Evidence map›Paper›PMID 26080440›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2015

Inflammation induces dermal Vγ4+ γδT17 memory-like cells that travel to distant skin and accelerate secondary IL-17-driven responses.

Francisco Ramírez-Valle, Elizabeth E Gray, Jason G Cyster

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed, 1 pooled it
8.9field-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

115 citing papers in PubMed, 1 synthesis or guideline pooled it, 198 citations in OpenAlex.

  1. γδ T cells in oral diseases.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Pooled it
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55 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

3 authors at 2 institutions in 1 country.

Francisco Ramírez-ValleDepartment of Microbiology and Immunology, University of California, San Francisco, CA 94143; Department of Dermatology, University of California, San Francisco, CA 94143;
Elizabeth E GrayDepartment of Microbiology and Immunology, University of California, San Francisco, CA 94143;
Jason G CysterDepartment of Microbiology and Immunology, University of California, San Francisco, CA 94143; Howard Hughes Medical Institute, University of California, San Francisco, CA 94143 jason.cyster@ucsf.edu.
University of California, San Francisco · USHoward Hughes Medical Institute · US

Funding

UCSF Dermatology Training GrantT32AR007175 · NIAMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Wilson Liao, Michael David Rosenblum · 1986 to 2026
$6.1M
Cellular and Genetic Analysis of Lymphocyte EgressR01AI074847 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI CYSTER, JASON G · 2007 to 2016
$3.8M
Howard Hughes Medical InstituteNIAID NIH HHS AI074847NIAID NIH HHS R01 AI074847NIAMS NIH HHS T32 AR007175
6 · The paper itself

Abstract

Gamma delta (γδ) T cells represent a major IL-17 committed T-cell population (γδT17 cells) in the mouse dermis. Following exposure to the inflammatory agent imiquimod (IMQ) the Vγ4(+) subset of γδT cells produce IL-17 in the skin and expand rapidly in draining lymph nodes (LNs). Local IMQ treatment in humans is known to exacerbate psoriasis skin lesion activity at distant sites. Whether expanded γδT17 cells sensitize distant sites to inflammation has been unknown. Here we show that expanded Vγ4(+) γδT17 cells egress from LNs in a fingolimod (FTY720)-sensitive manner and use C-C chemokine receptor type 2 to accumulate in inflamed skin where they augment neutrophil recruitment and inflammation. They also travel to noninflamed skin and peripheral LNs and remain in elevated numbers at these distant sites for at least 3 mo. Sensitized mice show more rapid skin inflammation and greater proliferation and IL-17 production by Vγ4(+) γδT cells upon imiquimod challenge. Transfer experiments confirm that memory-like Vγ4(+) γδT17 cells respond more rapidly. Memory-like Vγ4(+) γδT17 cells are distinguished by greater IL-1R1 expression and more proliferation in response to IL-1β. These findings establish that local skin inflammation leads to faster and stronger secondary responses to the same stimulus through long-term and systemic changes in the composition and properties of the dermal γδT-cell population.

Indexed as

Immunologic MemoryAminoquinolinesAnimalsImiquimodInflammationInterleukin-17MiceReceptors, Antigen, T-Cell, gamma-deltaSkinT-LymphocytesAminoquinolinesImiquimodInterleukin-17Receptors, Antigen, T-Cell, gamma-deltaimmunological memoryinflammationγδT cells

Identifiers

PMID26080440
PMCPMC4491769
OpenAlexW1570798316

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.