Evidence map›Paper›PMID 18768852›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2008

Defects in skin gamma delta T cell function contribute to delayed wound repair in rapamycin-treated mice.

Robyn E Mills, Kristen R Taylor, Katie Podshivalova, Dianne B McKay, Julie M Jameson

Open access · bronzeAbstract read
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
44citing papers in PubMed, 1 pooled it
1.4field-weighted citation impact, top 19% 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

44 citing papers in PubMed, 1 synthesis or guideline pooled it, 78 citations in OpenAlex.

  1. Pooled it
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  3. Development and Evaluation ofPharmaceuticals (Basel, Switzerland) · 2025
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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

5 authors at 1 institution in 1 country.

Robyn E MillsDepartment of Immunology, The Scripps Research Institute, La Jolla, CA 92037, USA.
Kristen R Taylor
Katie Podshivalova
Dianne B McKay
Julie M Jameson
Scripps Research Institute · US

Funding

PATHOGENESIS AND IMMUNOLOGY OF DISEASET32AI007244 · NIAID · SCRIPPS RESEARCH INSTITUTE, THE · PI NEMAZEE, DAVID · 1985 to 2022
$8.8M
The Role of Inflammation in Ischemic Organ InjuryR01DK075718 · NIDDK · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI MCKAY, DIANNE B · 2008 to 2012
$2.1M
Gamma Delta T cell and keratinocyte cross-talk in diabetic woundsR21DK073098 · NIDDK · SCRIPPS RESEARCH INSTITUTE, THE · PI JAMESON, JULIE M · 2005 to 2006
$505k
NIAID NIH HHS AI07244NIAID NIH HHS T32 AI007244NIDDK NIH HHS DK073098NIDDK NIH HHS R01 DK075718NIDDK NIH HHS R21 DK073098
6 · The paper itself

Abstract

Disruptions in the normal program of tissue repair can result in poor wound healing, which perturbs the integrity of barrier tissues such as the skin. Such defects in wound repair occur in transplant recipients treated with the immunosuppressant drug rapamycin (sirolimus). Intraepithelial lymphocytes, such as gammadelta T cells in the skin, mediate tissue repair through the production of cytokines and growth factors. The capacity of skin-resident T cells to function during rapamycin treatment was analyzed in a mouse model of wound repair. Rapamycin treatment renders skin gammadelta T cells unable to proliferate, migrate, and produce normal levels of growth factors. The observed impairment of skin gammadelta T cell function is directly related to the inhibitory action of rapamycin on mammalian target of rapamycin. Skin gammadelta T cells treated with rapamycin are refractory to IL-2 stimulation and attempt to survive in the absence of cytokine and growth factor signaling by undergoing autophagy. Normal wound closure can be restored in rapamycin-treated mice by addition of the skin gammadelta T cell-produced factor, insulin-like growth factor-1. These studies not only reveal that mammalian target of rapamycin is a master regulator of gammadelta T cell function but also provide a novel mechanism for the increased susceptibility to nonhealing wounds that occurs during rapamycin administration.

Indexed as

AnimalsCell LineDisease Models, AnimalEpidermisImmunosuppressive AgentsMiceMice, Inbred C57BLMice, KnockoutOrgan Culture TechniquesProtein KinasesReceptors, Antigen, T-Cell, gamma-deltaSirolimusSkinTime FactorsT-Lymphocyte SubsetsTOR Serine-Threonine KinasesImmunosuppressive AgentsmTOR protein, mouseProtein KinasesReceptors, Antigen, T-Cell, gamma-deltaSirolimusTOR Serine-Threonine Kinases

Identifiers

PMID18768852
PMCPMC2547144
OpenAlexW2171557486

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.