Decreased Expression of the Decoy Interleukin-1 Receptor Type II in Human Endometriosis

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This study investigated the expression of the decoy interleukin-1 receptor type II (IL-1RII) in human endometriosis and found it to be decreased in affected tissues.

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Abstract

Many of the biological changes occurring in the endometrium during the menstrual cycle bear a striking resemblance to those associated with inflammatory and reparative processes. Hence, it would not be surprising to find that cytokines known for their pro-inflammatory properties, such as interleukin-1 (IL-1), could play a key role in the physiology of this tissue and that their action would be tightly controlled by local mechanisms. In the present study, immunohistochemical and Western blot analyses show that in normal women (n = 39), the endometrial tissue expresses, in a cycle-dependent manner, the IL-1 receptor type II (IL-1RII), a molecule of which the only biological property known to date is that of capturing IL-1, inhibiting thereby its binding to the functional type I IL-1 receptor. IL-RII immunostaining was particularly intense within the lumen of the glands and at the apical side of surface epithelium. Interestingly, the intensity of staining was markedly less pronounced in the endometrium of women with endometriosis (n = 54), a disease believed to arise from the abnormal development of endometrial tissue outside the uterus, especially in the early stages of the disease (stages I and II). This study is the first to show the local expression in endometrial tissue of IL-1RII, a potent and specific down-regulator of IL-1 action and its decreased expression in women suffering from endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Receptors, Interleukin-1 Adult Blotting, Western Endometriosis Endometriosis Endometrium Endometrium Endometrium Female Humans Immunohistochemistry Receptors, Interleukin-1 Receptors, Interleukin-1 Type II

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europepmc
last seen: 2026-09-01T06:12:48.306406+00:00
openalex
last seen: 2026-06-10T17:14:06.276822+00:00
pubmed
last seen: 2026-05-13T22:13:30.513821+00:00
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