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To address this gap, we investigated the impact of spontaneous pregravid obesity, independent of obesogenic diet, on fetal immune ontogeny in a rhesus macaque model. Using spectral flow cytometry, multiplex cytokine profiling, functional stimulation assays, and single\u2370cell RNA sequencing, we profiled immune composition, function, transcriptional profiles, and intercellular communication in umbilical cord blood as well as fetal spleen and lung. Pregravid obesity was associated with altered fetal organ growth, elevated inflammatory mediators, altered frequencies of immune cell populations, and hyperresponsiveness to stimulation by splenic and lung leukocytes. Single\u2370cell transcriptomic analyses revealed tissue\u2370specific reprogramming of innate immune cells, including heightened inflammatory, migratory, and metabolic signatures with impaired antigen presentation. Moreover, there was evidence of impaired T cell differentiation, premature effector differentiation, and B cell dysfunction. Cell\u2013cell communication analysis identified loss of tolerogenic signaling and enhanced proinflammatory pathways across spleen and lung myeloid cells. These findings demonstrate that spontaneous pregravid obesity fundamentally reshapes fetal circulating and tissue\u2370resident immune cells, providing mechanistic insight into the increased susceptibility to infection, respiratory diseases, and immune dysregulation observed in offspring of mothers with obesity.<\/jats:p>","DOI":"10.64898\/2026.03.27.714880","type":"posted-content","created":{"date-parts":[[2026,3,31]],"date-time":"2026-03-31T15:50:25Z","timestamp":1774972225000},"source":"Crossref","is-referenced-by-count":1,"title":["Spontaneous Pregravid Obesity Reshapes Fetal Immune Ontogeny in a Nonhuman Primate Model"],"prefix":"10.64898","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8107-724X","authenticated-orcid":false,"given":"Brianna M.","family":"Doratt","sequence":"first","affiliation":[{"name":"Department of Microbiology, Immunology, and Molecular Genetics, College of Medicine, University of Kentucky, Lexington, KY, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sheridan","family":"Wagner","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Molecular Genetics, College of Medicine, University of Kentucky, Lexington, KY, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Uriel","family":"Avila","sequence":"additional","affiliation":[{"name":"Division of Metabolic Health and Disease, Oregon National Primate Research Center, Beaverton, OR, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Travis","family":"Hodge","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Oregon National Primate Research Center, Beaverton, OR, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lauren D.","family":"Martin","sequence":"additional","affiliation":[{"name":"Division of Comparative Medicine, Oregon National Primate Research Center, Beaverton, OR, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Oleg","family":"Varlamov","sequence":"additional","affiliation":[{"name":"Division of Metabolic Health and Disease, Oregon National Primate Research Center, Beaverton, OR, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3203-2405","authenticated-orcid":false,"given":"Ilhem","family":"Messaoudi","sequence":"additional","affiliation":[{"name":"Department of Microbiology, Immunology, and Molecular Genetics, College of Medicine, University of Kentucky, Lexington, KY, United States"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"54368","reference":[{"key":"2026040304250484000_2026.03.27.714880v1.1","doi-asserted-by":"crossref","unstructured":"1. 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