| First Author | Clark DA | Year | 1998 |
| Journal | J Immunol | Volume | 160 |
| Issue | 2 | Pages | 545-9 |
| PubMed ID | 9551885 | Mgi Jnum | J:45186 |
| Mgi Id | MGI:1194525 | Doi | 10.4049/jimmunol.160.2.545 |
| Citation | Clark DA, et al. (1998) Cytokine-dependent abortion in CBA x DBA/2 mice is mediated by the procoagulant fgl2 prothombinase. J Immunol 160(2):545-9 |
| abstractText | 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 prothombinase 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. |
