IMMUNOLOGY2026™ Conference Recordings For Attendees-IL-9 at the Maternal-Fetal Interface Drives a Novel Immunological Mechanism of Preterm Labor and Birth

IL-9 at the Maternal-Fetal Interface Drives a Novel Immunological Mechanism of Preterm Labor and Birth

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Video Summary

The speaker described research on IL-9 signaling at the maternal-fetal interface as a potential novel cause of idiopathic preterm labor and birth. In humans, IL-9 was found mainly in decidual CD4 and CD8 T cells and was increased in idiopathic preterm labor. In a mouse model, intrauterine IL-9 injection caused preterm birth and neonatal death, while IL-9 neutralization or IL-9 receptor knockout protected against these outcomes. Unlike infectious/inflammatory preterm birth, IL-9 did not cause fetal growth restriction, systemic inflammation, or progesterone withdrawal. Mechanistically, IL-9 promoted cervical shortening, fetal membrane activation with MMP-9-driven collagen degradation, and immune signaling changes involving macrophages. IL-9 also crossed into the fetal compartment. Finally, prophylactic vitamin D3 reduced IL-9-mediated preterm birth and neonatal mortality, suggesting possible translational relevance.

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Date April 17, 2026 4:00 PM - 4:15 PM

Room 253

Session Regulation of Immunity and Inflammation in the Genital Tract

Speaker Eva Kareus

Track Mucosal And Regional Immunology (MUC)

Year 2026

Keywords

IL-9 signaling

idiopathic preterm birth

maternal-fetal interface

vitamin D3

MMP-9 collagen degradation

April 17, 2026 4:00 PM - 4:15 PM

253

Regulation of Immunity and Inflammation in the Genital Tract

Eva Kareus

Mucosal And Regional Immunology (MUC)

2026