Evidence map›Paper›PMID 39587108›Full record

ArticleNature communications2024

Promotion of TLR7-MyD88-dependent inflammation and autoimmunity in mice through stem-loop changes in Lnc-Atg16l1.

Zongheng Yang, Shuchen Ji, Lun Liu, Shuo Liu, Bingjing Wang, Yuanwu Ma, Xuetao Cao

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed.

  1. Review
  2. Article
  3. T cell-intrinsic PRR signaling in immunity and pathology.Acta biochimica et biophysica Sinica · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
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  12. Review
  13. [Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2025
    Article
  14. Review
  15. Article
  16. Article
  17. Article
  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Zongheng Yang *Department of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.ORCID 0000-0001-9662-6435
Shuchen Ji *Department of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Lun LiuDepartment of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Shuo LiuDepartment of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.ORCID 0000-0002-0293-585X
Bingjing WangDepartment of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China.
Yuanwu MaInstitute of Laboratory Animal Science, Chinese Academy of Medical Sciences, Beijing, China.
Xuetao CaoDepartment of Immunology, Center for Immunotherapy, Peking Union Medical College, Chinese Academy of Medical Sciences, Beijing, China. caoxt@immunol.org.ORCID 0000-0001-9677-7647

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82388201
6 · The paper itself

Abstract

Uncontrolled TLR signaling can cause inflammatory immunopathology and trigger autoimmune diseases. For example, TLR7 promotes pathogenesis of systemic lupus erythematosus. However, whether RNA structural changes affect nucleic acids-sensing TLRs signaling and impact disease progression is unclear. Here by iCLIP-seq we identify a TLR7-binding long non-coding RNA, Lnc-Atg16l1, and find that it promotes TLR7 and other MyD88-dependent TLRs signaling in various types of immune cells. Depletion of Lnc-Atg16l1 attenuates development of TLR7-linked autoimmune phenotypes in the mouse SLE model. Mechanistically, we find that Lnc-Atg16l1 binds to TLR7 at bases near U84 and MyD88 at bases around A129. The analysis of Lnc-Atg16l1 in situ structures show that it strengthens the interaction between TIR domain of TLR7 and MyD88 through specific stem-loop structure changes as a molecular scaffold after TLR7 activation to promote TLR7 downstream signaling. Therefore, we discover a mechanism for host RNA regulation of innate signaling and autoimmune disease through its structural changes. These findings provide insights into the pro-inflammatory function of self RNA in a structure-dependent manner and suggest a potential target for TLR-related autoimmune disorders.

Indexed as

AutoimmunityInflammationMembrane GlycoproteinsMyeloid Differentiation Factor 88RNA, Long NoncodingSignal TransductionToll-Like Receptor 7AnimalsDisease Models, AnimalFemaleHEK293 CellsHumansLupus Erythematosus, SystemicMiceMice, Inbred C57BLMice, KnockoutMembrane GlycoproteinsMyd88 protein, mouseMyeloid Differentiation Factor 88RNA, Long NoncodingTlr7 protein, mouseToll-Like Receptor 7

Identifiers

PMID39587108
PMCPMC11589596

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Registered trials

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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.