Evidence map›Paper›PMID 34335595›Full record

ReviewFrontiers in immunology2021

Revisiting the Antigen-Presenting Function of β Cells in T1D Pathogenesis.

Yang Li, Fei Sun, Tian-Tian Yue, Fa-Xi Wang, Chun-Liang Yang, Jia-Hui Luo, Shan-Jie Rong, Fei Xiong, Shu Zhang, Cong-Yi Wang

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
4.7field-weighted citation impact, top 5% of its field
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

29 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. METTL3-mediated mMolecular biology reports · 2025
    Review
  12. Review
  13. Review
  14. Article
  15. Article
  16. Article
  17. Engineered extracellular vesicles as "supply vehicles" to alleviate type 1 diabetes.Extracellular vesicles and circulating nucleic acids · 2024
    Article
  18. Review
  19. Article
  20. Review
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

10 authors at 2 institutions in 1 country.

Yang LiThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei SunThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Tian-Tian YueThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fa-Xi WangThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Chun-Liang YangThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Jia-Hui LuoThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Shan-Jie RongThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Fei XiongThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Shu ZhangThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Cong-Yi WangThe Center for Biomedical Research, Department of Respiratory and Critical Care Medicine, NHC Key Laboratory of Pulmonary Diseases, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.
Huazhong University of Science and Technology · CNTongji Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is characterized by the unresolved autoimmune inflammation and islet β cell destruction. The islet resident antigen-presenting cells (APCs) including dendritic cells and macrophages uptake and process the β cell-derived antigens to prime the autoreactive diabetogenic T cells. Upon activation, those autoreactive T cells produce copious amount of IFN-γ, TNF-α and IL-1β to induce β cell stress and death. Autoimmune attack and β cell damage intertwine together to push forward this self-destructive program, leading to T1D onset. However, β cells are far beyond a passive participant during the course of T1D development. Herein in this review, we summarized how β cells are actively involved in the initiation of autoimmune responses in T1D setting. Specifically, β cells produce modified neoantigens under stressed condition, which is coupled with upregulated expression of MHC I/II and co-stimulatory molecules as well as other immune modules, that are essential properties normally exhibited by the professional APCs. At the cellular level, this subset of APC-like β cells dynamically interacts with plasmacytoid dendritic cells (pDCs) and manifests potency to activate autoreactive CD4 and CD8 T cells, by which β cells initiate early autoimmune responses predisposing to T1D development. Overall, the antigen-presenting function of β cells helps to explain the tissue specificity of T1D and highlights the active roles of structural cells played in the pathogenesis of various immune related disorders.

Indexed as

Antigen PresentationAnimalsB-LymphocytesDiabetes Mellitus, Type 1HumansIslets of Langerhansantigen presentationautoimmune diabetescrosstalkinnate immunityβ cell

Identifiers

PMID34335595
PMCPMC8318689
OpenAlexW3182602740

What OpenQuestion holds

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LicenceCC BY
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Registered trials

None linked

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.