The Role of Macrophages in Defense Against Neoplastic Disease

Mh, Levy; Ef, Wheelock

doi:10.1016/s0065-230x(08)60110-4

Cited by 134 publications

(49 citation statements)

References 140 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Macrophage activation has been correlated with suppression of tumour growth (Keller, 1975;Keller & Hess, 1972) and may reflect an increased participation of macrophages in the rejection process via a nonspecific or specific process (Di Luzio, 1975;Keller, 1975;Levy & Wheelock, 1974 Keller, 1975;Levy & Wheelock, 1974). Macrophages can induce lvsis of tumour cells, and such lytic ability appears to be related to contactinduced destruction and associated release of lysosomal enzymes (Hibbs, 1974;Journey & Amos, 1962;Keller, 1973;Keller & Hess, 1972).…”

Section: Discussionmentioning

confidence: 99%

“…MACROPHAGES may represent a primitive and effective cellular anti-tumour surveillance mechanism (Diller et al, 1963;Di Luzio, 1975;Hibbs et al, 1972a,b;Levy & Wheelock, 1974;Old et al, 1960;Stern, 1960). Stimulation of the macrophage system increases resistance to tumour challenge (Diller et al, 1963;Stern, 1960) and macrophage depression decreases resistance to tumour growth.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Circulating immunoreactive and bioassayable opsonic plasma fibronectin during experimental tumour growth

Saba¹,

Gregory²,

Blumenstock³

1980

Br J Cancer

View full text Add to dashboard Cite

Immunoreactive and bioassayable plasma fibronectin (opsonic α 2 surface-binding (SB) glycoprotein) was measured during experimental Sarcoma-180 tumour growth in mice. Male C57BL/6 mice were challenged s.c. with 2 × 10 6 viable Sarcoma-180 tumour cells and evaluated sequentially in parallel with saline-injected controls over a 21-day experimental period. Before challenge, immunoreactive plasma fibronectin was 1050-1150 μg/ml. Minimal tumour growth occurred until 6 days after tumour challenge. There was then a rapid increase in primary tumour size, especially over the 7-14-day interval, with a plateau of growth over the 18-21-day interval. Immunoreactive plasma fibronectin was significantly ( P < 0·05) raised at 3 and 7 days after tumour challenge. A rapid rise ( P < 0·001) to 2816·6 ± 158·9 μg/ml was observed at 14 days followed by a modest decline at 21 days. Bioassayable opsonic activity increased ( P < 0·5) with the rise in immunoreactive fibronectin 3 and 7 days after tumour challenge, but the rapid rise in immunoreactive fibronectin over the 7-14-day interval was associated with a significant ( P < 0·5) fall in bioassayable opsonic activity. Thus, the rapid rise in immunoreactive plasma fibronectin parallels the rapid rate of tumour growth, but is associated with a fall in opsonically active plasma fibronectin. Dissociation between immunoreactive and opsonically active plasma fibronectin may be mediated by inhibition and/or alteration of circulating fibronectin during rapid tumour growth. Alternatively, it may reflect increased release of antigenically related protein (i.e. cell-surface fibronectin) during rapid tumour growth, which may have limited biological opsonic activity. Images Fig. 2

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Circulating immunoreactive and bioassayable opsonic plasma fibronectin during experimental tumour growth

Saba¹,

Gregory²,

Blumenstock³

1980

Br J Cancer

View full text Add to dashboard Cite

show abstract

“…Their observed potential for recognizing and destroying neoplastic cells, thus preventing the development of cancer, is another remarkable property that merits further study (14). More than two decades ago, Gorer (15) noted that macrophages were prominent during the rejection of tumor cells.…”

Section: Helpful Effects Of Macrophage Functionmentioning

confidence: 99%

Macrophage damage in relation to the pathogenesis of lung diseases.

Brain¹

1980

Environ Health Perspect

View full text Add to dashboard Cite

Pulmonary macrophages are important since their migratory patterns and behavior are often pivotal events in the pathogenesis of pulmonary disease. Alveolar macrophages act to decrease the probability of particle penetration through epithelial barriers, and their phagocytic and lytic potentials provide most of the known bactericadal properties of the lung. Macrophages are also involved in immune responses and in defense against neoplasms. Increased inert or infectious particles stimulate the recruitment of additional macrophages. Most free cells containing particles eventually reach the airways and are quickly carried to the pharynx and swallowed. In addition, evidence has now accumulated that macrophages play a part in the pathogenesis of pulmonary diseases. For example, the ingestion of some particles by macrophages causes a release of lysosomal enzymes into the macrophage cytoplasm. These enzymes may kill the macrophage, and dead or dying macrophages release a substance with attracts fibroblasts that elicit fibrogenic responses. Other toxic particles, such as cigarette smoke, my lead to a release of proteases and other toxic enzymes. All particles are capable of competitive inhibition of phagocytosis in macrophages and many may be cytotoxic and further depress phagocytosis. In addition, connective tissue macrophages may contribute to lung disease by concentrating and storing potent carcinogens or other toxic particles close to a reactive bronchial epithelium for long periods. Thus, even through macrophages serve as a first line of defense for the alveolar surface, they may also be capable of injuring the host while exercising their defensive role.

show abstract

“…Macrophages and lymphocytes possibly play an important rote in the host defense.against neoplasms [1,2]. In vitro the process of the tumor cell lysis by specific T lymphocytes has been resolved into 3 steps.…”

Section: Introductionmentioning

confidence: 99%