Confirming the role of PGE2 as a Th2promoting factor, acting at the APC level. Notably, COX-2 activity is necessary for strong Ab response following vaccination; especially when vaccines are poorly immunogenic or the target population is poorly responsive to immunization. However one wonders which of the following metabolites of AA downstream pathway like LTB4, cysteinyl leukotrienes, 12–15-hetes, PGE2, and PGD2 are actually responsible for the beneficial effect. In future we propose to address these issues of delineating the pathway by appropriate use of pharmacological inhibitors. Many DC-based clinical trials for cancer treatment have shown its safety and feasibility. The clinical efficacy of this therapy still needs to be improvised. Advances in biology lead to frequent improvements in the vaccine production protocols and therapeutics. Recent reports also illustrate that there is emerging evidence that PGE2 plays crucial roles in reciprocal crosstalk between dendritic cells and natural killer cell biology. AB1010 Several NK cell functions are influenced by PGE2, accentuating the role of PGE2 on DC– NK cell crosstalk and its subsequent impact on immune regulations in normal and immunopathological processes. Some of the previous reports show that in vitro generated DCs are less efficient in migration and other functional activities due to use of the cytokine IL-4 in the protocols. IL-4 is known to adversely affect the AA metabolism. In vitro manipulation of cellular vaccines is crucial for their successful use in clinics and thus our methodology, though it shows an incremental increase in the output, may add a new dimension in improvising the production of a potent immunotherapeutic agent. In other words these findings will be helpful in the better contriving of DC based vaccines for cancer immunotherapy with enhanced functionality. Although it has been demonstrated that acute starvation, which is frequently observed in clinical practice, sometimes augments the cytolytic activity of NK cells against neoplastic cells, the molecular mechanisms underlying this phenomenon remain unclear. In addition, few studies have addressed the question of whether such augmentation of NK cell activity by nutritional alteration is of practical benefit. It has been shown that many transformed cells, including virusinfected and tumor cells, can be attacked by tumor necrosis factor– related apoptosis-inducing ligand -expressing NK cells. A variety of mechanisms are involved in the control of neoplastic cells by NK cells. One is the direct release of cytolytic granules containing perforin, granzymes, and granulysin via the granule exocytosis pathway. Another mechanism is mediated by death-inducing ligands such as Fas ligand and TRAIL. TRAIL, an Apo2 ligand, is a type II transmembrane protein belonging to the TNF family. There are 5 TRAIL receptors: two can induce apoptotic signals and the others act as decoy receptors.