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, Vol. 160, No. 2, 15.01.1998, p. 545-9.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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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 -