New insights into pattern recognition receptors and their ligands in gynecologic pathologies

Yoshihiko Yamada, Yamada Y, Shigetomi H, Hiroshi Shigetomi, Onogi A, Akira Onogi, Shoji Haruta, Haruta S, Ryuji Kawaguchi, Kawaguchi R, Yoshida S, Shozo Yoshida, Furukawa N, Naoto Furukawa, Nagai A, Akira Nagai, Yasuhito Tanase, Tanase Y, Taihei Tsunemi, Tsunemi T, Hidekazu Oi, Oi H, Kobayashi H, Hiroshi Kobayashi
Human immunology · 2010 · vol. 72(3) , pp. 213–218 · doi:10.1016/j.humimm.2010.12.009 · PMID:21167248 · W2058393441
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⚙ AI-generated summary by claude@2026-06, 2026-06-10 ⓘ

This review explores pattern recognition receptors and their ligands, discussing their involvement and potential therapeutic roles in gynecologic pathologies.

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Abstract

In the ovary, clear cell carcinoma (CCC) and endometrioid adenocarcinoma occur in the setting of endometriosis. In this review, we discuss the role of innate immune responses, specifically endogenous ligands (also known as "alarmins"), their pattern recognition receptors (PRRs) and their signaling pathways, in the pathogenesis of ovarian cancer, in particular, endometriosis-associated ovarian cancer. This article reviews the English-language literature for pathogenesis and pathophysiological studies on endometriosis and ovarian cancer. Here, we show that iron functions as an endogenous ligand and can induce chromosomal instability through production of reactive oxygen intermediates-induced oxidative stress. Several important CCC-related genes overlap with those known to be associated with hepatocyte nuclear factor-1β-dependent oxidative stress. Aberrant expression of PRRs and HNF-1β in endometriosis has been reported in the setting of chronic inflammation and oxidative stress pathways, which lie downstream of these genes. A concerted overexpression of alarmins, their receptors and HNF-1β might be required for endometriosis carcinogenesis. Recent advances in innate immunity illuminate the molecular mechanism underlying inflammation-induced carcinogenesis. Upregulation of PRRs expression may synergize with activation of HNF-1β signaling to accelerate endometriosis proliferation and cause carcinogenesis.

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Condition tags

endometriosis

MeSH descriptors

Endometriosis Immunity, Innate Ovarian Neoplasms Receptors, Pattern Recognition Receptors, Pattern Recognition Chromosomal Instability Endometriosis Endometriosis Endometriosis Endometriosis Female Hepatocyte Nuclear Factor 1-beta Hepatocyte Nuclear Factor 1-beta Hepatocyte Nuclear Factor 1-beta Humans Iron Iron Iron Ligands Ovarian Neoplasms

Citation neighborhood

Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

References (88)

Cited by (5)

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License: CC0 · commercial use OK