E. Somigliana et al., HUMAN ENDOMETRIAL STROMAL CELLS AS A SOURCE OF SOLUBLE INTERCELLULAR-ADHESION MOLECULE (ICAM)-1 MOLECULES, Human reproduction, 11(6), 1996, pp. 1190-1194
Intercellular adhesion molecule (ICAM)-1-mediated cell-cell adhesion i
s essential for various immunological functions, including natural kil
ler (NK) cell-mediated cytotoxicity against endometrium, The present s
tudy was designed to establish whether shedding of ICAM-1 from culture
d endometrial stromal cells occurred and to characterize its potential
functional significance in endometrial physiology and pathology, The
shed sICAM-1 molecule was detected and quantified in supernatants from
endometrial stromal cultures and in peritoneal fluids by a specific e
nzyme-linked immunosorbent assay, The results of this study indicate t
hat cultured endometrial stromal cells constitutively shed ICAM-1 from
their surface, This ability is regulated during the menstrual cycle,
as it appears to be higher in the proliferative than ire the secretory
phase of the cycle (16.93 +/- 2.2 and 7.7 +/- 1.76 ng/ml respectively
). In order to evaluate whether the release of sICAM-1 could interfere
with cell-mediated lysis of endometrium, we compared the determinatio
ns of sICAM-1 in endometrial supernatants with the ability of such sup
ernatants to suppress NK cell-mediated cytotoxicity toward endometrial
targets, A significant correlation (r = 0.6, P < 0.05) was found betw
een the sICAM-1 concentration in endometrial supernatants and the perc
entage of inhibition of NK cell-mediated lysis exerted by the same sup
ernatant samples, Finally, endometrial stromal shedding of sICAM-1 app
ears to be related to endometriosis since endometrial stromal cultures
obtained from patients with advanced stages of the disease released s
ignificantly higher amounts of the soluble protein compared to the con
trol group (P < 0.05), sICAM-1 is a soluble molecule which can interfe
re with immunological functions, and its shedding may be one of the me
chanisms by which refluxed endometrial cells escape immunosurveillance
.