article · American Journal of Reproductive Immunology
The postdelivery decline in chemokines observed in this study has not previously been reported. This shift may result from two mechanisms: greater-than-expected placental chemokine production or the degradation of key signaling molecules during parturition and early uterine involution. Additionally, the rise in proinflammatory markers from enrollment to postdelivery suggests a persistent inflammatory state, either unaffected by fetal delivery or worsened by tissue damage in the gestational parent.
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DOI: 10.1111/aji.70147
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