{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,27]],"date-time":"2026-07-27T19:12:16Z","timestamp":1785179536366,"version":"3.55.0"},"reference-count":44,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2026,7,12]],"date-time":"2026-07-12T00:00:00Z","timestamp":1783814400000},"content-version":"vor","delay-in-days":192,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,1,1]],"date-time":"2026-01-01T00:00:00Z","timestamp":1767225600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Immunology Research"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:p>\n                    Mitochondrial transcription factor A (TFAM) is a key regulator of mitochondrial DNA transcription and replication. T cell\u2010specific TFAM\u2010deficient mice are immunocompromised, often succumbing to viral infection, and their T cells are unresponsive to T\u2010cell antigen receptor (TCR) stimulation, suggesting that TFAM\u2010mediated mitochondrial activity regulates T\u2010cell activity, such as effector function and memory formation. In contrast to the attenuation of immune response, TFAM deficiency may also induce inflammatory responses, raising the possibility that TFAM deficiency results in inflammation\u2010mediated autoimmune responses. Thus, besides regulating T\u2010cell function, TFAM plays important roles in autoimmune responses. However, its role in autoimmune diseases remains uncertain. We aimed to investigate the role of TFAM in autoimmune diseases using T cell\u2010specific TFAM\u2010deficient mice. We detected anti\u2010double\u2010strand (ds) DNA antibody, and interferon alpha (IFN\u03b1) and IFN\u03b3 in the serum of TFAM\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    CD4Cre mice after 30 weeks of age. Mononuclear cell infiltration was observed in the kidneys. TFAM\u2010deficient T cells exhibited leakage of mitochondrial DNA into the cytoplasm. Cytoplasmic mitochondrial DNA was associated with activation of TANK\u2010binding kinase 1 (TBK1) and IFN regulatory factor 3 (IRF3)\u2014the downstream molecules of the nucleic acid sensor cyclic guanosine monophosphate\u2013adenosine monophosphate synthase\/stimulator of IFN genes (cGAS\/STING) machinery. mRNA expression of type I IFN genes was elevated in T cells from TFAM\n                    <jats:sup>fl\/fl<\/jats:sup>\n                    CD4Cre mice. The suppressive function of Foxp3\n                    <jats:sup>+<\/jats:sup>\n                    regulatory T (Treg) cells, which play a major role in establishment of peripheral tolerance, was reduced in the absence of TFAM. Our findings suggest that T cells in TFAM\u2010deficient conditions may contribute to immune instability and autoimmune responses by inducing type I IFN\u2010mediated inflammatory responses.\n                  <\/jats:p>","DOI":"10.1155\/jimr\/2594317","type":"journal-article","created":{"date-parts":[[2026,7,13]],"date-time":"2026-07-13T06:52:36Z","timestamp":1783925556000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["Mitochondrial Transcription Factor A Deficiency in T Cells Leads to Activation of the Cyclic Guanosine Monophosphate\u2013Adenosine Monophosphate Synthase\/Stimulator of Interferon Genes Pathway and Production of Autoantibodies in 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