumoricidal potential provides further strong support to the implementation of IL-15 DCs in DC-based antitumor immunotherapy strategies and to the use of IL-15 as an immunostimulatory adjunct in cancer therapy. Few new drug Mepiroxol targets have been validated despite considerable advances in our understanding of M. tuberculosis biochemistry, metabolism and identification of many essential genes and pathways. While it has become apparent that not all essential metabolic processes represent good drug targets, years of drug development efforts have shown that the bacterial cell wall is an excellent target for antibacterials. Several successful antitubercular drugs, including isoniazid and ethionamide, inhibit enzymes required for mycolic acid synthesis. Mycolic acids are C60-C90 branched-chain b-hydroxylated fatty acids that are covalently bound to arabinogalactan-peptidoglycan forming the skeleton of the cell wall. They are also found in the abundant non-covalently associated outer membrane ester glycolipids trehalose monomycolates and trehalose dimycolates or as free lipids in mycobacterial biofilms. Mycolic acids display important characteristics such as permeability to antibiotics and persistence within the infected host. The biosynthetic machinery of mycolates involves type I and type II fatty acid synthases, FAS-I and FAS-II, respectively. FAS-II is composed of four dissociable enzymes that act successively and reiteratively to elongate the growing acylatedacyl carrier protein. FabH links FAS-I and FAS-II, providing a b-ketoacyl-ACP product with two added carbon atoms which is then reduced by the reductase MabA, followed by a dehydratation step carried out by the set of dehydratases Cinoxacin HadABC and then reduction by the enoyl-ACP reductase InhA. The subsequent steps of elongation of the growing acyl-ACP chain with the condensation of a malonyl-ACP unit at each round are performed by the condensases KasA and KasB. Most FAS-II enzymes are unique and essential, thus representing excellent drug targets.