Natural Innate and Adaptive Immunity to Cancer
Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.Annual Review of Immunology (Impact Factor: 39.33). 04/2010; 29(1):235-71. DOI: 10.1146/annurev-immunol-031210-101324
The immune system can identify and destroy nascent tumor cells in a process termed cancer immunosurveillance, which functions as an important defense against cancer. Recently, data obtained from numerous investigations in mouse models of cancer and in humans with cancer offer compelling evidence that particular innate and adaptive immune cell types, effector molecules, and pathways can sometimes collectively function as extrinsic tumor-suppressor mechanisms. However, the immune system can also promote tumor progression. Together, the dual host-protective and tumor-promoting actions of immunity are referred to as cancer immunoediting. In this review, we discuss the current experimental and human clinical data supporting a cancer immunoediting process that provide the fundamental basis for further study of immunity to cancer and for the rational design of immunotherapies against cancer.
Full-text previewDOI: · Available from: theprovengetrials.org
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed. The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual current impact factor. Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence agreement may be applicable.
[Show abstract] [Hide abstract]
- "Furthermore , such a model offers scope to devise and apply innovative immunotherapeutics possessing potent anti-neoplastic effects. Both innate (rapid and non-specific) and adaptive (specific with memory) immunity are required to prevent neoplastic development (Vesely et al., 2011). The failure of immunosurveillance during tumourigenesis implies that the immune system is ignorant of and/or rendered impotent to the impending danger of tumour formation. "
ABSTRACT: Oral canine malignant melanoma (CMM) is a spontaneously occurring aggressive tumour with relatively few medical treatment options, which provides a suitable model for the disease in humans. Historically, multiple immunotherapeutic strategies aimed at provoking both innate and adaptive anti-tumour immune responses have been published with varying levels of activity against CMM. Recently, a plasmid DNA vaccine expressing human tyrosinase has been licensed for the adjunct treatment of oral CMM. This article reviews the immunological similarities between CMM and the human counterpart; mechanisms by which tumours evade the immune system; reasons why melanoma is an attractive target for immunotherapy; the premise of whole cell, dendritic cell (DC), viral and DNA vaccination strategies alongside preliminary clinical results in dogs. Current “gold standard” treatments for advanced human malignant melanoma are evolving quickly with remarkable results being achieved following the introduction of immune checkpoint blockade and adoptively transferred cell therapies. The rapidly expanding field of cancer immunology and immunotherapeutics means that rational targeting of this disease in both species should enhance treatment outcomes in veterinary and human clinics.
[Show abstract] [Hide abstract]
- "On the contrary, immune cells present in the tumor microenvironment are deregulated and participate in cancer progression by secreting ROS, as well as pro-inflammatory, growth and angiogenic factors. This cellular reprogramming of immune cells, the difficulty to develop an antibody against self-antigens to specifically target cancer cells and ineffective or mutated antigen processing and presentation pathways, the loss of specific membrane markers and a resistance to cell death can mask the tumor from immune cell detection and protect against destruction (Hanahan and Weinberg 2011; Vesely et al. 2011). An alcoholic extract or instant coffee powders prepared from Coffea arabica were reported to act as immunostimulants based on their ability to increase the level of total leukocytes in the blood of mice, induce the secretion of free radicals and IL-2 by mouse immunocytes and activate B lymphocytes. "
ABSTRACT: Coffee is the second most popular beverage in the world after water with a consumption of approximately two billion cups per day. Due to its low cost and ease of preparation, it is consumed in almost all countries and by all social classes of the population through different modes of preparation. Despites its simple appearance, a cup of coffee is in fact a complex mixture that contains hundreds of molecules, the composition and concentration of which vary widely and depend on factors including the origin of the coffee tree or its metabolism. Although an excessive consumption of coffee can be harmful, many molecules that are present in this black decoction exert anticancer properties. This review aims to describe the different primary coffee-containing substances that exert chemopreventive and bioactive activities against the different hallmarks and enabling characteristics of cancer, thus explaining the anticancer health benefit of black coffee.
[Show abstract] [Hide abstract]
- "Likewise , mRNA levels of Ifit1 and Ifit2 , two type I IFN - stimulated genes ( ISGs ) , were also elevated in Ptgs2 À / À tumors ( Figure 2D ) , indicative of enhanced type I interferon ( IFN - a / b ) signaling , which is central to immune - mediated tumor control ( Gajewski et al . , 2013 ; Vesely et al . , 2011 ) . We failed to detect a reduction in the expression of type 2 cytokines , such as IL - 4 , IL - 5 , or IL - 13 , or markers associated with M2 macrophage polarization , such as iNOS , arginase I , Gas - 3 , or E - cadherin ( Figure S5 ; data not shown ) , despite the fact that they have been reported to be induced by prostanoids withi"
ABSTRACT: The mechanisms by which melanoma and other cancer cells evade anti-tumor immunity remain incompletely understood. Here, we show that the growth of tumors formed by mutant Braf(V600E) mouse melanoma cells in an immunocompetent host requires their production of prostaglandin E2, which suppresses immunity and fuels tumor-promoting inflammation. Genetic ablation of cyclooxygenases (COX) or prostaglandin E synthases in Braf(V600E) mouse melanoma cells, as well as in Nras(G12D) melanoma or in breast or colorectal cancer cells, renders them susceptible to immune control and provokes a shift in the tumor inflammatory profile toward classic anti-cancer immune pathways. This mouse COX-dependent inflammatory signature is remarkably conserved in human cutaneous melanoma biopsies, arguing for COX activity as a driver of immune suppression across species. Pre-clinical data demonstrate that inhibition of COX synergizes with anti-PD-1 blockade in inducing eradication of tumors, implying that COX inhibitors could be useful adjuvants for immune-based therapies in cancer patients.