Evidence map›Paper›PMID 30396745›Full record

ReviewJournal of autoimmunity2019

PD-1 immunobiology in systemic lupus erythematosus.

Colleen S Curran, Sarthak Gupta, Ignacio Sanz, Elad Sharon

Open access · greenAbstract readReview
In one paragraph

Review in Journal of autoimmunity, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 67 papers.

0numbers the graph read from it
0cells of the map it votes in
67citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

67 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Defective B cell tolerance in SLE lymph nodes underpins VHmedRxiv : the preprint server for health sciences · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Immune Modulatory Effects of PD-1/PD-L1 in Myasthenia Gravis: Insights From Peripheral Blood Mononuclear Cell Analysis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Surface PD-1 expression in T cells is suppressed by HNRNPK through an exonic splicing silencer on exon 3.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  16. Article
  17. Review
  18. Article
  19. Article
  20. Immune Checkpoint Inhibitors and Lupus Erythematosus.Pharmaceuticals (Basel, Switzerland) · 2024
    Review

7 more citing papers are in PubMed but not listed here.

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

4 authors at 4 institutions in 1 country.

Colleen S CurranCritical Care Medicine Department, Clinical Center, National Institutes of Health, Bethesda, MD, USA. Electronic address: colleen.curran@nih.gov.
Sarthak GuptaSystemic Autoimmunity Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA. Electronic address: sarthak.gupta@nih.gov.
Ignacio SanzEmory University School of Medicine, Atlanta, GA, USA. Electronic address: ignacio.sanz@emory.edu.
Elad SharonCancer Therapy Evaluation Program, Division of Cancer Treatment & Diagnosis, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA. Electronic address: sharone@mail.nih.gov.
Emory University · USNational Cancer Institute · USNational Institutes of Health · USNational Institutes of Health Clinical Center · US

Funding

Intramural NIH HHS Z99 CA999999
6 · The paper itself

Abstract

Programmed death (PD)-1 receptors and their ligands have been identified in the pathogenesis and development of systemic lupus erythematosus (SLE). Two key pathways, toll-like receptor and type I interferon, are significant to SLE pathogenesis and modulate the expression of PD-1 and the ligands (PD-L1, PD-L2) through activation of NF-κB and/or STAT1. These cell signals are regulated by tyrosine kinase (Tyro, Axl, Mer) receptors (TAMs) that are aberrantly activated in SLE. STAT1 and NF-κB also exhibit crosstalk with the aryl hydrocarbon receptor (AHR). Ligands to AHR are identified in SLE etiology and pathogenesis. These ligands also regulate the activity of the Epstein-Barr virus (EBV), which is an identified factor in SLE and PD-1 immunobiology. AHR is important in the maintenance of immune tolerance and the development of distinct immune subsets, highlighting a potential role of AHR in PD-1 immunobiology. Understanding the functions of AHR ligands as well as AHR crosstalk with STAT1, NF-κB, and EBV may provide insight into disease development, the PD-1 axis and immunotherapies that target PD-1 and its ligand, PD-L1.

Indexed as

Disease SusceptibilityAnimalsAutoimmunityBiomarkersEpstein-Barr Virus InfectionsGene Expression RegulationHerpesvirus 4, HumanHumansImmunityLupus Erythematosus, SystemicProgrammed Cell Death 1 ReceptorReceptors, Aryl HydrocarbonSignal TransductionBiomarkersProgrammed Cell Death 1 ReceptorReceptors, Aryl HydrocarbonAryl hydrocarbon receptorEpstein-Barr virusPD-1Systemic lupus erythematosus

Identifiers

PMID30396745
PMCPMC7449827
OpenAlexW2898677536

What OpenQuestion holds

Textmetadata
LicenceTDM
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.