title: Involvement of decidual Valpha14 NKT cells in abortion.
abstract: The immunological mechanisms that regulate abortion are largely unknown. Here, we found that a distinct subset of lymphocytes, Valpha14 NKT cells expressing an invariant antigen receptor encoded by Valpha14/Jalpha281 and Vbeta7 segments, accumulated in the decidua during pregnancy and provoked abortion upon stimulation with alpha-galactosylceramide (alpha-GalCer), a specific ligand for Valpha14 NKT cells. The alpha-GalCer-mediated abortion was not observed in Valpha14 NKT-, IFN-gamma-, tumor necrosis factor alpha-, or perforin-knock-out mice and appeared to be due to the degeneration of embryonic trophoblasts mediated by the activated Valpha14 NKT cells whose perforin-dependent killing and production of IFN-gamma and tumor necrosis factor alpha were essential. The possible role of the decidual Valpha14 NKT cells in the pathogenesis of abortion is discussed.
authors.affiliation: CREST (Core Research for Evolutional Science and Technology) Project and Department of Molecular Immunology, Graduate School of Medicine, Chiba University, Japan.
authors.forename: K
authors.initials: K
authors.lastname: Ito
authors.forename: M
authors.initials: M
authors.lastname: Karasawa
authors.forename: T
authors.initials: T
authors.lastname: Kawano
authors.forename: T
authors.initials: T
authors.lastname: Akasaka
authors.forename: H
authors.initials: H
authors.lastname: Koseki
authors.forename: Y
authors.initials: Y
authors.lastname: Akutsu
authors.forename: E
authors.initials: E
authors.lastname: Kondo
authors.forename: S
authors.initials: S
authors.lastname: Sekiya
authors.forename: K
authors.initials: K
authors.lastname: Sekikawa
authors.forename: M
authors.initials: M
authors.lastname: Harada
authors.forename: M
authors.initials: M
authors.lastname: Yamashita
authors.forename: T
authors.initials: T
authors.lastname: Nakayama
authors.forename: M
authors.initials: M
authors.lastname: Taniguchi
mesh_terms: D000028:Abortion, Induced; D000818:Animals; D016207:Cytokines / Q000378:metabolism; D003656:Decidua / Q000166:cytology*; D005260:Female; D005434:Flow Cytometry; D005699:Galactosylceramides / Q000009:adverse effects; D007371:Interferon-gamma / Q000378:metabolism; D007694:Killer Cells, Natural / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D008297:Male; D008562:Membrane Glycoproteins / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D011247:Pregnancy; D016693:Receptors, Antigen, T-Cell, alpha-beta / Q000378:metabolism*; D013047:Specific Pathogen-Free Organisms; D014327:Trophoblasts / Q000187:drug effects / Q000473:pathology; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism
chemical_list: D016207:Cytokines; D005699:Galactosylceramides; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D016693:Receptors, Antigen, T-Cell, alpha-beta; D014409:Tumor Necrosis Factor-alpha; D054353:Perforin; D007371:Interferon-gamma