Evidence map›Paper›PMID 30021216›Full record

ArticleJournal of innate immunity2018

Potential Role of Gr-1+ CD8+ T Lymphocytes as a Source of Interferon-γ and M1/M2 Polarization during the Acute Phase of Murine Legionella pneumophila Pneumonia.

Yu Kusaka, Chiaki Kajiwara, Sho Shimada, Yoshikazu Ishii, Yasunari Miyazaki, Naohiko Inase, Theodore J Standiford, Kazuhiro Tateda

Open access · goldAbstract read
In one paragraph

Article in Journal of innate immunity, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.5field-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

13 citing papers in PubMed, 16 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Catch Me if You Can or Actors on the Run.Journal of innate immunity · 2019
    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

8 authors at 3 institutions in 2 countries.

Yu KusakaDepartment of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo, Japan.
Chiaki KajiwaraDepartment of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo, Japan.
Sho ShimadaDepartment of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo, Japan.
Yoshikazu IshiiDepartment of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo, Japan.
Yasunari MiyazakiDepartment of Respiratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Naohiko InaseDepartment of Respiratory Medicine, Tokyo Medical and Dental University, Tokyo, Japan.
Theodore J StandifordDepartment of Internal Medicine, Division of Pulmonary and Critical Care Medicine, University of Michigan, Ann Arbor, Michigan, USA.
Kazuhiro TatedaDepartment of Microbiology and Infectious Diseases, Toho University School of Medicine, Tokyo, Japan.
Toho University · JPTokyo Medical and Dental University · JPUniversity of Michigan–Ann Arbor · US

Funding

Novel IL-1 Family Members in Lung Innate ImmunityR01HL123515 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI STANDIFORD, THEODORE J. · 2015 to 2018
$2.5M
NHLBI NIH HHS R01 HL123515
6 · The paper itself

Abstract

In this study, we analyzed interferon (IFN)-γ-producing cells and M1/M2 macrophage polarization in Legionella pneumophila pneumonia following anti-Gr-1 antibody treatment. Anti-Gr-1 treatment induced an M1-to-M2 shift of macrophage subtypes in the lungs and weakly in the peripheral blood, which was associated with increased mortality in legionella-infected mice. CD8+ T lymphocytes and natural killer cells were the dominant sources of IFN-γ in the acute phase, and anti-Gr-1 treatment reduced the number of IFN-γ-producing CD8+ T lymphocytes. In the CD3-gated population, most Gr-1-positive cells were CD8+ T lymphocytes in the lungs and lymph nodes (LNs) of infected mice. Additionally, the number of IFN-γ-producing Gr-1+ CD8+ T lymphocytes in the lungs and LNs increased 2 and 4 days after L. pneumophila infection, with anti-Gr-1 treatment attenuating these populations. Antibody staining revealed that Gr-1+ CD8+ T lymphocytes were Ly6C-positive cells rather than Ly6G, a phenotype regarded as memory type cells. Furthermore, the adoptive transfer of Gr-1+ CD8+ T lymphocytes induced increases in IFN-γ, M1 shifting and reduced bacterial number in the Legionella pneumonia model. These data identified Ly6C+ CD8+ T lymphocytes as a source of IFN-γ in innate immunity and partially associated with reduced IFN-γ production, M2 polarization, and high mortality in anti-Gr-1 antibody-treated mice with L. pneumophila pneumonia.

Indexed as

Acute DiseaseAnimalsAntibodies, BlockingCD8-Positive T-LymphocytesCell DifferentiationCytokinesDisease Models, AnimalFemaleHumansImmunologic MemoryInterferon-gammaLegionella pneumophilaLegionnaires' DiseaseMacrophagesMicePneumoniaAntibodies, BlockingCytokinesGr-1 protein, mouseInterferon-gammaReceptors, ChemokineGr-1+ CD8+ T lymphocytesLegionella pneumophilaMacrophage polarization

Identifiers

PMID30021216
PMCPMC6757147
OpenAlexW2884989865

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.