Journal
EUROPEAN JOURNAL OF IMMUNOLOGY
Volume 48, Issue 6, Pages 937-949Publisher
WILEY
DOI: 10.1002/eji.201747162
Keywords
Adoptive transfer; Dendritic cell (DC); Invariant NKT cell (iNKT cell); Miscarriage; alpha-galactosylceramide (alpha-GalCer)
Categories
Funding
- JSPS KAKENHI [JP17K11255]
- Grants-in-Aid for Scientific Research [17K11255] Funding Source: KAKEN
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Unexpected fetal loss is one of the common complications of pregnancy; however, the pathogenesis of many miscarriages, particularly those not associated with infections, is unknown. We previously found that activated DEC-205(+) dendritic cells (DCs) and NK1.1(+) invariant natural killer T (iNKT) cells are recruited into the myometrium of mice when miscarriage is induced by the intraperitoneal administration of -galactosylceramide (-GalCer). Here we demonstrate that the adoptive transfer of DEC-205(+) bone marrow-derived DCs cocultured with -GalCer (DEC-205(+) BMDCs-c/w--GalCer) directly induced marked fetal loss by syngeneic pregnant C57BL/6 (B6) mice and allogeneic mice (B6 (f) x BALB/c (o)), which was accompanied by the accumulation of activated iNKT cells in the myometrium. Further, the adoptive transfer of NK1.1(+) iNKT cells obtained from B6 mice injected with -GalCer facilitated miscarriages in syngeneic J18((-/-)) (iNKT cell-deficient) mice. These results suggest that DEC-205(+) DCs and NK1.1(+) iNKT cells play crucial roles required for the initiation of fetal loss associated with stimulation by glycolipid antigens and sterile inflammation.
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