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Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6 (CROSBI ID 134354)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Martinez de la Torre, Y. ; Buracchi, C. ; Borroni, E. M. ; Dupor, J. ; Bonecchi, R. ; Nebuloni, M. ; Pasqualini, F. ; Doni, A. ; Lauri, E. ; Agostinis, C. et al. Protection against inflammation- and autoantibody-caused fetal loss by the chemokine decoy receptor D6 // Proceedings of the National Academy of Sciences of the United States of America, 104 (2007), 7; 2319-2324-x

Podaci o odgovornosti

Martinez de la Torre, Y. ; Buracchi, C. ; Borroni, E. M. ; Dupor, J. ; Bonecchi, R. ; Nebuloni, M. ; Pasqualini, F. ; Doni, A. ; Lauri, E. ; Agostinis, C. ; Bulla, R. ; Cook, D. N. ; Haribabu, B. ; Meroni, P. ; Rukavina, Daniel ; Vago, L. ; Tedesco, F. ; Vecchi, A. ; Lira, S. A. ; Locati, M. ; Mantovani, A.

engleski

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

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.

trophoblast; leukocyte; placenta; decoy receptor D6

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Podaci o izdanju

104 (7)

2007.

2319-2324-x

objavljeno

0027-8424

Povezanost rada

Temeljne medicinske znanosti

Indeksiranost