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We identified biallelic loss-of-function mutations in\n            <jats:italic>LTBR,<\/jats:italic>\n            encoding the lymphotoxin beta receptor (LT\u03b2R), primarily expressed on stromal cells. Patients with LT\u03b2R deficiency had hypogammaglobulinemia, diminished memory B cells, regulatory and follicular T helper cells, and dysregulated expression of several tumor necrosis factor family members. B cell differentiation in an ex vivo coculture system was intact, implying that the observed B cell defects were not intrinsic in nature and instead resulted from LT\u03b2R-dependent stromal cell interaction signaling critical for SLO formation. Collectively, we define a human inborn error of immunity caused primarily by a stromal defect affecting the development and function of SLOs.\n          <\/jats:p>","DOI":"10.1126\/sciimmunol.adq8796","type":"journal-article","created":{"date-parts":[[2024,11,22]],"date-time":"2024-11-22T19:03:32Z","timestamp":1732302212000},"update-policy":"https:\/\/doi.org\/10.34133\/aaas_crossmark","source":"Crossref","is-referenced-by-count":13,"title":["LT\u03b2R deficiency causes lymph node aplasia and impaired B cell differentiation"],"prefix":"10.1126","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0009-0005-3243-1846","authenticated-orcid":true,"given":"Bernhard","family":"Ransmayr","sequence":"first","affiliation":[{"name":"St. Anna Children\u2019s Cancer Research Institute, Vienna, Austria."},{"name":"CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Vienna, Austria."},{"name":"Ludwig Boltzmann Institute for Rare and Undiagnosed Diseases, Vienna, 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