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Molecular immunological approaches to biotherapy of human cancers--a review, hypothesis and implications.\nBecker Y.\nAnticancer Res. 2006 Mar-Apr;26(2A):1113-34. Review.\nPMID: 16619514 \n\nPolarized Th1 cells produce interleukin (IL)-2, IL-12 and interferon (IFN)-gamma, and polarized Th2 cells and the hematopoietic cells produce IL-4, IL-5, IL-6, IL-10 and IL-13. In healthy individuals there is a Th1/Th2 cytokine balance, but during microbial-induced inflammation the pathogens induce an overproduction of the Th2 cytokines that inhibit the adaptive immune response against the pathogen. A review of studies on the Th1/Th2 cytokine balance in humans harboring different tumor types revealed that tumor cells induce increased Th2 cytokine levels in patients' sera that can serve as indicators for the existence of tumors. I\n

The precise mechanism of the anti-tumor effect of imiquimod in BCC is not known. It has been postulated that ultraviolet radiation induces mutations in the tumor-suppressor genes and alters the immuno-surveillance, so that tumor cells escape from cytotoxic T cells and apoptosis.[1] Th-2 cytokines, that downregulate tumor surveillance, are raised in BCC.[1],[5] Imiquimod acts on toll-like receptor-7 (TLR-7) present on dendritic cells, macrophages and monocytes and induces expression of interferons, Th-1 cytokines (IL-1, IL-6, IL-10 and IL-12), tumor necrosis factor-a and G-CSF, thereby counteracting Th2 cytokines and promoting tumor surveillance.[1],[5] It also enhances the activity of natural killer cells and epidermal Langerhans' cells. The tumor regression is achieved probably by induction of Fas receptors on the tumor cells resulting in their apoptosis.[10]

Journal of Skin CancerVolume 2011 (2011), Article ID 571734, 6 pagesdoi:10.1155/2011/571734 © 2011 Mary H. Lien and Vernon K. Sondak.

We describe how innate and adaptive immune cascades trigger the release of cytokines and chemokines, resulting in the initiation and progression of atherosclerosis. We discuss how cytokines have direct and indirect effects on myocardial function.

The cellular and extracellular matrix accumulations that comprise the lesions of atherosclerosis are driven by local release of cytokines at sites of predilection for lesion formation, and by the specific attraction and activation of cells expressing rece

Diagram.

Atherosclerosis is the predominant underlying pathology of cardiovascular disease...atherosclerotic lesions are characterized by abundance of immune cells and their effector molecules, eventually leading to unstable angina, myocardial infarction, or strok

Unlike simple starvation, where body fat is lost preferentially, cancer cachexia is associated with depletion of both fat and skeletal muscle mass. Although anorexia is frequently associated with cachexia a reduction of nutrient intake alone could not explain the progressive wasting. Instead the process appears to be mediated by circulatory tumor-produced catabolic factors acting either alone or in concert with certain cytokines. A knowledge of the mechanisms involved should lead to the development of effective pharmacological intervention. Effective therapy should not only improve the quality of life of the cancer patient, but should lead to an increase in survival. Since cachexia is so common in cancer host products may be required for tumor homeostasis. Thus further knowledge in this area may lead to the development of new agents for the treatment of cancer.

Fatty acids, the immune response, and autoimmunity: a question of n-6 essentiality and the balance between n-6 and n-3.

Study provides the first evidence of a direct relationship between the depression of protein synthesis in skeletal muscle by PIF and Ang II, through activation of PKR, and eIF2{alpha} phosphorylation, and the enhanced degradation of the myofibrillar protein myosin, through activation of NF-{kappa}B resulting in an increased expression and activity of the ubiquitin-proteasome proteolytic pathway. This suggests that agents that target PKR may be effective in the treatment of muscle atrophy in cancer cachexia or other wasting conditions.

Eley, HL and Tisdale, MJ: Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham UK. January 2007

Skeletal Muscle Atrophy: Link between Depression of Protein Synthesis and Increase in Degradation -- Eley and Tisdale 282 (10): 7087 -- Journal of Biological Chemistry. Eley, HL and Tisdale, MJ: Nutritional Biomedicine, School of Life and Health Sciences, Aston University, Birmingham UK. January 2007

This study shows that by modulating the eicosanoid metabolism using a combination of n-3 fatty acids and cyclooxygenase-2 inhibitor, some of the signs and symptoms associated with a Systemic Immune-Metabolic Syndrome (SIMS) could be ameliorated.