{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,1]],"date-time":"2026-11-01T02:36:16Z","timestamp":1793500576733,"version":"4.5.0"},"reference-count":29,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T00:00:00Z","timestamp":1776729600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Anti\u2013interferon-\u03b3 autoantibodies (AIGAs) are an established cause of adult-onset immunodeficiency (AOID), predisposing individuals to disseminated intracellular infections such as\n                      <jats:italic>Talaromyces marneffei<\/jats:italic>\n                      (TM). However, their role in promoting persistent immune dysregulation and subsequent lymphomagenesis remains poorly understood.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Case presentation<\/jats:title>\n                    <jats:p>\n                      A 63-year-old Chinese female with high-titer AIGAs (1:2500) initially presented with disseminated TM. Despite antifungal therapy, her clinical course was complicated by recurrent opportunistic infections\u2014including\n                      <jats:italic>Varicella-zoster virus<\/jats:italic>\n                      (VZV) and\n                      <jats:italic>Mycobacterium persicum<\/jats:italic>\n                      (\n                      <jats:italic>M. persicum<\/jats:italic>\n                      ), and steroid-dependent inflammatory episodes. Approximately two years after the initial presentation, she developed an\n                      <jats:italic>Epstein-Barr virus<\/jats:italic>\n                      (EBV)-positive aggressive B-cell lymphoma, confirmed by mass biopsy and PET\/CT. Despite treatment with rituximab and broad-spectrum antimicrobials, she died of Gram-negative septic shock. Whole-exome sequencing (WES) revealed a CREBBP p.Q278P mutation, providing a genetic perspective on her disease susceptibility.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>This case illustrates a rare progression from AIGAs-associated immunodeficiency to EBV-driven lymphoma, suggesting a \u201ctriple-hit\u201d pathogenic model that warrants further investigation, comprising: (1) AIGAs-associated AOID; (2) chronic antigenic stimulation from persistent infections that may exacerbate immune dysregulation; and (3) a CREBBP mutation that may act as a genetic contributor to malignant transformation. This case underscores the necessity for rigorous tumor surveillance and individualized treatment in patients with AIGAs-associated immunodeficiency.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.3389\/fimmu.2026.1783319","type":"journal-article","created":{"date-parts":[[2026,4,21]],"date-time":"2026-04-21T09:40:12Z","timestamp":1776764412000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":2,"title":["Case Report: From Talaromyces marneffei infection to EBV-positive lymphoma in an adult with anti-IFN-\u03b3 autoantibody-associated immunodeficiency"],"prefix":"10.3389","volume":"17","author":[{"given":"Yan","family":"Ning","sequence":"first","affiliation":[{"name":"Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Guangxi Medical University","place":["Nanning, Guangxi, 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