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- W4386640462 abstract "Pregnancy success is critically dependent on specific maternal immune and endocrine adaptions to induce immune tolerance towards the allogenic fetus. Hereby, second pregnancies have been observed to be less prone to obstetric complications and the acquisition of immune memory has been proposed. We could recently show that CD4+ regulatory T (Treg) cells are crucially involved in ameliorating the course of subsequent pregnancies. However, the lack of specific immune markers to reliably detect memory CD4+ Treg cells still aggravates the investigation of immune memory during pregnancy. Therefore, we employed a sophisticated screening approach combining high throughput flow cytometry and machine learning, a method called Infinity Flow. Cells from the uterus-draining lymph nodes were harvested within 7 days postpartum from parous mice allogenically mated twice and virgin control mice. Confirming previous results using conventional flow cytometry, the proportion of the CD4+ Treg cell cluster from parous mice was visibly larger compared to virgin mice. Within the CD4+ Treg cluster, we further observed the highest fold change between virgin and parous samples for Integrin-b7 followed by CD73 and Ly6C. Among the Top10 marker, we could also detect the memory marker CD44 as well as the folate receptor (FR)4 and CD137. We could independently verify higher gene expression levels for FR4 and CD73 in CD4+ Treg cells sorted from parous mice compared to virgin mice. Our results indicate CD73 and FR4 as novel immune memory markers to allow the detection of pregnancy-generated CD4+ Treg cells. A thorough validation in an in-vivo setting remains necessary." @default.
- W4386640462 created "2023-09-13" @default.
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- W4386640462 date "2023-09-01" @default.
- W4386640462 modified "2023-09-27" @default.
- W4386640462 title "Pregnancy-induced memory CD4+ regulatory T cells: identification of specific immune memory markers using Infinity Flow" @default.
- W4386640462 doi "https://doi.org/10.1016/j.jri.2023.104052" @default.
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