Maternal obesity is associated with a higher number of regulatory‐T‐cells in newborns without affecting suppression
Background Maternal obesity (MO) is associated with a higher risk of immune‐mediated diseases in the offspring and higher leptin levels in cord blood (CB). This study evaluates the number and function of lymphocyte subtypes in CB related to MO and its relationship with leptin concentration and lepti...
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Published in | American journal of reproductive immunology (1989) Vol. 89; no. 4; pp. e13687 - n/a |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
Denmark
Wiley Subscription Services, Inc
01.04.2023
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Subjects | |
Online Access | Get full text |
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Summary: | Background
Maternal obesity (MO) is associated with a higher risk of immune‐mediated diseases in the offspring and higher leptin levels in cord blood (CB). This study evaluates the number and function of lymphocyte subtypes in CB related to MO and its relationship with leptin concentration and leptin receptor expression.
Methods
Pregnant women with (n = 32) or without obesity (n = 41) were enrolled at delivery. Cord blood mononuclear cells were separated with Ficoll‐Hypaque. B and CD4+, regulatory and effector T cells were quantified by Flow Cytometry. Cord blood leptin concentration was measured by ELISA, and the leptin receptor (sLepR) on Treg cells was determined by Flow Cytometry.
Results
MO was associated with higher numbers of CD4+, Treg and effector T cells in the CB of their offspring, without differences in the suppressive function of Tregs. Female offspring had a higher number of these cells and a higher cord leptin concentration. Tregs expressed higher levels of sLepR than effector T cells, without differences between groups.
Conclusions
MO is associated with changes in the newborn's immune profile, more evident in female newborns with higher leptin concentrations. More studies are needed to identify the mechanisms by which the high levels of cord leptin in the newborn of women with obesity could affect the offspring's immune system. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1046-7408 1600-0897 |
DOI: | 10.1111/aji.13687 |