ArticleJournal of immunology research2026
Mitochondrial Transcription Factor A Deficiency in T Cells Leads to Activation of the Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase/Stimulator of Interferon Genes Pathway and Production of Autoantibodies in Mice.
Article in Journal of immunology research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
2 citing papers in PubMed.
- Steaming and Sodium Bicarbonate-Assisted Aqueous Extraction ofFoods (Basel, Switzerland) · 2026Article
- Mitochondrial Transcription Factor A Deficiency in T Cells Leads to Activation of the Cyclic Guanosine Monophosphate-Adenosine Monophosphate Synthase/Stimulator of Interferon Genes Pathway and Production of Autoantibodies in Mice.Journal of immunology research · 2026Article
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Authors and funding
6 authors.
Funding
Abstract
Mitochondrial transcription factor A (TFAM) is a key regulator of mitochondrial DNA transcription and replication. T cell-specific TFAM-deficient mice are immunocompromised, often succumbing to viral infection, and their T cells are unresponsive to T-cell antigen receptor (TCR) stimulation, suggesting that TFAM-mediated mitochondrial activity regulates T-cell 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-mediated autoimmune responses. Thus, besides regulating T-cell 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-specific TFAM-deficient mice. We detected anti-double-strand (ds) DNA antibody, and interferon alpha (IFNα) and IFNγ in the serum of TFAM
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