Evidence map›Paper›PMID 36265003›Full record

ArticlePLoS pathogens2022

The PD-1/PD-L1 pathway is induced during Borrelia burgdorferi infection and inhibits T cell joint infiltration without compromising bacterial clearance.

Jennifer D Helble, Julie E McCarthy, Machlan Sawden, Michael N Starnbach, Linden T Hu

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 20% 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

12 citing papers in PubMed, 11 citations in OpenAlex.

  1. Seroprevalence ofPathogens (Basel, Switzerland) · 2026
    Observational
  2. Strain-specific immune response patterns toInfection and immunity · 2026
    Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Hitchhiker's Guide toJournal of bacteriology · 2024
    Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
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 2 institutions in 1 country.

Jennifer D HelbleDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Julie E McCarthyDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Machlan SawdenDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.
Michael N StarnbachDepartment of Microbiology, Harvard Medical School, Boston, Massachusetts, United States of America.
Linden T HuDepartment of Molecular Biology and Microbiology, Tufts University School of Medicine, Boston, Massachusetts, United States of America.ORCID 0000-0003-1659-5558
Tufts University · USHarvard University · US

Funding

Cytotoxic T Cell Mediated Immunity to ChlamydiaR01AI039558 · NIAID · HARVARD UNIVERSITY (MEDICAL SCHOOL) · PI STARNBACH, MICHAEL N · 2001 to 2025
$15.6M
Role of human innate immune mutations in loss of tolerance to Borrelia burgdorferiR01AI150157 · NIAID · TUFTS UNIVERSITY BOSTON · PI HU, LINDEN T · 2020 to 2024
$3.0M
NIAID NIH HHS R01 AI039558NIAID NIH HHS R01 AI150157
6 · The paper itself

Abstract

The Lyme disease bacterial pathogen, Borrelia burgdorferi, establishes a long-term infection inside its mammalian hosts. Despite the continued presence of the bacteria in animal models of disease, inflammation is transitory and resolves spontaneously. T cells with limited effector functions and the inability to become activated by antigen, termed exhausted T cells, are present in many long-term infections. These exhausted T cells mediate a balance between pathogen clearance and preventing tissue damage resulting from excess inflammation. Exhausted T cells express a variety of immunoinhibitory molecules, including the molecule PD-1. Following B. burgdorferi infection, we found that PD-1 and its ligand PD-L1 are significantly upregulated on CD4+ T cells and antigen presenting cell subsets, respectively. Using mice deficient in PD-1, we found that the PD-1/PD-L1 pathway did not impact bacterial clearance but did impact T cell expansion and accumulation in the ankle joint and popliteal lymph nodes without affecting B cell populations or antibody production, suggesting that the PD-1/PD-L1 pathway may play a role in shaping the T cell populations present in affected tissues.

Indexed as

Borrelia burgdorferiLyme DiseaseAnimalsB7-H1 AntigenCD4-Positive T-LymphocytesInflammationMammalsMiceProgrammed Cell Death 1 ReceptorB7-H1 AntigenProgrammed Cell Death 1 Receptor

Identifiers

PMID36265003
PMCPMC9624412
OpenAlexW4306896953

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.