Evidence map›Paper›PMID 27777971›Full record

ArticleJCI insight2016

Anti-coreceptor therapy drives selective T cell egress by suppressing inflammation-dependent chemotactic cues.

Aaron J Martin, Matthew Clark, Gregory Gojanovich, Fatima Manzoor, Keith Miller, Douglas E Kline, Y Maurice Morillon, Bo Wang, Roland Tisch

Open access · goldAbstract read
In one paragraph

Article in JCI insight, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.9field-weighted citation impact, top 18% 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

8 citing papers in PubMed, 7 citations in OpenAlex.

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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 2 institutions in 1 country.

Aaron J MartinDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Matthew ClarkDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Gregory GojanovichDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Fatima ManzoorDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Keith MillerDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Douglas E KlineDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Y Maurice MorillonDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Bo WangDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
Roland TischDepartment of Microbiology and Immunology, University of North Carolina at Chapel Hill School of Medicine, Chapel Hill, North Carolina, USA.
University of North Carolina at Chapel Hill · USNational Cancer Institute · US

Funding

Virology Research Program (Program 4)P30CA016086 · NCI · UNIV OF NORTH CAROLINA CHAPEL HILL · PI David Darr · 1985 to 2026
$201.5M
Islet-Specific Tolerance Induced by T Cell Co-Receptor Therapy in Type 1 DiabetesR01DK100256 · NIDDK · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TISCH, ROLAND M · 2014 to 2018
$1.7M
Human CD8+ T Cell Tolerance by Nondepleting Humanized CD8-Specific AntibodyR21AI115752 · NIAID · UNIV OF NORTH CAROLINA CHAPEL HILL · PI TISCH, ROLAND M · 2015 to 2016
$433k
NCI NIH HHS P30 CA016086NIAID NIH HHS R21 AI115752NIDDK NIH HHS R01 DK100256
6 · The paper itself

Abstract

There continues to be a need for immunotherapies to treat type 1 diabetes in the clinic. We previously reported that nondepleting anti-CD4 and -CD8 Ab treatment effectively reverses diabetes in new-onset NOD mice. A key feature of the induction of remission is the egress of the majority of islet-resident T cells. How this occurs is undefined. Herein, the effects of coreceptor therapy on islet T cell retention were investigated. Bivalent Ab binding to CD4 and CD8 blocked TCR signaling and T cell cytokine production, while indirectly downregulating islet chemokine expression. These processes were required for T cell retention, as ectopic IFN-γ or CXCL10 inhibited Ab-mediated T cell purging. Importantly, treatment of humanized mice with nondepleting anti-human CD4 and CD8 Ab similarly reduced tissue-infiltrating human CD4

Indexed as

ChemotaxisAnimalsAntibodiesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesHumansInflammationIslets of LangerhansMiceMice, Inbred NODReceptors, Antigen, T-CellAntibodiesReceptors, Antigen, T-Cell

Identifiers

PMID27777971
PMCPMC5070954
OpenAlexW2535939331

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.