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Poxvirus-based vaccines have a long record of efficacy as both anti-tumour agents and vectors for gene therapy in different human tumour models. Interestingly, several studies of these vaccines have now entered the clinical evaluation phase for safety and effectiveness. A desirable outcome of antigen specific cancer immunotherapy is the disruption of host self-tolerance against endogenous tumour-associated antigens (TAAs). Nonetheless, recent studies have found reductions in vaccine efficacy due to host anti-vaccine immune reactions. Thus, newer approaches bringing together poxvirus-based vaccination and immunostimulation are being developed, and new poxvirus strains are being examined in tumour therapy studies. Our review summarizes the current knowledge on the efficacy of poxvirus-based vaccination on human tumours, with a particular focus on approaches aimed at increasing innate and specific immune responses. Special attention will be devoted to the new poxvirus strains that are currently under consideration for tumour therapy; the current knowledge on clinical trials and outcomes will also be reviewed.

CD36 is a scavenger receptor known to play a critical role in the development of atherosclerosis by mediating the uptake of oxidized low-density lipoproteins (oxLDL) by macrophages, thus leading to foam cell formation. It is now generally recognized that the immune system has a pivotal role in the pathogenesis of atherosclerosis, whose progression is determined by ongoing inflammatory reactions. Recently, several studies pointed out that opioid peptides exert anti-inflammatory activities. Therefore the aim of the present study was to evaluate a possible endomorphin-1 (EM-1) immunomodulatory activity on human foam cells. Our results showed that EM-1 reduced Nile Red-stained lipid droplets content, decreased the expression of CD36 receptor and modulated tumor necrosis factor-α (TNF-α) and interferon-γ (IFN-γ) release from lipid-laden macrophages. Furthermore, Naloxone, an opioid receptors antagonist, reverted the anti-atherogenic and anti-inflammatory observed effects of EM-1. These data demonstrated, for the first time, an unprecedented ability of EM-1 to act as a novel modulator for macrophage-to-foam cell transformation, and for inflammatory cytokines profile, suggesting possible novel endomorphin-based anti-atherosclerotic approaches for the prevention and treatment of atherosclerosis., (Copyright © 2010 Elsevier Inc. All rights reserved.)

Malignant mesothelioma (MM) is a highly fatal tumor of inner body membranes, the extensive growth of which is supported by both a weak immunogenicity and the ability to reprogram surrounding immune cells towards tumor-supporting phenotypes. Interleukin-17 (IL-17) is a major inflammatory cytokine which is now accepted as the paradigmatic cytokine of many autoimmune diseases; however, its role in tumor immunology has only been partially unraveled, and no data exist regarding its possible involvement in MM. Thus, in this work we evaluated the ability of MM to induce IL-17 production in immune cells and the effects of IL-17 on MM growth and invasiveness. Our data show for the first time that macrophages and CD4+ T-cells are polarized by MM to produce IL-17, and that this cytokine exerts multiple tumor-supporting effects on both cell growth and invasiveness. These data provide novel evidence of the crosstalk occurring between MM and immune cells and suggest potential targets for the development of new pharmacological approaches for MM treatment. [ABSTRACT FROM AUTHOR]

Abstract: Brain Natriuretic Peptide (BNP), besides retaining vasodilatory, diuretic and natriuretic properties, is a vasoactive hormone that it is also involved in several cardiac diseases as well as severe sepsis and septic shock. All these conditions are characterized by an ongoing inflammatory response consisting in a complex interaction of pleiotropic mediators derived from plasma or cells, including monocytes and macrophages. However, the relationship between this hormone and inflammation remains to be elucidated. Therefore, the aim of the present study was to evaluate a possible BNP immunomodulatory activity on macrophages. Our results demonstrate that BNP regulates the production of major inflammatory molecules, such as reactive oxygen- and nitrogen species (ROS and RNS), leukotriene B4 (LTB4), prostaglandin E2 (PGE2); modulates the cytokines (TNF-α, IL-12 and IL-10) profile, and affects cell motility. These results furnish novel and brand-new proofs on BNP ability of modulating the production of inflammatory mediators in macrophages whose role has broad implications in inflammatory states where increased BNP levels have been reported. [Copyright &y& Elsevier]