Evidence map›Paper›PMID 25488990›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2015

B7H1/CD80 interaction augments PD-1-dependent T cell apoptosis and ameliorates graft-versus-host disease.

Ruishu Deng, Kaniel Cassady, Xiaofan Li, Sheng Yao, Mingfeng Zhang, Jeremy Racine, Jeffrey Lin, Lieping Chen, Defu Zeng

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed, 1 pooled it
2.9field-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

38 citing papers in PubMed, 1 synthesis or guideline pooled it, 65 citations in OpenAlex.

  1. Pooled it
  2. Trial
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  5. Article
  6. Review
  7. Article
  8. Blockade of trans PD-L1 interaction with CD80 augments antitumor immunity.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  9. Article
  10. Review
  11. Article
  12. Article
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  15. Immune-Checkpoint Blockade Therapy in Lymphoma.International journal of molecular sciences · 2020
    Review
  16. Article
  17. Review
  18. Article
  19. Review
  20. MHC-mismatched mixed chimerism restores peripheral tolerance of noncross-reactive autoreactive T cells in NOD mice.Proceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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

9 authors at 3 institutions in 2 countries.

Ruishu DengDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA 91010;
Kaniel CassadyDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA 91010; Irell and Manella Graduate School of Biological Sciences, City of Hope, Duarte, CA 91010;
Xiaofan LiDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology, Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, China;
Sheng YaoDepartment of Immunobiology, Yale University School of Medicine, New Haven, CT 06520; and.
Mingfeng ZhangDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA 91010;
Jeremy RacineDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA 91010; Irell and Manella Graduate School of Biological Sciences, City of Hope, Duarte, CA 91010;
Jeffrey LinEugene and Ruth Roberts Summer Student Academy of City of Hope, Duarte, CA 91010.
Lieping ChenDepartment of Hematology, Fujian Institute of Hematology, Fujian Medical University Union Hospital, Fuzhou 350001, China;
Defu ZengDepartment of Diabetes Research, Beckman Research Institute, City of Hope, Duarte, CA 91010; Department of Hematology and Hematopoietic Cell Transplantation, Beckman Research Institute, City of Hope, Duarte, CA 91010; Irell and Manella Graduate School of Biological Sciences, City of Hope, Duarte, CA 91010; dzeng@coh.org.ORCID http://orcid.org/0000-0001-9585-1411
City of Hope · USFujian Medical University · CNYale University · US

Funding

Transgenic Mouse FacilityP30CA033572 · NCI · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI STANLEY R. HAMILTON · 1985 to 2026
$86.3M
Role of autoreactivity in the pathogenesis of chronic GVHDR01AI066008 · NIAID · CITY OF HOPE/BECKMAN RESEARCH INSTITUTE · PI ZENG, DEFU · 2005 to 2020
$6.1M
NCI NIH HHS P30 CA033572NIAID NIH HHS R01 AI066008
6 · The paper itself

Abstract

Interactions of B7H1 (programmed death ligand 1 [PD-L1]) with its two ligands, PD-1 and CD80, on T cells play a pivotal role in controlling T cell activation, proliferation, anergy, and apoptosis. However, the interactions between the two pathways remain unknown. Using an alloimmune response model of graft-versus-host disease (GVHD), we report in this study that: 1) Comparison of proliferation and apoptosis of wild-type (WT) and PD-1(-/-)CD4(+) conventional T (Tcon) cells in WT and B7H1(-/-) recipients revealed that B7H1/CD80 interaction per se augments T cell proliferation, and this interaction augments T cell apoptosis mediated by B7H1/PD-1 interaction. This observation was recapitulated in an in vitro MLR assay. 2) Specific blockade of the B7H1/CD80 axis by anti-B7H1 mAb reduces WT-alloreactive Tcon cell proliferation, IL-2 production, expression of PD-1, and apoptosis, resulting in worsening GVHD. In contrast, specific blockade of B7H1/CD80 interaction reduces donor PD-1(-/-) Tcon cell proliferation without an impact on apoptosis, resulting in ameliorating GVHD. 3) B7H1 fused to an Ig Fc domain (B7H1-Ig), when produced in vivo by hydrodynamic injection of B7H1-Ig plasmid, ameliorates GVHD by augmenting proliferation and apoptosis of WT- alloreactive Tcon cells. Conversely, B7H1-Ig treatment has no impact on apoptosis but augments PD-1(-/-) T cell proliferation and worsens GVHD. These results indicate that B7H1/CD80 interaction augments Tcon cell proliferation, IL-2 production, and expression of PD-1, which leads to increased apoptosis mediated by the B7H1/PD-1 pathway. Additionally, by engaging both PD-1 and CD80, B7H1-Ig can be a powerful therapeutic reagent for downregulating the T cell immune response.

Indexed as

AnimalsApoptosisB7-1 AntigenB7-H1 AntigenCD4-Positive T-LymphocytesCell ProliferationGene Expression RegulationGraft vs Host DiseaseInterleukin-2MiceMice, Inbred BALB CMice, KnockoutProgrammed Cell Death 1 ReceptorRecombinant Fusion ProteinsB7-1 AntigenB7-H1 AntigenInterleukin-2Pdcd1 protein, mouseProgrammed Cell Death 1 ReceptorRecombinant Fusion Proteins

Identifiers

PMID25488990
PMCPMC4282988
OpenAlexW1899957715

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.