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Here, we use functional genomics data from studies of <jats:italic>BCL11B<\/jats:italic> to investigate the contribution of neuronal and immune processes to SCZ pathophysiology. We identified the gene targets of BCL11B in brain striatal cells (n = 223 genes), double negative 4 (DN4) developing T cells (n = 114 genes) and double positive (DP) developing T cells (n = 518 genes) using an integrated analysis of RNA\u2010seq and ChIP\u2010seq data. No gene\u2010set was enriched for genes containing common variants associated with SCZ but the DP gene\u2010set was enriched for genes containing missense de novo mutations (DNMs; <jats:italic>p<\/jats:italic> = .001) using data from 3,447 SCZ trios. Post hoc analysis revealed the enrichment to be stronger for DP genes negatively regulated by BCL11B. Biological processes enriched for genes negatively regulated by BCL11B in DP gene\u2010set included immune system development and cytokine signaling. These analyses, leveraging a GWAS\u2010identified SCZ risk gene and data on gene expression and transcription factor binding, indicate that DNMs in immune pathways contribute to SCZ risk.<\/jats:p>","DOI":"10.1002\/ajmg.b.32811","type":"journal-article","created":{"date-parts":[[2020,7,30]],"date-time":"2020-07-30T06:36:01Z","timestamp":1596090961000},"page":"370-379","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["Genes regulated by <scp>BCL11B<\/scp> during T\u2010cell development are enriched for de novo mutations found in schizophrenia patients"],"prefix":"10.1002","volume":"183","author":[{"given":"Laura","family":"Fahey","sequence":"first","affiliation":[{"name":"Cognitive Genetics and Cognitive Therapy Group, Centre for Neuroimaging &amp; Cognitive Genomics, School of Psychology and Discipline of Biochemistry National University of Ireland Galway  Galway Ireland"},{"name":"School of Mathematics, Statistics and Applied Mathematics National University of Ireland Galway  Galway Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-3037-7426","authenticated-orcid":false,"given":"Gary","family":"Donohoe","sequence":"additional","affiliation":[{"name":"Cognitive Genetics and Cognitive Therapy Group, Centre for Neuroimaging &amp; Cognitive Genomics, School of Psychology and Discipline of Biochemistry National University of Ireland Galway  Galway Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6702-8564","authenticated-orcid":false,"given":"Pilib \u00d3.","family":"Broin","sequence":"additional","affiliation":[{"name":"School of Mathematics, Statistics and Applied Mathematics National University of Ireland Galway  Galway Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-3413-570X","authenticated-orcid":false,"given":"Derek W.","family":"Morris","sequence":"additional","affiliation":[{"name":"Cognitive Genetics and Cognitive Therapy Group, Centre for Neuroimaging &amp; Cognitive Genomics, School of Psychology and Discipline of Biochemistry National University of Ireland Galway  Galway Ireland"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[2020,7,29]]},"reference":[{"key":"e_1_2_8_2_1","doi-asserted-by":"publisher","DOI":"10.1084\/jem.20070863"},{"key":"e_1_2_8_3_1","doi-asserted-by":"publisher","DOI":"10.1038\/ejhg.2015.218"},{"key":"e_1_2_8_4_1","unstructured":"Andrews S.(2012). 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