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Identification of a unique intervillous cellular signature in chronic histiocytic intervillositis
Juliette Krop1, Lotte E van der Meeren2, Marie-Louise P van der Hoorn3
1Department of Immunology, Leiden University Medical Centre, Leiden, the Netherlands.
Insights
Chronic histiocytic intervillositis (CHI) involves CD68+ cells in the placenta, linked to poor pregnancy outcomes. This study identified unique CHI cell clusters, offering potential new therapeutic targets for this rare condition.
Area of Science:
- Reproductive immunology
- Placental pathology
Background:
- Chronic histiocytic intervillositis (CHI) is a rare placental lesion associated with adverse pregnancy outcomes.
- The underlying pathophysiological mechanisms of CHI are not fully understood but are thought to be immunologically driven.
Purpose of the Study:
- To investigate the phenotype of the cellular infiltrate in Chronic histiocytic intervillositis (CHI).
- To gain a better understanding of the immunological mechanisms underlying CHI.
Main Methods:
- Utilized imaging mass cytometry for in-depth visualization of maternal immune cells within the intervillous space.
- Examined the spatial orientation of immune cells in relation to the fetal syncytiotrophoblast.
Main Results:
- Identified three phenotypically distinct CD68+, HLA-DR+, CD38+ cell clusters specific to CHI.
- Observed decreased expression of the immunosuppressive enzyme CD39 on syncytiotrophoblast cells near these identified cell clusters.
Conclusions:
- The findings provide novel insights into the phenotype of CD68+ cells in CHI.
- The identified unique cell clusters in CHI may serve as targets for future therapeutic strategies.
Introduction:
Chronic histiocytic intervillositis (CHI) is a rare histopathological lesion in the placenta characterized by an infiltrate of CD68+ cells in the intervillous space. CHI is associated with adverse pregnancy outcomes such as miscarriage, fetal growth restriction, and (late) intrauterine fetal death. The adverse pregnancy outcomes and a variable recurrence rate of 25-100% underline its clinical relevance. The pathophysiologic mechanism of CHI is unclear, but it appears to be immunologically driven. The aim of this study was to obtain a better understanding of the phenotype of the cellular infiltrate in CHI.
Method:
We used imaging mass cytometry to achieve in-depth visualization of the intervillous maternal immune cells and investigated their spatial orientation in situ in relation to the fetal syncytiotrophoblast.
Results:
We found three phenotypically distinct CD68+HLA-DR+CD38+ cell clusters that were unique for CHI. Additionally, syncytiotrophoblast cells in the vicinity of these CD68+HLA-DR+CD38+ cells showed decreased expression of the immunosuppressive enzyme CD39.
Discussion:
The current results provide novel insight into the phenotype of CD68+ cells in CHI. The identification of unique CD68+ cell clusters will allow more detailed analysis of their function and could result in novel therapeutic targets for CHI.
