Abstract

Objective: Intercellular adhesion molecule (ICAM)-1, a member of the immunoglobulin supergene family of adhesion molecules, has been shown to play a crucial role in inflammatory and immune responses. The interaction between ICAM-1 and its ligands is essential for cell-mediated cytotoxicity, the interaction of T and B cells and lymphocyte-endothelial cell adhesion. The soluble form of ICAM-1 (sICAM-1) represents the shedding domain of the surface molecule and has been suggested to interfere with the molecular mechanisms that mediate the immunesurveillance, thus promoting cellular spreading potential. ICAM-1 and its soluble form seem to play an important role in the eziopathogenetic mechanisms of various inflammatory and autoimmune diseases, including endometriosis. We have previously shown that ectopic endometrial cells release significantly higher levels of sICAM-1 when compared to corresponding eutopic cells and that shedding of the protein by eutopic endometrium is significantly increased in patients with endometriosis. Moreover, concentrations of the protein directly correlate with the number of peritoneal endometriotic lesions. However, contribution of ICAM-1 gene polymorphisms to this disease remains unknown. A single-base ICAM-1 polymorphism has been described in exon 4 changing codon 241 in the ICAM-1 gene. The aim of this study was to examine the potential association of G/R241 ICAM-1 gene polymorphism with the clinical expression of endometriosis.

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