SYNERGIC IN-VITRO EFFECTS OF INTERLEUKIN-2 AND TAU-INTERFERON ON THE MIGRATION OF BLOOD MONOCYTES FROM CONTROL SUBJECTS AND PATIENTS WITH LUNG-CANCER

Citation
P. Vaillant et al., SYNERGIC IN-VITRO EFFECTS OF INTERLEUKIN-2 AND TAU-INTERFERON ON THE MIGRATION OF BLOOD MONOCYTES FROM CONTROL SUBJECTS AND PATIENTS WITH LUNG-CANCER, Cancer, 72(7), 1993, pp. 2141-2147
Citations number
36
Categorie Soggetti
Oncology
Journal title
CancerACNP
ISSN journal
0008543X
Volume
72
Issue
7
Year of publication
1993
Pages
2141 - 2147
Database
ISI
SICI code
0008-543X(1993)72:7<2141:SIEOIA>2.0.ZU;2-V
Abstract
Background. Macrophages can play a major role against cancer by exerti ng their cytotoxic activity against tumor cells. The presence of macro phages in tumor stroma is related to the recruitment of circulating bl ood monocytes through the release of chemotactic factors by cancer cel ls. However, fewer blood monocytes from patients with cancer, such as lung cancer, migrate from in vivo and in vitro, compared with blood mo nocytes control subjects. Methods. Two cytokines, interleukin-2 (IL-2) and tau-interferon (tau-INF), proposed in the treatment of cancer, we re tested for their ability to modulate the migratory response in modi fied Boyden chemotactic chambers of blood monocytes obtained from cont rol subjects and patients with lung cancer in the presence of two chem otactic factors: N-formylmethionyl-leucyl-phenylalamine and complement fraction C5a (C5a). Results. Incubation with IL-2 and tau-INF resulte d in a dose-dependent depression of the migration of blood monocytes f rom control subjects and patients with lung cancer. IL-2 depression wa s induced by IL-2 concentrations of 10(5) units/ml, and tau-IFN effect s were measured for concentrations of 100 mu/ml. Furthermore, when low concentrations of IL-2 were tested in combination with low concentrat ions of tau-IFN, dose-dependent depression of blood monocyte migration occurred. Conclusions. Dose-dependent depression of blood monocyte mi gration may modulate the inflammatory component of tumor stroma in pat ients with lung cancer treated with these cytokines. It may also expla in, in part, the high incidence of infections in patients treated with IL-2.