Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6

Yeny Martinez De La Torre, Chiara Buracchi, Elena M. Borroni, Jana Dupor, Raffaella Bonecchi, Manuela Nebuloni, Fabio Pasqualini, Andrea Doni, Eleonora Lauri, Chiara Agostinis, Roberta Bulla, Donald N. Cook, Bodduluri Haribabu, Pierluigi Meroni, Daniel Rukavina, Luca Vago, Francesco Tedesco, Annunciata Vecchi, Sergio A. Lira, Massimo LocatiAlberto Mantovani

Research output: Contribution to journalArticlepeer-review


Fetal loss in animals and humans is frequently associated with inflammatory conditions. D6 is a promiscuous chemokine receptor with decoy function, expressed in lymphatic endothelium, that recognizes and targets to degradation most inflammatory CC chemokines. Here, we report that D6 is expressed in placenta on invading extravillous trophoblasts and on the apical side of syncytiotrophoblast cells, at the very interface between maternal blood and fetus. Exposure of D6-/- pregnant mice to LPS or antiphospholipid autoantibodies results in higher levels of inflammatory CC chemokines and increased leukocyte infiltrate in placenta, causing an increased rate of fetal loss, which is prevented by blocking inflammatory chemokines. Thus, the promiscuous decoy receptor for inflammatory CC chemokines D6 plays a nonredundant role in the protection against fetal loss caused by systemic inflammation and antiphospholipid antibodies.

Original languageEnglish
Pages (from-to)2319-2324
Number of pages6
JournalProceedings of the National Academy of Sciences of the United States of America
Issue number7
Publication statusPublished - Feb 13 2007


  • Leukocyte
  • Placenta
  • Trophoblast

ASJC Scopus subject areas

  • Genetics
  • General


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