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Human Decidual CD1a+ Dendritic Cells Undergo Functional Maturation Program Mediated by Gp96 (CROSBI ID 323109)

Prilog u časopisu | izvorni znanstveni rad | međunarodna recenzija

Gulić, Tamara ; Laskarin, Gordana ; Glavan, Lana ; Grubić Kezele, Tanja ; Haller, Herman ; Rukavina, Daniel. Human Decidual CD1a+ Dendritic Cells Undergo Functional Maturation Program Mediated by Gp96 // International journal of molecular sciences, 24 (2023), 3; 2278-2293. doi: 10.3390/ijms24032278

Podaci o odgovornosti

Gulić, Tamara ; Laskarin, Gordana ; Glavan, Lana ; Grubić Kezele, Tanja ; Haller, Herman ; Rukavina, Daniel.

engleski

Human Decidual CD1a+ Dendritic Cells Undergo Functional Maturation Program Mediated by Gp96

Heat shock proteins (hsps), in certain circumstances, could shape unique features of decidual dendritic cells (DCs) that play a key role in inducing immunity as well as maintaining tolerance. The aim of the study was to assess the binding of gp96 to Toll-like receptor (TLR) 4 and CD91 receptors on decidual CD1a+ DCs present at the maternal-fetal interface in vitro as well as the influence of CD1a+ DCs maturation status. Immunohistology and immunofluorescence of paraffin-embedded first-trimester decidua tissue sections of normal and pathological (missed abortion MA and blighted ovum BO) pregnancies were performed together with flow cytometry detection of antigens in CD1a+ DCs after gp96 stimulation of decidual mononuclear cells. Gp96 efficiently bound CD91 and TLR4 receptors on decidual CD1a+ DCs in a dose-dependent manner and increased the expression of CD83 and HLA-DR. The highest concentration of gp96 (1000 ng/mL) increased the percentage of Interferon-γ (INF-γ) and IL-15 expressing gp96+ cells. Gp96 binds CD91 and TLR4 on decidual CD1a+ DCs, which causes their maturation and significantly increases INF-γ and IL-15 in the context of Th1 cytokine/chemokine domination, which could support immune response harmful for ongoing pregnancy.

decidual dendritic cells ; chemokine ; cytokine ; gp96 ; pregnancy

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Podaci o izdanju

24 (3)

2023.

2278-2293

objavljeno

1422-0067

10.3390/ijms24032278

Trošak objave rada u otvorenom pristupu

APC

Povezanost rada

Kliničke medicinske znanosti, Temeljne medicinske znanosti

Poveznice
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