CXCL8 blockade reduces fibrosis in endometriosis

Endometriosis is a common condition that leads to pain and infertility, but treatment options are limited. The disease is associated with chronic inflammation, and several inflammatory chemokines have been implicated in its progression. Here, the authors examined the expression of inflammatory genes in endometriotic tissue samples and identified the chemokine CXCL8 (also known as IL-8) and its receptors CXCR1 and CXCR2 as being highly upregulated in women with endometriosis. CXCL8 was also highly expressed in cynomolgus monkeys that spontaneously developed endometriosis, and preliminary experiments suggested that targeting CXCL8 reduced fibrotic disease in these animals. The authors engineered a long-lasting antibody against CXCL8 (AMY109) and showed that therapeutic delivery of this agent reduced disease in a surgically induced model of endometriosis in cynomolgus monkeys. AMY109 seemed to reduce the fibrotic disease associated with endometriosis, at least in part by blocking neutrophil recruitment and activation. The authors report that trials of AMY109 in humans are now underway. This is a preview of subscription content, access via your institution Access options Access Nature and 54 other Nature Portfolio journals Get Nature+, our best-value online-access subscription 27,99 € / 30 days cancel any time Subscribe to this journal Receive 12 print issues and online access 251,40 € per year only 20,95 € per issue Buy this article - Purchase on SpringerLink - Instant access to the full article PDF. 39,95 € Prices may be subject to local taxes which are calculated during checkout References Original article Nishimoto-Kakiuchi, A. et al. A long-acting anti–IL-8 antibody improves inflammation and fibrosis in endometriosis. Sci. Transl. Med. https://doi.org/10.1126/scitranslmed.abq5858 (2023) Author information Authors and Affiliations Corresponding author Rights and permissions About this article Cite this article Bordon, Y. CXCL8 blockade reduces fibrosis in endometriosis. Nat Rev Immunol 23, 203 (2023). https://doi.org/10.1038/s41577-023-00861-1 Published: Version of record: Issue date: DOI: https://doi.org/10.1038/s41577-023-00861-1