Evidence map›Paper›PMID 30952980›Full record

ArticleNature biomedical engineering2019

Depletion of PD-1-positive cells ameliorates autoimmune disease.

Peng Zhao, Peng Wang, Shuyun Dong, Zemin Zhou, Yanguang Cao, Hideo Yagita, Xiao He, Song Guo Zheng, Simon J Fisher, Robert S Fujinami and 1 more

Open access · greenAbstract read
In one paragraph

Article in Nature biomedical engineering, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 7% 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

48 citing papers in PubMed, 74 citations in OpenAlex.

  1. Understanding the Therapeutic Potential of PD-1 Agonism in Inflammatory and Autoimmune Disorders.BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy · 2026
    Review
  2. Article
  3. Review
  4. Article
  5. The CNS Meninges and the Synovial Joint: Parallel Immunological Structures in Autoimmune Disease.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  6. Article
  7. Review
  8. Review
  9. 3-in-oneiScience · 2025
    Article
  10. Progenitor exhausted PD-1Nature cardiovascular research · 2025
    Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. PD-1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 4 institutions in 2 countries.

Peng ZhaoDepartment of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, University of Utah, Salt Lake City, UT, USA.
Peng WangDepartment of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, University of Utah, Salt Lake City, UT, USA.
Shuyun DongDepartment of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, University of Utah, Salt Lake City, UT, USA.
Zemin ZhouDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Yanguang CaoDivision of Pharmacotherapy and Experimental Therapeutics, The UNC Eshelman School of Pharmacy, University of North Carolina at Chapel Hill, Chapel Hill, NC, USA.
Hideo YagitaDepartment of Immunology, Juntendo University School of Medicine, Tokyo, Japan.
Xiao HeDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Song Guo ZhengDivision of Rheumatology, Department of Medicine, Penn State Milton S. Hershey Medical Center, Hershey, PA, USA.
Simon J FisherDivision of Endocrinology, Metabolism, and Diabetes, Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA.
Robert S FujinamiDepartment of Pathology, University of Utah School of Medicine, Salt Lake City, UT, USA.
Mingnan ChenDepartment of Pharmaceutics and Pharmaceutical Chemistry, College of Pharmacy, University of Utah, Salt Lake City, UT, USA. mingnan.chen@utah.edu.ORCID http://orcid.org/0000-0002-7080-9804
University of Utah · USJuntendo University · JPPenn State Milton S. Hershey Medical Center · USUniversity of North Carolina at Chapel Hill · US

Funding

Therapeutic immunoregulation mediated by TGF-??-induced iTregs in autoimmune arthR01AR059103 · NIAMS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI JARJOUR, WAEL N · 2010 to 2020
$3.9M
Virus-Host Interactions that Lead to EpilepsyR01NS065714 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2010 to 2018
$2.9M
Targeted depletion of programmed death-1 positive cells, a method that not only stops autoimmune attack but also preserves adaptive immunityR01AI139535 · NIAID · UNIVERSITY OF UTAH · PI CHEN, MINGNAN · 2019 to 2024
$2.7M
Viral-induced axonopathy: mechanisms of damage and repairR01NS091939 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S, LANE, THOMAS E · 2016 to 2020
$1.7M
Virus Infection Leads to Autoreactive T Cells Having Multiple TCRsR01NS082102 · NINDS · UNIVERSITY OF UTAH · PI FUJINAMI, ROBERT S · 2013 to 2017
$1.6M
DIABETES ASSOCIATED BRAIN DAMAGE FOLLOWING SEVERE HYPOGLYCEMIAR01NS070235 · NINDS · WASHINGTON UNIVERSITY · PI FISHER, SIMON J · 2010 to 2014
$1.5M
Enhancing cytotoxic T lymphocyte (CTL) responses by directly loading CTL epitope vaccines onto MHC Class I complexes on the dendritic cell surfaceR21EB024083 · NIBIB · UNIVERSITY OF UTAH · PI CHEN, MINGNAN · 2017 to 2018
$417k
NIAID NIH HHS R01 AI139535NIAMS NIH HHS R01 AR059103NIBIB NIH HHS R21 EB024083NINDS NIH HHS R01 NS065714NINDS NIH HHS R01 NS070235NINDS NIH HHS R01 NS082102NINDS NIH HHS R01 NS091939
6 · The paper itself

Abstract

Targeted suppression of autoimmune diseases without collateral suppression of normal immunity remains an elusive yet clinically important goal. Targeted blockade of programmed-cell-death-protein-1 (PD-1)-an immune checkpoint factor expressed by activated T cells and B cells-is an efficacious therapy for potentiating immune activation against tumours. Here we show that an immunotoxin consisting of an anti-PD-1 single-chain variable fragment, an albumin-binding domain and Pseudomonas exotoxin targeting PD-1-expressing cells, selectively recognizes and induces the killing of the cells. Administration of the immunotoxin to mouse models of autoimmune diabetes delays disease onset, and its administration in mice paralysed by experimental autoimmune encephalomyelitis ameliorates symptoms. In all mouse models, the immunotoxin reduced the numbers of PD-1-expressing cells, of total T cells and of cells of an autoreactive T-cell clone found in inflamed organs, while maintaining active adaptive immunity, as evidenced by full-strength immune responses to vaccinations. The targeted depletion of PD-1-expressing cells contingent to the preservation of adaptive immunity might be effective in the treatment of a wide range of autoimmune diseases.

Indexed as

Adaptive ImmunityADP Ribose TransferasesAmino Acid SequenceAnimalsAutoimmune DiseasesBacterial ToxinsDiabetes Mellitus, Type 1Encephalomyelitis, Autoimmune, ExperimentalExotoxinsFemaleHumansMice, Inbred C57BLMice, Inbred NODProgrammed Cell Death 1 ReceptorProtein DomainsPseudomonas aeruginosa Exotoxin AADP Ribose TransferasesBacterial ToxinsExotoxinsProgrammed Cell Death 1 ReceptorPseudomonas aeruginosa Exotoxin AVirulence Factors

Identifiers

PMID30952980
PMCPMC6452906
OpenAlexW2918647367

What OpenQuestion holds

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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.