title: CD1d-restricted NKT cells modulate placental and uterine leukocyte populations during chlamydial infection in mice.
abstract: Invariant CD1d-restricted natural killer T cells play an important immunoregulatory role and can influence a broad spectrum of immunological responses including against bacterial infections. They are present at the fetal-maternal interface and although it has been reported that experimental systemic iNKT cell activation can induce mouse abortion, their role during pregnancy remain poorly understood. In the present work, using a physiological Chlamydia muridarum infection model, we have shown that, in vaginally infected pregnant mice, C. muridarum is cleared similarly in C57BL/6 wild type (WT) and CD1d(-/-) mice. We have also shown that infected- as well as uninfected-CD1d(-/-) mice have the same litter size as WT counterparts. Thus, CD1d-restricted cells are required neither for the resolution of chlamydial infection of the lower-genital tract, nor for the maintenance of reproductive capacity. However, unexpected differences in T cell populations were observed in uninfected pregnant females, as CD1d(-/-) placentas contained significantly higher percentages of CD4(+) and CD8(+) T cells than WT counterparts. However, infection triggered a significant decrease in the percentages of CD4(+) T cells in CD1d(-/-) mice. In infected WT pregnant mice, the numbers of uterine CD4(+) and CD8(+) T cells, monocytes and granulocytes were greatly increased, changes not observed in infected CD1d(-/-) mice. An increase in the percentage of CD8(+) T cells seems independent of CD1d-restricted cells as it occurred in both WT and CD1d(-/-) mice. Thus, in the steady state, the lack of CD1d-restricted NKT cells affects leukocyte populations only in the placenta. In Chlamydia-infected pregnant mice, the immune response against Chlamydia is dampened in the uterus. Our results suggest that CD1d-restricted NKT cells play a role in the recruitment or homeostasis of leukocyte populations at the maternal-fetal interface in the presence or absence of Chlamydia infection.
authors.affiliation: Laboratory of Inflammation, Gestation and Autoimmunity, Jacques Monod Institute, CNRS and University Paris-Diderot, 15 rue Hélène Brion, 75205 Paris Cedex 13, France; Centre d'Immunologie de Marseille-Luminy (CIML), Aix-Marseille University UM2, France; INSERM U1104 and CNRS UMR7280, Marseille, France.
authors.forename: Mohamed
authors.initials: M
authors.lastname: Habbeddine
authors.forename: Philippe
authors.initials: P
authors.lastname: Verbeke
authors.forename: Christiane
authors.initials: C
authors.lastname: Delarbre
authors.forename: René
authors.initials: R
authors.lastname: Moutier
authors.forename: Stéphane
authors.initials: S
authors.lastname: Prieto
authors.forename: David M
authors.initials: DM
authors.lastname: Ojcius
authors.forename: Colette
authors.initials: C
authors.lastname: Kanellopoulos-Langevin
mesh_terms: D000818:Animals; D055610:Antigens, CD1d / Q000378:metabolism*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D018414:CD8-Positive T-Lymphocytes / Q000276:immunology; D002690:Chlamydia Infections / Q000276:immunology* / Q000473:pathology; D023502:Chlamydia muridarum / Q000276:immunology*; D004195:Disease Models, Animal; D005260:Female; D007962:Leukocytes / Q000276:immunology; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009000:Monocytes / Q000276:immunology; D055611:Natural Killer T-Cells / Q000276:immunology*; D010920:Placenta / Q000276:immunology* / Q000473:pathology; D011247:Pregnancy; D011251:Pregnancy Complications, Infectious / Q000276:immunology* / Q000473:pathology; D014599:Uterus / Q000276:immunology* / Q000473:pathology
chemical_list: D055610:Antigens, CD1d; C584692:CD1d antigen, mouse
keywords: Chlamydia infection; Leukocyte populations; Mouse models; NKT cells; Pregnancy