Evidence map›Paper›PMID 20472828›Full record

ArticleBlood2010

B7-H1/CD80 interaction is required for the induction and maintenance of peripheral T-cell tolerance.

Jang-June Park, Ryusuke Omiya, Yumiko Matsumura, Yukimi Sakoda, Atsuo Kuramasu, Mathew M Augustine, Sheng Yao, Fumihiko Tsushima, Hidehiko Narazaki, Sudarshan Anand and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in Blood, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 194 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
194citing papers in PubMed, 2 pooled it
7.6field-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.

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

194 citing papers in PubMed, 2 syntheses or guidelines pooled it, 322 citations in OpenAlex.

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  5. PD-L1Haematologica · 2018
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134 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

14 authors at 3 institutions in 1 country.

Jang-June ParkMarlene and Stewart Greenebaum Cancer Center, University of Maryland, Baltimore, USA.
Ryusuke Omiya
Yumiko Matsumura
Yukimi Sakoda
Atsuo Kuramasu
Mathew M Augustine
Sheng Yao
Fumihiko Tsushima
Hidehiko Narazaki
Sudarshan Anand
Yingjia Liu
Scott E Strome
Lieping Chen
Koji Tamada
University of Maryland, Baltimore · USJohns Hopkins Medicine · USJohns Hopkins University · US

Funding

PD-1/PD-L1 modulation in cancer therapyR01CA142779 · NCI · JOHNS HOPKINS UNIVERSITY · PI PARDOLL, DREW M., TAUBE, JANIS M · 2010 to 2025
$8.2M
MOLECULAR MECHANISMS OF TUMOR-INDUCED TOLERANCER01CA097085 · NCI · YALE UNIVERSITY · PI CHEN, LIEPING · 2002 to 2011
$3.5M
LIGHT co-stimulatory therapy on GVHD and GVLR01HL088954 · NHLBI · UNIVERSITY OF MARYLAND BALTIMORE · PI STROME, SCOTT E. · 2007 to 2011
$2.0M
NCI NIH HHS CA97085NCI NIH HHS R01 CA097085NCI NIH HHS R01 CA142779NHLBI NIH HHS HL088954NHLBI NIH HHS R01 HL088954
6 · The paper itself

Abstract

T-cell tolerance is the central program that prevents harmful immune responses against self-antigens, in which inhibitory PD-1 signal given by B7-H1 interaction plays an important role. Recent studies demonstrated that B7-H1 binds CD80 besides PD-1, and B7-H1/CD80 interaction also delivers inhibitory signals in T cells. However, a role of B7-H1/CD80 signals in regulation of T-cell tolerance has yet to be explored. We report here that attenuation of B7-H1/CD80 signals by treatment with anti-B7-H1 monoclonal antibody, which specifically blocks B7-H1/CD80 but not B7-H1/PD-1, enhanced T-cell expansion and prevented T-cell anergy induction. In addition, B7-H1/CD80 blockade restored Ag responsiveness in the previously anergized T cells. Experiments using B7-H1 or CD80-deficient T cells indicated that an inhibitory signal through CD80, but not B7-H1, on T cells is responsible in part for these effects. Consistently, CD80 expression was detected on anergic T cells and further up-regulated when they were re-exposed to the antigen (Ag). Finally, blockade of B7-H1/CD80 interaction prevented oral tolerance induction and restored T-cell responsiveness to Ag previously tolerized by oral administration. Taken together, our findings demonstrate that the B7-H1/CD80 pathway is a crucial regulator in the induction and maintenance of T-cell tolerance.

Indexed as

AnimalsAntigens, DifferentiationAutoantigensB7-1 AntigenB7-H1 AntigenBlotting, WesternCell ProliferationEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryHumansImmune ToleranceImmunizationImmunoglobulin GImmunoprecipitationMembrane GlycoproteinsAntigens, DifferentiationAutoantigensB7-1 AntigenB7-H1 AntigenCd274 protein, mouseImmunoglobulin GMembrane GlycoproteinsOvalbuminPdcd1 protein, mousePeptide FragmentsPeptidesProgrammed Cell Death 1 ReceptorReceptors, Antigen, T-CellRNA, Messenger

Identifiers

PMID20472828
PMCPMC2938239
OpenAlexW2087186136

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.