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One environmental factor, maternal immune activation (MIA)\u2014in which pathogenic infection during pregnancy increases ASD risk in offspring\u2014disproportionately affects males. However, the basis for this male-specific vulnerability, and the mechanisms by which inflammatory signals cross the maternal-fetal interface to affect the male embryo, remain largely unknown. Using the poly(I:C) mouse model of neurodevelopmental disorders, we characterize fetal, placental, and amniotic changes occurring within twenty-four hours of MIA. We find that 30% of embryos exhibit large-scale teratogenic abnormalities\u2014ranging from decreased fetal weight to altered sensory organ development\u2014while 70% develop normally. These abnormalities occur exclusively in a subset of males, never in females. Single-nucleus transcriptomics revealed robust induction of pro-inflammatory gene programs in the placentas of affected males across a broad range of cell types, and most prominently in spongiotrophoblasts\u2014fetally derived cells that partly form the maternal-fetal border. These cells simultaneously downregulate extracellular matrix and hormone biosynthesis pathways, coinciding with a breakdown in placental structural integrity and the accumulation of immune cells and cytokines in the amniotic fluid. One such cytokine, IL-6, is required for MIA-evoked developmental abnormalities to emerge. Our data indicate that MIA drives a rapid shift from an immunosuppressive to a pro-inflammatory maternal-fetal interface in a vulnerable subset of male embryos, producing acute, sex-restricted developmental deficits. We propose that male embryos may express unique proteins capable of triggering this inflammatory response, which\u2014combined with MIA-induced loss of maternal immunosuppression\u2014selectively derails male embryonic development.<\/jats:p>","DOI":"10.64898\/2026.02.02.703351","type":"posted-content","created":{"date-parts":[[2026,2,3]],"date-time":"2026-02-03T15:15:15Z","timestamp":1770131715000},"source":"Crossref","is-referenced-by-count":2,"title":["Maternal-fetal immune conflict contributes to male-specific impairments in a mouse model of neurodevelopmental disorders"],"prefix":"10.64898","author":[{"given":"Irene","family":"Sanchez-Martin","sequence":"first","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bharti","family":"Kukreja","sequence":"additional","affiliation":[{"name":"Division of Newborn Medicine, Boston Children\u2019s Hospital; Boston, MA, 02115, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Paige","family":"Henderson","sequence":"additional","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"},{"name":"Graduate Program in Genetics, Stony Brook University, Stony Brook, NY, 11794, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qianyu","family":"Lin","sequence":"additional","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"DiMartino","sequence":"additional","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Valerie","family":"Bagan","sequence":"additional","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Justin","family":"Park","sequence":"additional","affiliation":[{"name":"Cold Spring Harbor Laboratory; Cold Spring Harbor, NY, 11724, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian T.","family":"Kalish","sequence":"additional","affiliation":[{"name":"Division of Newborn Medicine, Boston Children\u2019s Hospital; Boston, MA, 02115, USA"},{"name":"F.M. 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