Expression of interleukin-10 and its receptor is up-regulated in early pregnant versus cycling human endometrium.

Previous reports suggest that systemic and/or placental presence of T helper 2-type cytokines would be supportive of normal pregnancy. Among these cytokines, IL-10 is thought to be produced at the feto-maternal interface to control fetal-ablating immune responses. However, expression of IL-10 in nonhemopoietic maternal cells of the human uterus has not been characterized in detail. Thus, we studied the expression and modulation of the cytokine and its receptor in human endometrial cells obtained in different phases of the cycle and in early pregnancy. Both cycling and pregnant endometrium express the genes for IL-10 and its receptor, but secretion of the cytokine was significantly increased in decidual cultures compared with that by endometrial cells in both proliferative and secretory phases of the cycle. Similarly, the expression of IL-10 receptor mRNA was up-regulated in early decidua compared with that in menstrual cycle-dependent endometrium. IL-1beta, but not gonadal steroid hormones, was able to directly increase endometrial/decidual IL-10 production. Based on the activity of IL-10 in other nonhemopoietic cell populations, we also evaluated its potential effects on TNFalpha secretion and proliferation of endometrial/decidual cells, but we were unable to demonstrate any direct role of IL-10 as a regulator of these specific functions. It is evident that IL-10 and its receptor are normal constituents of endometrium and early decidua, and their up-regulation during early pregnancy may participate in the T helper type 2 predominance at the feto-maternal interface. The inability of the cytokine to exert autocrine effects on TNFalpha secretion and proliferation of decidual cells leads to speculation that the cytokine acts mostly as a paracrine mediator able to affect maternal immune responses.