DISTRIBUTION OF CELL-ADHESION MOLECULES ON CD56++, CD3-, CD16- LARGE GRANULAR LYMPHOCYTES AND ENDOTHELIAL-CELLS IN 1ST-TRIMESTER HUMAN DECIDUA

Human decidua exhibits a unique infiltrate of large granular lymphocytes (LGL) with a natural killer (NK) cell phenotype (CD56+ +, CD16-, CD3-). The mechanisms underlying the binding of circulating LGL to vascular endothelium in the decidua and their migration into the decidual stroma were investigated immunohistochemically in first-trimester decidua with antibodies against endothelial adhesion molecules and their counter-receptors on leukocytes. Decidual and peripheral blood LGL were also investigated by flow cytometry. In the immunohistochemical investigations, moderate to large numbers of lymphoid cells in the decidua were found to express the alpha4 and alpha(L) integrin subunits, platelet endothelial cell adhesion molecule (PECAM) and intercellular adhesion molecule-1 (ICAM-1). PECAM and ICAM-1 were found on the endothelium of large numbers of decidual blood vessels of all types. Vascular cell adhesion molecule (VCAM), however, was found on the endothelium of only small to moderate numbers of arterioles and venules and a few capillaries, the latter being the main site of migration of leukocytes into the stroma. Weak staining for endothelial leukocyte adhesion molecule (ELAM) was seen only in a moderate number of blood vessels. Flow cytometry revealed expression of the alpha(L) integrin subunit by 72 +/- 10% and 97 +/- 3% of decidual and peripheral blood CD56+ LGL, respectively, of the alpha4 integrin subunit by 85 +/- 7% and 90 +/- 5%, of PECAM by 40 +/- 12% and 30 +/- 15%, and of ICAM-1 by 22 +/- 10% and 1 +/- 1%. These findings suggest that interaction between the integrin beta2alpha(L) and ICAM-1 is the more important mechanism of binding to endothelium in the migration of CD56+ LGL out of the peripheral blood into the decidua.