{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T13:15:08Z","timestamp":1788527708881,"version":"build-2803163510"},"reference-count":63,"publisher":"MDPI AG","issue":"17","license":[{"start":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T00:00:00Z","timestamp":1788480000000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Biology"],"abstract":"<jats:p>Autism spectrum disorder (ASD) is a neurodevelopmental condition characterized by social communication deficits and repetitive behaviors, now affecting approximately 1 in 31 children. While traditionally defined behaviorally, ASD is increasingly understood as a disorder of brain connectivity arising from altered synaptic formation and refinement. This narrative review synthesizes evidence on neuroimmune dysregulation in ASD, focusing on immune-mediated synaptic pruning mechanisms. We conducted a comprehensive literature search in PubMed, Scopus, and Web of Science (2010\u20132026), prioritizing high-impact peer-reviewed research. Convergent findings suggest that the classical complement cascade (C1q-C3) tags specific synapses for elimination, while microglia participate in the phagocytic removal of tagged connections. Genetic studies have reported associations between ASD and variants in complement-related genes (C1q, C3, CR3, and C4A, although the strongest evidence for C4A-mediated pruning comes from schizophrenia research), as well as in microglial function genes (TREM2, PTEN, SHANK3). Neuroimaging reveals a dynamic pattern of local hyperconnectivity transitioning to long-range hypoconnectivity during development, particularly affecting prefrontal, insular, and cerebellar regions. Systemic inflammation, including gut\u2013brain axis dysbiosis and maternal immune activation, may amplify neuroimmune dysregulation. We conclude that ASD can be understood, in part, as a disorder of synaptic immunology, where disrupted neuroimmune communication during critical developmental windows may contribute to altered connectivity. The complement\u2013microglia axis therefore represents a potential mechanistic target for future therapeutic investigation.<\/jats:p>","DOI":"10.3390\/biology15171539","type":"journal-article","created":{"date-parts":[[2026,9,4]],"date-time":"2026-09-04T12:20:46Z","timestamp":1788524446000},"page":"1539","update-policy":"https:\/\/doi.org\/10.3390\/mdpi_crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["Neuroimmune Dysregulation and Synaptic Pruning in Autism Spectrum Disorder"],"prefix":"10.3390","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0004-8905-2911","authenticated-orcid":false,"given":"Abdel","family":"Bernal-Reyes","sequence":"first","affiliation":[{"name":"Department of Immunology, Instituto de Ciencias B\u00e1sicas y Precl\u00ednicas \u201cVictoria de Gir\u00f3n\u201d, Universidad de Ciencias M\u00e9dicas de La Habana, La Habana 10600, Cuba"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ormany","family":"Soriano-Torres","sequence":"additional","affiliation":[{"name":"Department of Immunology, Instituto de Ciencias B\u00e1sicas y Precl\u00ednicas \u201cVictoria de Gir\u00f3n\u201d, Universidad de Ciencias M\u00e9dicas de La Habana, La Habana 10600, Cuba"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Iris Dany Carmenate","family":"Rodr\u00edguez","sequence":"additional","affiliation":[{"name":"Hospital Pedi\u00e1trico Provincial \u201cDocente Jos\u00e9 Mart\u00ed\u201d, Sancti Spiritus 60100, Cuba"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Deanira","family":"Patrone","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine, Division of Biotechnology, Molecular Biology and Histology, University of Campania \u201cL. Vanvitelli\u201d, 80138 Naples, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nicola","family":"Antonucci","sequence":"additional","affiliation":[{"name":"Biomedical Centre for Autism Research and Treatment, 70126 Bari, Italy"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3779-2596","authenticated-orcid":false,"given":"Dario","family":"Siniscalco","sequence":"additional","affiliation":[{"name":"Department of Experimental Medicine, Division of Biotechnology, Molecular Biology and Histology, University of Campania \u201cL. 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