Cytokine-dependent abortion in CBA x DBA/2 mice is mediated by the procoagulant fgl2 prothrombinase [correction of prothombinase]

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Cytokine-dependent abortion in CBA x DBA/2 mice is mediated by the procoagulant fgl2 prothrombinase [correction of prothombinase]. / Clark, D A; Chaouat, G; Arck, P C; Mittrücker, Hans-Willi; Levy, G A.

in: J IMMUNOL, Jahrgang 160, Nr. 2, 15.01.1998, S. 545-9.

Publikationen: SCORING: Beitrag in Fachzeitschrift/ZeitungSCORING: ZeitschriftenaufsatzForschungBegutachtung

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@article{3d072a79f3064115af517835e1bf11b6,
title = "Cytokine-dependent abortion in CBA x DBA/2 mice is mediated by the procoagulant fgl2 prothrombinase [correction of prothombinase]",
abstract = "Spontaneous resorption in the CBA x DBA/2 model is attributed to NK cells, macrophages, and Th1-type cytokines. In vivo depletion of NK cells by anti-asialoGM1 Ab or macrophage depletion by silicon dioxide treatment reduced abortion rates, which could no longer be boosted by injecting TNF-alpha (which activates NK cells) or IFN-gamma (which activates macrophages). TNF-alpha + gamma-IFN coadministration aborted >80% of the embryos whether or not NK cells or macrophages had been depleted or estradiol + progesterone was injected to correct potential reduction in ovarian function by cytokines. The cytokines also aborted IRF1+/+ C57BL/6 but not IRF1-/- females pregnant by IRF1+/+ DBA/2. Both spontaneous and cytokine-boosted abortions in CBA x DBA/2 were blocked by Ab to fgl2 prothrombinase [corrected] expressed by cytokine-stimulated vascular endothelial cells and monocytes; in vivo Ab depletion of granulocytes also prevented TNF-alpha + IFN-gamma-induced abortions. Cytokine-triggered thrombotic/inflammatory processes in maternal uteroplacental blood vessels causes abortion.",
keywords = "Abortion, Spontaneous, Animals, Crosses, Genetic, Cytokines, DNA-Binding Proteins, Endothelium, Vascular, Female, Fibrinogen, Granulocytes, Immune Sera, Injections, Intraperitoneal, Interferon Regulatory Factor-1, Interferon-gamma, Killer Cells, Natural, Macrophages, Mice, Mice, Inbred C57BL, Mice, Inbred CBA, Mice, Inbred DBA, Mice, Knockout, Phosphoproteins, Pregnancy, Thromboplastin",
author = "Clark, {D A} and G Chaouat and Arck, {P C} and Hans-Willi Mittr{\"u}cker and Levy, {G A}",
year = "1998",
month = jan,
day = "15",
language = "English",
volume = "160",
pages = "545--9",
journal = "J IMMUNOL",
issn = "0022-1767",
publisher = "American Association of Immunologists",
number = "2",

}

RIS

TY - JOUR

T1 - Cytokine-dependent abortion in CBA x DBA/2 mice is mediated by the procoagulant fgl2 prothrombinase [correction of prothombinase]

AU - Clark, D A

AU - Chaouat, G

AU - Arck, P C

AU - Mittrücker, Hans-Willi

AU - Levy, G A

PY - 1998/1/15

Y1 - 1998/1/15

N2 - Spontaneous resorption in the CBA x DBA/2 model is attributed to NK cells, macrophages, and Th1-type cytokines. In vivo depletion of NK cells by anti-asialoGM1 Ab or macrophage depletion by silicon dioxide treatment reduced abortion rates, which could no longer be boosted by injecting TNF-alpha (which activates NK cells) or IFN-gamma (which activates macrophages). TNF-alpha + gamma-IFN coadministration aborted >80% of the embryos whether or not NK cells or macrophages had been depleted or estradiol + progesterone was injected to correct potential reduction in ovarian function by cytokines. The cytokines also aborted IRF1+/+ C57BL/6 but not IRF1-/- females pregnant by IRF1+/+ DBA/2. Both spontaneous and cytokine-boosted abortions in CBA x DBA/2 were blocked by Ab to fgl2 prothrombinase [corrected] expressed by cytokine-stimulated vascular endothelial cells and monocytes; in vivo Ab depletion of granulocytes also prevented TNF-alpha + IFN-gamma-induced abortions. Cytokine-triggered thrombotic/inflammatory processes in maternal uteroplacental blood vessels causes abortion.

AB - Spontaneous resorption in the CBA x DBA/2 model is attributed to NK cells, macrophages, and Th1-type cytokines. In vivo depletion of NK cells by anti-asialoGM1 Ab or macrophage depletion by silicon dioxide treatment reduced abortion rates, which could no longer be boosted by injecting TNF-alpha (which activates NK cells) or IFN-gamma (which activates macrophages). TNF-alpha + gamma-IFN coadministration aborted >80% of the embryos whether or not NK cells or macrophages had been depleted or estradiol + progesterone was injected to correct potential reduction in ovarian function by cytokines. The cytokines also aborted IRF1+/+ C57BL/6 but not IRF1-/- females pregnant by IRF1+/+ DBA/2. Both spontaneous and cytokine-boosted abortions in CBA x DBA/2 were blocked by Ab to fgl2 prothrombinase [corrected] expressed by cytokine-stimulated vascular endothelial cells and monocytes; in vivo Ab depletion of granulocytes also prevented TNF-alpha + IFN-gamma-induced abortions. Cytokine-triggered thrombotic/inflammatory processes in maternal uteroplacental blood vessels causes abortion.

KW - Abortion, Spontaneous

KW - Animals

KW - Crosses, Genetic

KW - Cytokines

KW - DNA-Binding Proteins

KW - Endothelium, Vascular

KW - Female

KW - Fibrinogen

KW - Granulocytes

KW - Immune Sera

KW - Injections, Intraperitoneal

KW - Interferon Regulatory Factor-1

KW - Interferon-gamma

KW - Killer Cells, Natural

KW - Macrophages

KW - Mice

KW - Mice, Inbred C57BL

KW - Mice, Inbred CBA

KW - Mice, Inbred DBA

KW - Mice, Knockout

KW - Phosphoproteins

KW - Pregnancy

KW - Thromboplastin

M3 - SCORING: Journal article

C2 - 9551885

VL - 160

SP - 545

EP - 549

JO - J IMMUNOL

JF - J IMMUNOL

SN - 0022-1767

IS - 2

ER -