Suppression of natural killer cell function and production of soluble ICAM-1: Endometrial stroma versus melanoma

Citation
P. Vigano et al., Suppression of natural killer cell function and production of soluble ICAM-1: Endometrial stroma versus melanoma, AM J REPROD, 46(5), 2001, pp. 342-348
Citations number
26
Categorie Soggetti
Immunology
Journal title
AMERICAN JOURNAL OF REPRODUCTIVE IMMUNOLOGY
ISSN journal
10467408 → ACNP
Volume
46
Issue
5
Year of publication
2001
Pages
342 - 348
Database
ISI
SICI code
1046-7408(200111)46:5<342:SONKCF>2.0.ZU;2-L
Abstract
PROBLEM: It has been suggested that specific mechanisms commonly used by di fferent cellular systems to evade immunologic recognition are involved in t he development of endometriosis. To gain insight into this aspect, we looke d at the relationship between two of these mechanisms in endometrial stroma and the melanoma system for which the ability to create an environment of immune privilege has been well established. METHOD OF STUDY: Media conditioned by endometrial stromal cultures and mali gnant melanoma A375 were examined to test their effects on peripheral blood mononuclear cell-mediated cytotoxicity directed against K562 target. Moreo ver, these media were tested for the concentration of the soluble form of i ntercellular adhesion molecule-1 (sICAM-1), which has been suggested as a m arker for spreading potential. RESULTS: Media conditioned by endometrial stromal cultures exerted a signif icant suppressive effect on cell cytotoxicity when compared with those deri ved from malignant melanoma Moreover, the constitutive release of sICAM-1 w as significantly higher in supernatants from endometrial stromal than in me lanoma cells. CONCLUSIONS: These results indicate that two specific properties suggested to be involved in the ability of tumor cells to evade the immune system are more pronounced in the endometrium than in a malignant melanoma. Since the properties evaluated have been previously demonstrated to be even more not able in endometrial samples derived from endometriosis patients. a role of these mechanisms in the development of the disease may be hypothesized.