ReviewFrontiers in immunology2026
Research progress on the relationship between the TdT gene and autoimmune diseases.
Review in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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0 citing papers in PubMed.
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autoimmune diseases (AIDs) are caused by defects in immune tolerance or abnormalities in immune regulation, leading to damage to host organs. The pathogenesis of AIDs is complex, and their clinical manifestations are diverse. Currently, the pathogenesis of AIDs is not fully understood. Accumulating evidence from experimental models suggests that TdT-mediated antigen receptor diversification may influence autoimmune responses and immune regulation. Although emerging evidence from human autoimmune diseases has been reported, the current understanding of the relationship between TdT and AIDs remains limited. Understanding the mechanisms by which TdT influences autoimmune responses may provide new insights into disease pathogenesis and future therapeutic exploration. This review summarizes relevant information on the TdT gene and discusses current evidence regarding the relationship between TdT and AIDs, with particular emphasis on findings from experimental models and emerging evidence from human autoimmune diseases.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.