Evidence map›Paper›PMID 20421645›Full record

ArticleJournal of immunology (Baltimore, Md. : 1950)2010

Diabetic mice display a delayed adaptive immune response to Mycobacterium tuberculosis.

Therese Vallerskog, Gregory W Martens, Hardy Kornfeld

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of immunology (Baltimore, Md. : 1950), 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
100citing papers in PubMed, 3 pooled it
3.8field-weighted citation impact, top 6% 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

100 citing papers in PubMed, 3 syntheses or guidelines pooled it, 159 citations in OpenAlex.

  1. Pooled it
  2. Diabetes Mellitus and Latent Tuberculosis Infection: A Systematic Review and Metaanalysis.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2017
    Pooled it
  3. Pooled it
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  12. Review
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  15. The Many Hosts of Mycobacteria 9 (MHM9): A conference report.Tuberculosis (Edinburgh, Scotland) · 2023
    Article
  16. Review
  17. Article
  18. Review
  19. Article
  20. The cause-effect relation of tuberculosis on incidence of diabetes mellitus.Frontiers in cellular and infection microbiology · 2023
    Review

40 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 1 institution in 1 country.

Therese VallerskogDepartment of Medicine, University of Massachusetts Medical School, Worcester, MA 01655, USA.
Gregory W Martens
Hardy Kornfeld
University of Massachusetts Chan Medical School · US

Funding

PILOT AND FEASIBILITY PROGRAMP30DK032520 · NIDDK · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI CZECH, MICHAEL P · 1986 to 2010
$14.6M
Impact of Diabetes and Hyperlipidemia on Host DefenseR01HL081149 · NHLBI · UNIV OF MASSACHUSETTS MED SCH WORCESTER · PI KORNFELD, HARDY · 2006 to 2019
$5.3M
NHLBI NIH HHS HL081149NHLBI NIH HHS R01 HL081149NIDDK NIH HHS DK32520NIDDK NIH HHS P30 DK032520
6 · The paper itself

Abstract

Diabetes mellitus (DM) is a major risk factor for tuberculosis (TB) but the defect in protective immunity responsible for this has not been defined. We previously reported that streptozotocin-induced DM impaired TB defense in mice, resulting in higher pulmonary bacterial burden, more extensive inflammation, and higher expression of several proinflammatory cytokines known to play a protective role in TB. In the current study, we tested the hypothesis that DM leads to delayed priming of adaptive immunity in the lung-draining lymph nodes (LNs) following low dose aerosol challenge with virulent Mycobacterium tuberculosis. We show that M. tuberculosis-specific IFN-gamma-producing T cells arise later in the LNs of diabetic mice than controls, with a proportionate delay in recruitment of these cells to the lung and stimulation of IFN-gamma-dependent responses. Dissemination of M. tuberculosis from lung to LNs was also delayed in diabetic mice, although they showed no defect in dendritic cell trafficking from lung to LNs after LPS stimulation. Lung leukocyte aggregates at the initial sites of M. tuberculosis infection developed later in diabetic than in nondiabetic mice, possibly related to reduced levels of leukocyte chemoattractant factors including CCL2 and CCL5 at early time points postinfection. We conclude that TB increased susceptibility in DM results from a delayed innate immune response to the presence of M. tuberculosis-infected alveolar macrophages. This in turn causes late delivery of Ag-bearing APC to the lung draining LNs and delayed priming of the adaptive immune response that is necessary to restrict M. tuberculosis replication.

Indexed as

Adaptive ImmunityAnimalsCell MovementDendritic CellsDiabetes Mellitus, ExperimentalInterferon-gammaLymph NodesMiceMice, Inbred C57BLMycobacterium tuberculosisTuberculosis, PulmonaryInterferon-gamma

Identifiers

PMID20421645
PMCPMC2874741
OpenAlexW2138679301

What OpenQuestion holds

Textmetadata
LicenceTDM
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.