ArticleMicrobes and infection2013
CD1d-restricted NKT cells modulate placental and uterine leukocyte populations during chlamydial infection in mice.
Article in Microbes and infection, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Single-cell map of innate-like lymphocyte response toiScience · 2025Article
- Review
- Article
- The Pathophysiological Relevance of the iNKT Cell/Mononuclear Phagocyte Crosstalk in Tissues.Frontiers in immunology · 2018Review
- Decidual vascular endothelial cells promote maternal-fetal immune tolerance by inducing regulatory T cells through canonical Notch1 signaling.Immunology and cell biology · 2016Article
- Leukocyte population dynamics and detection of IL-9 as a major cytokine at the mouse fetal-maternal interface.PloS one · 2014Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
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.
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