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CD1d-restricted NKT cells modulate placental and uterine leukocyte populations during chlamydial infection in mice
Institution:1. Laboratory of Inflammation, Gestation and Autoimmunity, Jacques Monod Institute, CNRS and University Paris-Diderot, 15 rue Hélène Brion, 75205 Paris Cedex 13, France;2. Centre d''Immunologie de Marseille-Luminy (CIML), Aix-Marseille University UM2, France;3. INSERM U1104 and CNRS UMR7280, Marseille, France;4. Health Sciences Research Institute and School of Natural Sciences, University of California, 5200 North Lake Road, Merced, CA 95343, USA;1. Departamento de Biotecnología y Bioingeniería, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV-IPN), Av. IPN # 2508, Col. San Pedro Zacatenco, Delg. Gustavo A. Madero, CP 07360 México, DF, Mexico;2. Departamento de Infectómica y Patogénesis Molecular, Centro de Investigación y de Estudios Avanzados del Instituto Politécnico Nacional (CINVESTAV-IPN), Av. IPN # 2508, Col. San Pedro Zacatenco, Delg. Gustavo A. Madero, CP 07360 México, DF, Mexico;3. Laboratório de Ultraestrutura Celular, Universidade Santa Úrsula, Rua Jornalista Orlando Dantas 36, Botafogo, CEP 22231-010 Rio de Janeiro, Brazil;1. Institute of Application Science, Harbin University of Science and Technology, Harbin 150080, China;2. Key Laboratory of Engineering Dielectric and Its Application, Ministry of Education, Harbin University of Science and Technology, Harbin 150080, China;1. Hydrosolutions Ltd., 8005 Zürich, Switzerland;2. Institute of Environmental Engineering, ETH Zürich, 8093 Zürich, Switzerland;3. IBG-3 Agrosphere, Forschungszentrum Jülich, 52425 Jülich, Germany;4. Institute of Hydraulic Engineering, University of Stuttgart, 70569 Stuttgart, Germany
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.
Keywords:NKT cells  Mouse models  Leukocyte populations  Pregnancy
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