title: Anti-interferon-gamma antibody treatment, growth of Lewis lung tumours in mice and tumour-associated cachexia.
abstract: C57BL/6N mice bearing Lewis lung tumours were treated with anti-gamma-interferon (IFN-gamma) monoclonal antibodies. Early, but not late, treatment inhibited tumour growth, suggesting that endogenous IFN-gamma promotes initial tumour cell proliferation. Tumour development was associated with failure to gain weight or with progressive weight loss. Anti-IFN-gamma given early or late counteracted this wasting syndrome, which indicates that IFN-gamma production subsists during tumour growth and is directly or indirectly responsible for tumour-associated cachexia. Studies of body composition in cachectic mice revealed fat tissue to be particularly affected. Fat loss was enhanced by IFN-gamma and antagonised by anti-IFN-gamma. Tumour-bearing mice were also hypersensitive to the lethal effect of endotoxin; anti-IFN-gamma was unable to mitigate this sensitisation, suggesting that IFN-gamma does not exert its cachexia-inducing effect through augmentation of the host response to an endogenous endotoxin source.
authors.affiliation: Laboratory of Immunobiology, Rega Institute, University of Leuven, Belgium.
authors.forename: P
authors.initials: P
authors.lastname: Matthys
authors.forename: H
authors.initials: H
authors.lastname: Heremans
authors.forename: G
authors.initials: G
authors.lastname: Opdenakker
authors.forename: A
authors.initials: A
authors.lastname: Billiau
mesh_terms: D000818:Animals; D000911:Antibodies, Monoclonal / Q000627:therapeutic use*; D001835:Body Weight / Q000502:physiology; D002100:Cachexia / Q000209:etiology / Q000517:prevention & control*; D004435:Eating / Q000502:physiology; D005260:Female; D007371:Interferon-gamma / Q000276:immunology* / Q000502:physiology; D008175:Lung Neoplasms / Q000150:complications / Q000473:pathology / Q000628:therapy*; D051379:Mice; D008810:Mice, Inbred C57BL
chemical_list: D000911:Antibodies, Monoclonal; D007371:Interferon-gamma