Evidence map›Paper›PMID 28479600›Full record

ArticleCellular & molecular immunology2018

A crucial role of the PD-1H coinhibitory receptor in suppressing experimental asthma.

Huafeng Liu, Xin Li, Li Hu, Min Zhu, Bailin He, Liqun Luo, Lieping Chen

Erratum issuedOpen access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

28 citing papers in PubMed, 40 citations in OpenAlex.

  1. Article
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  11. Review
  12. VISTA (PD-1H) Is a Crucial Immune Regulator to Limit Pulmonary Fibrosis.American journal of respiratory cell and molecular biology · 2023
    Article
  13. Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Review
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  20. Exploring the VISTA of microglia: immune checkpoints in CNS inflammation.Journal of molecular medicine (Berlin, Germany) · 2020
    Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Huafeng LiuLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Xin LiLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Li HuLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Min ZhuLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Bailin HeLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Liqun LuoLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China.
Lieping ChenLaboratory of Immunotherapy, Sun Yet-Sen University, Guangzhou, Guangdong, People's Republic of China. lieping.chen@yale.edu.
Sun Yat-sen University · CN

Funding

Yale Pathology Tissue Services Shared ResourceP30CA016359 · NCI · YALE UNIVERSITY · PI MEGAN C KING · 1985 to 2026
$85.0M
Yale SPORE in Lung Cancer (YSILC): The Biology and Personalized Treatment of Lung CancerP50CA196530 · NCI · YALE UNIVERSITY · PI Kurt A Schalper · 2015 to 2026
$31.1M
Personalizing NSCLC Therapy: Exploiting KRAS activated pathwaysR01CA155196 · NCI · YALE UNIVERSITY · PI HERBST, ROY S, PAPADIMITRAKOPOULOU, VASSILIKI · 2011 to 2015
$2.8M
NCI NIH HHS P30 CA016359NCI NIH HHS P50 CA196530NCI NIH HHS R01 CA155196
6 · The paper itself

Abstract

Programmed death one homolog (PD-1H) is a cell surface molecule of the B7/CD28 immune modulatory gene family. Although PD-1H has been shown to function as a coinhibitory receptor on T cells to limit naive T-cell activation and proliferation, its role in the regulation of the T-cell response to allergens is unknown. We report here that genetic ablation or blockade of PD-1H drastically promotes pulmonary inflammation with massive accumulation of eosinophils in a mouse model of experimental asthma, indicating a suppressive function of PD-1H in allergic inflammation. The loss of PD-1H led to elevated production of both innate cytokines (IL-6, MCP-1 and TNFα) and Th2 cytokines (IL-5 and IL-13) in the lung, indicating a critical role of PD-1H in suppressing the production of airway inflammatory cytokines. In addition, the loss of PD-1H also impaired the expansion of systemic and pulmonary regulatory T cells during asthma induction. These findings support a critical role of intrinsic PD-1H in the regulation of inflammatory responses to allergens. Finally, we showed that treatment with a PD-1H agonistic monoclonal antibody reduced the severity of asthma, which was accompanied by suppressed lung inflammation. Our findings support PD-1H as a potential target and suggest a possible strategy for the treatment of allergic asthma in humans.

Indexed as

AnimalsAntibodies, MonoclonalAsthmaCytokinesDisease Models, AnimalLungMembrane ProteinsMiceMice, Inbred BALB CMice, KnockoutTh2 CellsT-Lymphocytes, RegulatoryAntibodies, MonoclonalCytokinesMembrane ProteinsVsir protein, mouseAsthmaPD-1HTh2VISTA

Identifiers

PMID28479600
PMCPMC6203798
OpenAlexW2124797720

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.