Evidence map›Paper›PMID 16087865›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2005

Establishment of NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes.

Jian Wang, Taku Yoshida, Fumio Nakaki, Hiroshi Hiai, Taku Okazaki, Tasuku Honjo

2 registry-linked trialsOpen access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to 2 registered trials, which are not on this map. Cited by 246 papers, 7 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
246citing papers in PubMed, 7 pooled it
9.1field-weighted citation impact, top 2% 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.

NCT02259621 phase2active not recruitingnot on this mapstarted 2014, after this paper: background citation

Neoadjuvant Nivolumab, or Nivolumab in Combination With Ipilimumab, in Resectable Non-Small-Cell Lung Cancer.

TypeinterventionalSponsorSidney Kimmel Comprehensive Cancer Center at Johns HopkinsRan2014 to 2027Enrolled39ConditionsNon-Small Cell Lung CancerArmsNivolumab, Carboplatin, Paclitaxel, Ipilimumab
NCT03918252 phase2active not recruitingnot on this mapstarted 2019, after this paper: background citation

Neoadjuvant Immune Checkpoint Blockade in Resectable Malignant Pleural Mesothelioma

TypeinterventionalSponsorSidney Kimmel Comprehensive Cancer Center at Johns HopkinsRan2019 to 2028Enrolled30ConditionsMesotheliomaArmsNivolumab Injection, Ipilimumab Injection
3 · Its place in the literature

Who cites it

246 citing papers in PubMed, 7 syntheses or guidelines pooled it, 427 citations in OpenAlex.

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  19. The PD-1/PD-L1 pathway and Epstein-Barr virus.European journal of medical research · 2025
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186 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

6 authors at 2 institutions in 1 country.

Jian WangDepartment of Medical Chemistry and Molecular Biology, Graduate School of Medicine, Kyoto University, Yoshida-Konoe, Sakyo-ku, Kyoto 606-8501, Japan.
Taku Yoshida
Fumio Nakaki
Hiroshi Hiai
Taku Okazaki
Tasuku Honjo
Kyoto University · JPShiga Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mice deficient in programmed cell death 1 (PD-1, Pdcd1), an immunoinhibitory receptor belonging to the CD28/cytotoxic T lymphocyte-associated antigen-4 family, spontaneously develop lupus-like autoimmune disease and autoimmune dilated cardiomyopathy on C57BL/6 and BALB/c backgrounds, respectively. However, how PD-1 deficiency induces different forms of autoimmune diseases on these two strains was unknown. Here, we report that PD-1 deficiency specifically accelerates the onset and frequency of type I diabetes in NOD (nonobese diabetic) mice, with strong T helper 1 polarization of T cells infiltrating into islets. These results suggest that PD-1 deficiency accelerates autoimmune predisposition of the background strain, leading to the induction of different forms of autoimmune diseases depending on the genetic background of the strain. Using NOD-Pdcd1-/- mice as an efficient animal model of type I diabetes, we screened diabetes-susceptible loci by genetic linkage analysis. The diabetic incidence of NOD-Pdcd1-/- mice was controlled by five genetic loci, including three known recessive loci [Idd (insulin-dependent diabetes) 1, Idd17, and Idd20] and two previously unidentified dominant loci [Iddp (Idd under PD-1 deficiency) 1 and Iddp2].

Indexed as

Disease Models, AnimalGene DeletionAnimalsAntigens, SurfaceApoptosis Regulatory ProteinsCD8-Positive T-LymphocytesDiabetes Mellitus, Type 1Genetic LinkageGenetic Predisposition to DiseaseIncidenceIslets of LangerhansMiceMice, Inbred BALB CMice, Inbred C57BLMice, Inbred NODMice, KnockoutAntigens, SurfaceApoptosis Regulatory ProteinsPdcd1 protein, mouseProgrammed Cell Death 1 Receptor

Identifiers

PMID16087865
PMCPMC1188011
OpenAlexW2085604821

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

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.