ArticleChinese medical journal2026
Elucidating the functional dynamics of DNASE1L2 intron retention in tuberculosis progression.
Article in Chinese medical journal, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
15 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIntron retention (IR) is an important biological process associated with disease development. However, the role of IR in the progression of tuberculosis (TB) remains unexplored. Therefore, this study aimed to characterize the dynamic IR landscape during TB progression and elucidate the role of DNASE1L2 -IR in this process.
methodsWe conducted a comprehensive high-throughput sequencing analysis using 1729 samples from 19 public datasets and identified candidate IR events associated with TB progression. We then validated these candidate IR events in three macrophage infection models by quantitative polymerase chain reaction and revealed the underlying molecular mechanisms by investigating the subcellular localization and functional roles of their associated isoforms.
resultsIn an analysis of 1729 clinical specimens, we found genome-wide intron-splicing reprogramming in host cells during TB progression. Notably, deoxyribonuclease 1 like 2 ( DNASE1L2, a gene encoding deoxyribonuclease)-IR exhibited striking differences among healthy controls, individuals with latent TB infection, and individuals with active TB ( Padj <0.05), particularly between progressors and nonprogressors ( Padj <0.0001). Similar differences were observed in Mycobacterium tuberculosis ( M. tuberculosis ) infection models in vitro ; as the stimulation increased in concentration or duration, IR initially increased but subsequently decreased. DNASE1L2 -IR generated two transcript isoforms: a long isoform ( DNASE1L2 -L) and a short isoform ( DNASE1L2 -S). Upon stimulation, DNASE1L2-L appeared in the cytoplasm, whereas DNASE1L2-S remained membrane-anchored. Deoxyribonuclease activity assays revealed that compared with DNASE1L2-S, DNASE1L2-L exhibited significantly greater enzymatic activity against plasmid and M. tuberculosis DNA substrates and more effectively suppressed the release of interleukin-1beta and tumor necrosis factor alpha, indicating isoform-specific functional divergence in inflammatory regulation.
conclusionThese findings identify DNASE1L2 -IR splicing dynamics as a novel biomarker for monitoring TB progression and reveal a host-defense mechanism in which DNASE1L2 -IR regulates M. tuberculosis DNA degradation to modulate TB progression.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.