Proceedings of the National Academy of Sciences of the United States of America · 2007
Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Martinez de la Torre Yeny, Buracchi Chiara, Borroni Elena M, Dupor Jana, Bonecchi Raffaella, Nebuloni Manuela, Pasqualini Fabio, Doni Andrea, Lauri Eleonora, Agostinis Chiara, Bulla Roberta, Cook Donald N, Haribabu Bodduluri, Meroni Pierluigi, Rukavina Daniel, Vago Luca, Tedesco Francesco, Vecchi Annunciata, Lira Sergio A, Locati Massimo, Mantovani Alberto
Аннотация
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.