Evidence map›Paper›PMID 29400698›Full record

ArticleThe Journal of clinical investigation2018

Clonally expanded γδ T cells protect against Staphylococcus aureus skin reinfection.

Carly A Dillen, Bret L Pinsker, Alina I Marusina, Alexander A Merleev, Orly N Farber, Haiyun Liu, Nathan K Archer, Da B Lee, Yu Wang, Roger V Ortines and 13 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 76 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
76citing papers in PubMed, 1 pooled it
12.4field-weighted citation impact, top 1% 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

76 citing papers in PubMed, 1 synthesis or guideline pooled it, 102 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Circulating T-cell phenotypes are influenced by prior Staphylococcus aureus exposure in hemodialysis patients.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2026
    Article
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  10. LinkingAntibiotics (Basel, Switzerland) · 2024
    Review
  11. Article
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  13. Article
  14. Article
  15. Review
  16. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  17. Article
  18. Article
  19. Article
  20. Clinical Impact ofAntibiotics (Basel, Switzerland) · 2023
    Review

16 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

23 authors at 6 institutions in 2 countries.

Carly A DillenDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Bret L PinskerDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Alina I MarusinaDepartment of Dermatology, School of Medicine, UCD, Sacramento, California, USA.
Alexander A MerleevDepartment of Dermatology, School of Medicine, UCD, Sacramento, California, USA.
Orly N FarberLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Haiyun LiuDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Nathan K ArcherDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Da B LeeDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Yu WangDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Roger V OrtinesDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Steven K LeeDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Mark C MarchittoDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Shuting S CaiDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Alyssa G AshbaughDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Larissa S MayDepartment of Emergency Medicine, School of Medicine, UCD, Sacramento, California, USA.
Steven M HollandLaboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Alexandra F FreemanLaboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Loren G MillerDivision of Infectious Diseases.
Michael R YeamanDivision of Infectious Diseases.
Scott I SimonDepartment of Biomedical Engineering, UCD, Davis, California, USA.
Joshua D MilnerLaboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, NIH, Bethesda, Maryland, USA.
Emanual MaverakisDepartment of Dermatology, School of Medicine, UCD, Sacramento, California, USA.
Lloyd S MillerDepartment of Dermatology, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Johns Hopkins University · USNational Institute of Allergy and Infectious Diseases · USUniversity of California, San Francisco · USUniversity of California, Davis · USUniversity of California Davis Medical Center · USUniversity of California, Los Angeles · US

Funding

Genes And Gene Products As ImmunoadjuvantsZIAAI000647 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HOLLAND, STEVEN · 2009 to 2025
$22.6M
Transgenic Animal Models Of Human Immune DefectsZIAAI000646 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI HOLLAND, STEVEN · 2009 to 2025
$22.2M
Systems Immunolobiology of Antibiotic-Persistent MRSA InfectionU01AI124319 · NIAID · LUNDQUIST INSTITUTE FOR BIOMEDICAL INNOVATION AT HARBOR-UCLA MEDICAL CENTER · PI YEAMAN, MICHAEL R · 2016 to 2020
$10.1M
Primary Immune Deficiency ClinicZIAAI001247 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI FREEMAN, ALEXANDRA · 2019 to 2025
$8.7M
Pathogenesis and Treatment of Atopic DermatitisZIAAI001098 · NIAID · NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES · PI MILNER, JOSHUA · 2009 to 2019
$6.5M
Investigation and Development of New Therapeutic Avenues for SclerodermaDP2OD008752 · OD · UNIVERSITY OF CALIFORNIA AT DAVIS · PI MAVERAKIS, EMANUAL M. · 2011 to 2016
$2.8M
Engineering the innate immune response to Staphaureus infectionR01AI129302 · NIAID · UNIVERSITY OF CALIFORNIA AT DAVIS · PI LEACH, J. KENT, SIMON, SCOTT IRWIN · 2017 to 2021
$1.9M
STAT3-mediated immunity to Staphylococcus aureus in skinR01AR069502 · NIAMS · JOHNS HOPKINS UNIVERSITY · PI ARCHER, NATHAN K. · 2016 to 2020
$1.8M
Human in vivo Th17 cell responses in cutaneous immunity to Staphylococcus aureusR21AI126896 · NIAID · JOHNS HOPKINS UNIVERSITY · PI MILLER, LLOYD S · 2016 to 2017
$446k
NIAID NIH HHS R01 AI129302NIAID NIH HHS R21 AI126896NIAID NIH HHS U01 AI124319NIAMS NIH HHS R01 AR069502NIH HHS DP2 OD008752
6 · The paper itself

Abstract

The mechanisms that mediate durable protection against Staphylococcus aureus skin reinfections are unclear, as recurrences are common despite high antibody titers and memory T cells. Here, we developed a mouse model of S. aureus skin reinfection to investigate protective memory responses. In contrast with WT mice, IL-1β-deficient mice exhibited poor neutrophil recruitment and bacterial clearance during primary infection that was rescued during secondary S. aureus challenge. The γδ T cells from skin-draining LNs utilized compensatory T cell-intrinsic TLR2/MyD88 signaling to mediate rescue by trafficking and producing TNF and IFN-γ, which restored neutrophil recruitment and promoted bacterial clearance. RNA-sequencing (RNA-seq) of the LNs revealed a clonotypic S. aureus-induced γδ T cell expansion with a complementarity-determining region 3 (CDR3) aa sequence identical to that of invariant Vγ5+ dendritic epidermal T cells. However, this T cell receptor γ (TRG) aa sequence of the dominant CDR3 sequence was generated from multiple gene rearrangements of TRGV5 and TRGV6, indicating clonotypic expansion. TNF- and IFN-γ-producing γδ T cells were also expanded in peripheral blood of IRAK4-deficient humans no longer predisposed to S. aureus skin infections. Thus, clonally expanded γδ T cells represent a mechanism for long-lasting immunity against recurrent S. aureus skin infections.

Indexed as

AnimalsFemaleGene RearrangementInterferon-gammaInterleukin-17Interleukin-1betaInterleukin-22InterleukinsIntraepithelial LymphocytesMaleMiceMice, Inbred C57BLNeutrophil InfiltrationNeutrophilsReceptors, Antigen, T-Cell, gamma-deltaSequence Analysis, RNAInterferon-gammaInterleukin-17Interleukin-1betaInterleukin-22InterleukinsReceptors, Antigen, T-Cell, gamma-deltaTumor Necrosis Factor-alphaAdaptive immunityBacterial infectionsImmunologyInfectious diseaseSkin

Identifiers

PMID29400698
PMCPMC5824877
OpenAlexW2787421562

What OpenQuestion holds

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Registered trials

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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.