Alternative functions of the complement protein C1q at embryo implantation site

Chiara Agostinis, Francesco Tedesco, Roberta Bulla

Research output: Contribution to journalShort surveypeer-review


Complement component C1q is one of the recognition molecules of the complement system which can serve several functions unrelated to complement activation. This molecule is produced at foeto-maternal interface by macrophages as wells as by decidual endothelial cells and invading trophoblast. Foetal trophoblast cells migrating through the decidua in the early stages of pregnancy synthesize and express C1q on their surface, which is actively involved in promoting trophoblast endovascular and interstitial invasion of the decidua. These functions are mediated by two cell surface receptors, gC1qR and α4β1 integrin, which promote trophoblast adhesion and migration through the activation of ERK1/2 MAPKs. C1q−/− mice manifest increased frequency of foetal resorption, reduced foetal weight, and smaller litter size when compared to their wild-type counterparts, suggesting that defective local production of C1q may be involved in pregnancy disorders, such as pre-eclampsia. C1q acts also as a strong angiogenic factor and promotes neovascularization. These studies suggest novel and unexpected roles of this complement component in physiological and pathological pregnancies.

Original languageEnglish
Pages (from-to)74-80
Number of pages7
JournalJournal of Reproductive Immunology
Publication statusPublished - Feb 1 2017


  • C1q
  • Complement system
  • Innate immunity
  • Pre-eclampsia
  • Trophoblast invasion

ASJC Scopus subject areas

  • Immunology and Allergy
  • Immunology
  • Reproductive Medicine
  • Obstetrics and Gynaecology


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