Evidence map›Paper›PMID 35788761›Full record

ArticleNature metabolism2022

PD-1 signaling facilitates activation of lymphoid tissue inducer cells by restraining fatty acid oxidation.

Di Wu, Luni Hu, Mengwei Han, Yichen Deng, Yime Zhang, Guanqun Ren, Xingyu Zhao, Zongxian Li, Peng Li, Yinlian Zhang and 6 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature metabolism, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed, 1 pooled it
4.0field-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

33 citing papers in PubMed, 1 synthesis or guideline pooled it, 45 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. DNA From Neutrophil Extracellular Traps Restricts Group 3 Innate Lymphoid Cells Function in Intestinal Epithelial Repair via CCDC25.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2026
    Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. IL-22, a vital cytokine in autoimmune diseases.Clinical and experimental immunology · 2024
    Review
  15. Article
  16. Article
  17. Article
  18. Intestinal CXCR6Immunity · 2024
    Article
  19. Group 3 innate lymphoid cells in intestinal health and disease.Nature reviews. Gastroenterology & hepatology · 2024
    Review
  20. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

16 authors at 2 institutions in 1 country.

Di Wu *Institute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.ORCID http://orcid.org/0000-0003-0317-2337
Luni Hu *Institute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Mengwei Han *Institute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Yichen DengInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Yime ZhangInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Guanqun RenInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Xingyu ZhaoInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Zongxian LiInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Peng LiInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Yinlian ZhangInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China.
Shanwen ChenDivision of General Surgery, Peking University First Hospital, Beijing, China.
Jun LiDepartment of Gastroenterology, Peking University Third Hospital, Beijing, China.
Yanyan ShiResearch Center of Clinical Epidemiology, Peking University Third Hospital, Beijing, China.
Jianxin XueDepartment of Thoracic Oncology, Cancer Center and State Key Laboratory of Biotherapy, West China Hospital, Sichuan University, Chengdu, China.
Pengyuan WangDivision of General Surgery, Peking University First Hospital, Beijing, China.
Chao ZhongInstitute of Systems Biomedicine, Department of Immunology, NHC Key Laboratory of Medical Immunology (Peking University), Beijing Key Laboratory of Tumor Systems Biology, Peking University Health Science Center, Beijing, China. zhongc@pku.edu.cn.ORCID http://orcid.org/0000-0003-1744-6378
Peking University · CNSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-programmed death-1 (PD-1) immunotherapy that aims to restore T cell activity in cancer patients frequently leads to immune-related adverse events such as colitis. However, the underlying mechanism is still elusive. Here, we find that Pdcd1-deficient mice exhibit disrupted gut microbiota and aggravated dextran sulfate sodium (DSS)-induced colitis. In addition to T cells, PD-1 is also substantially expressed in colonic lymphoid tissue inducer (LTi) cells. During DSS-induced colitis, LTi cell activation is accompanied by increased PD-1 expression, whereas PD-1 deficiency results in reduced interleukin-22 (IL-22) production by LTi cells and exacerbated inflammation. Mechanistically, activated LTi cells reprogram their metabolism toward carbohydrate metabolism and fatty acid synthesis, while fatty acid oxidation (FAO) is unchanged. However, PD-1 deficiency leads to significantly elevated FAO in LTi cells, which in turn attenuates their activation and IL-22 production. Consistently, FAO suppression efficiently restores IL-22 production in Pdcd1

Indexed as

ColitisLymphoid TissueAnimalsFatty AcidsMiceT-Lymphocytes, Helper-InducerFatty Acids

Identifiers

PMID35788761
OpenAlexW4283792495

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.