Evidence map›Paper›PMID 22526678›Full record

ArticleInfection and immunity2012

Phenotypic, morphological, and functional heterogeneity of splenic immature myeloid cells in the host response to tularemia.

John W Rasmussen, Jason W Tam, Nihal A Okan, Patricio Mena, Martha B Furie, David G Thanassi, Jorge L Benach, Adrianus W M van der Velden

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
0.4field-weighted citation impact, top 38% 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

10 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
  2. Article
  3. ImmunoHorizons · 2022
    Article
  4. Article
  5. Infection and immunity · 2018
    Article
  6. Host-based lipid inflammation drives pathogenesis inProceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  7. Article
  8. Article
  9. Article
  10. 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 1 institution in 1 country.

John W RasmussenCenter for Infectious Diseases, Stony Brook University, Stony Brook, New York, USA.
Jason W Tam
Nihal A Okan
Patricio Mena
Martha B Furie
David G Thanassi
Jorge L Benach
Adrianus W M van der Velden
Stony Brook University · US

Funding

Viral Pathogenesis and TherapeuticsU54AI057158 · NIAID · WADSWORTH CENTER · PI LEVY, DAVID E · 2003 to 2014
$100.8M
Virulence Mechanism of Y. pestis and tularensisP01AI055621 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI BENACH, JORGE L. · 2004 to 2010
$20.7M
MOLECULAR AND CELL BIOLOGY OF INFECTIOUS DISEASEST32AI007539 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI KONOPKA, JAMES B · 1998 to 2023
$3.6M
Immature myeloid cells as targets for therapeutics to bacterial infectionR21AI092165 · NIAID · STATE UNIVERSITY NEW YORK STONY BROOK · PI VAN DER VELDEN, ADRIANUS WILHELMUS MARIA · 2012 to 2013
$427k
NIAID NIH HHS P01 AI055621NIAID NIH HHS R21 AI092165NIAID NIH HHS T32 AI007539NIAID NIH HHS U54 AI057158
6 · The paper itself

Abstract

Recent studies have linked accumulation of the Gr-1⁺ CD11b⁺ cell phenotype with functional immunosuppression in diverse pathological conditions, including bacterial and parasitic infections and cancer. Gr-1⁺ CD11b⁺ cells were the largest population of cells present in the spleens of mice infected with sublethal doses of the Francisella tularensis live vaccine strain (LVS). In contrast, the number of T cells present in the spleens of these mice did not increase during early infection. There was a significant delay in the kinetics of accumulation of Gr-1⁺ CD11b⁺ cells in the spleens of B-cell-deficient mice, indicating that B cells play a role in recruitment and maintenance of this population in the spleens of mice infected with F. tularensis. The splenic Gr-1⁺ CD11b⁺ cells in tularemia were a heterogeneous population that could be further subdivided into monocytic (mononuclear) and granulocytic (polymorphonuclear) cells using the Ly6C and Ly6G markers and differentiated into antigen-presenting cells following ex vivo culture. Monocytic, CD11b⁺ Ly6C(hi) Ly6G⁻ cells but not granulocytic, CD11b⁺ Ly6C(int) Ly6G⁺ cells purified from the spleens of mice infected with F. tularensis suppressed polyclonal T-cell proliferation via a nitric oxide-dependent pathway. Although the monocytic, CD11b⁺ Ly6C(hi) Ly6G⁻ cells were able to suppress the proliferation of T cells, the large presence of Gr-1⁺ CD11b⁺ cells in mice that survived F. tularensis infection also suggests a potential role for these cells in the protective host response to tularemia.

Indexed as

AnimalsB-LymphocytesCD11b AntigenDisease Models, AnimalFemaleFrancisella tularensisImmunophenotypingMiceMice, Inbred BALB CMice, Inbred C3HMice, Inbred C57BLMyeloid CellsReceptors, ChemokineSpleenT-LymphocytesTularemiaCD11b AntigenGr-1 protein, mouseReceptors, Chemokine

Identifiers

PMID22526678
PMCPMC3416475
OpenAlexW2136219290

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.