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In this study, phenazine biosynthesis\u2010like domain\u2010containing protein (PBLD) is identified as a key modulator of the STING\u2010dependent antiviral type I interferon (IFN) response by suppressing coiled\u2010coil domain\u2010containing protein 50 (CCDC50)\u2010mediated selective autophagic degradation of STING. Notably, viral infection downregulates PBLD expression through two distinct mechanisms: transcriptional suppression via reduced transcription factor EB (TFEB) activity, and post\u2010translational degradation through an enhanced membrane\u2010associated RING finger protein 2 (MARCH2)\u2010mediated ubiquitin\u2010proteasome pathway. Together, these mechanisms establish a negative feedback loop that facilitates viral immune evasion. Moreover,\n                    <jats:italic>Pbld<\/jats:italic>\n                    \u2010deficient mice exhibit increased susceptibility to human adenovirus type 4 (HAdV\u20104) infection compared with their wild\u2010type (WT) littermates. Importantly,\n                    <jats:italic>Pbld\u2010<\/jats:italic>\n                    deficiency in the 2,6,10,14\u2010tetramethylpentadecane (TMPD)\u2010induced lupus mice model attenuates STING expression and diminishes autoimmune phenotypes. Clinically, PBLD expression is elevated in patients with systemic lupus erythematosus and positively correlates with STING\u2010driven type I IFN signaling. Taken together, PBLD plays a dual role in STING\u2010mediated innate immunity against viral infection and autoimmunity, highlighting its potential as a therapeutic target for both antiviral infections and autoimmune diseases.\n                  <\/jats:p>","DOI":"10.1002\/advs.202514512","type":"journal-article","created":{"date-parts":[[2025,11,8]],"date-time":"2025-11-08T11:00:07Z","timestamp":1762599607000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["PBLD Orchestrates the STING\u2010Mediated Antiviral Immune Response and Autoimmune Diseases"],"prefix":"10.1002","volume":"13","author":[{"given":"Peili","family":"Hou","sequence":"first","affiliation":[{"name":"Ruminant Diseases Research Center, Key Laboratory of Animal Resistant Biology of Shandong College of Life Sciences Shandong Normal University  Jinan Shandong 250358 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