Identification of monocyte chemotactic activity produced by malignant cells

Article Abstract:

Macrophages, cells in the blood that engulf and destroy foreign organisms, mature and reside in tissues of the body. A solid tumor mass can consist of 80 percent macrophages. Macrophages can stimulate tumor growth by producing molecules that cause the tumor cells to multiply. Macrophages also stimulate the development of blood vessels which are necessary to deliver nutrients to the solid tumor so it can grow. However, macrophages can also inhibit tumor growth by the secretion of other molecules. Molecules secreted by human tumor cells that attract monocytes (single-nucleus cells) have been identified. The tumor cells that secrete these molecules include those from osteosarcoma (bone tumors), melanoma (tumors of melanocytes, cells of the skin which secrete a pigment), glioblastomas (tumors from gliocytes, cells in the brain), fibrosarcomas (tumors from the connective tissue that supports other body tissues and parts) and rhabdomyosarcomas (tumors of muscles). Tumors which did not produce such molecules include tumors from cells of the bladder, tumors of the skin, leiomyosarcoma (tumors from muscle cells from the uterus) and other osteosarcomas (tumors from bone). A similar molecule, smooth muscle-derived chemotactic factor (SMC-CF), is secreted by normal smooth muscle cells found in blood vessels. These similar molecules are thought to be involved in a common mechanism to recruit monocytes and macrophages to various tissues. The presence of macrophages in tumors is probably due to the secretion of these molecules by tumor cells. Since macrophages secrete other molecules that stimulate tumor growth, understanding how the macrophages are recruited may lead to the control of this process, which may be clinically important for the control of tumor growth.

Causes of, Tumors

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Localization of PDGF-B protein in macrophages in all phases of atherogenesis

Article Abstract:

In atherosclerosis, fatty deposits, or plaques, accumulate on the inner walls of the arteries. This restricts blood flow and can result in a heart attack, stroke, or gangrene of the extremities. The smooth muscle cells which line the arteries proliferate, as does fibrous connective tissue. Macrophages and T lymphocytes, cells of the immune system, accumulate near the thickened arterial wall. A fibrous cap of connective tissue forms over the immune cells and fatty deposits which have collected, resulting in a lesion. A few growth factors, such as platelet-derived growth factor-B (PDGF-B), interleukin-1, and transforming growth factor-beta 1, were found to be present in the arteries of animals that had ingested high levels of cholesterol over a long period of time, but these growth factors were not present in normal animals. The macrophages in the lesions have been shown to produce PDGF-B, which may cause the proliferation of smooth muscle cells. PDGF-B was found in macrophages in all stages in development of the lesions. PDGF-B is known to cause the growth of smooth muscle cells and is also chemotactic, causing the attraction and migration of smooth muscle cells to the site. It is thought that in the vicinity of the lesion, interactions occur between the macrophages, the T lymphocytes, and the endothelial cells which line the blood vessels, and that this allows the formation and release of growth factors and of other active molecules which contribute to the development of atherosclerosis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Development and progression, Growth, Growth factors, Atherosclerosis, Smooth muscle, Platelet-derived growth factor

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LFA-3, CD44, and CD45: physiologic triggers of human monocyte TNF and IL-1 release

Article Abstract:

Monocytes (a type of white blood cell) produce factors called monokines that have important regulatory effects on the immune system, but the physiologic stimuli for the release of these factors are not fully understood. One such stimulus might be contact between the monocyte and other cells. This was explored in a series of experiments by measuring the release of TNF-a (tumor necrosis factor-alpha) and IL-1B (interleukin-1B), two monokines, by monocytes when they were exposed to different specific monoclonal antibodies (proteins). Such exposure was thought to be similar to the situation a monocyte encounters when a molecule on its surface interacts with a molecule on the surface of cells it contacts. Results showed that monoclonal antibodies to CD44, CD45, and LFA-3 stimulated the monocytes to produce TNF-a and IL-1B, while the other five molecules tested induced no release. The properties of the three molecules against which the effective monoclonal antibodies were made are discussed; while not structurally related, all are capable of activating T cells (another white blood cell type), according to results from other studies. A discussion is provided of the ways release of factors by monokines upon contact with CD44, CD45, or LFA-3 could function to activate T cells. (Consumer Summary produced by Reliance Medical Information, Inc.)

Measurement, Interleukins, Tumor necrosis factor, Monokines

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