Evidence map›Paper›PMID 22409933›Full record

ArticleInfection and immunity2012

Dysfunction of natural killer T cells in patients with active Mycobacterium tuberculosis infection.

Seung-Jung Kee, Yong-Soo Kwon, Yong-Wook Park, Young-Nan Cho, Sung-Ji Lee, Tae-Jong Kim, Shin-Seok Lee, Hee-Chang Jang, Myung-Geun Shin, Jong-Hee Shin and 2 more

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 52 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed, 1 pooled it
3.1field-weighted citation impact, top 8% 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

52 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 citations in OpenAlex.

  1. Pooled it
  2. CD8+ lymphocytes in immunity against tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2026
    Review
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  10. Diagnostic accuracy ofFrontiers in immunology · 2024
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  11. Coevolution ofMicrobiology spectrum · 2023
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  13. Early innate cell interactions withFrontiers in immunology · 2023
    Review
  14. Frontiers in immunology · 2023
    Review
  15. Article
  16. Review
  17. Review
  18. Article
  19. Towards new TB vaccines.Seminars in immunopathology · 2020
    Review
  20. Host defense mechanisms against Mycobacterium tuberculosis.Cellular and molecular life sciences : CMLS · 2020
    Review
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

12 authors at 2 institutions in 1 country.

Seung-Jung KeeDepartment of Laboratory Medicine, Chonnam National University Medical School and Hospital, Gwangju, Republic of Korea.
Yong-Soo Kwon
Yong-Wook Park
Young-Nan Cho
Sung-Ji Lee
Tae-Jong Kim
Shin-Seok Lee
Hee-Chang Jang
Myung-Geun Shin
Jong-Hee Shin
Soon-Pal Suh
Dong-Wook Ryang
Chonnam National University Hospital · KRChonnam National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Natural killer T (NKT) cells are known to play a protective role in the immune responses of mice against a variety of infectious pathogens. However, little is known about the detailed information of NKT cells in patients with Mycobacterium tuberculosis infection. The aims of this study were to examine NKT cell levels and functions in patients with active M. tuberculosis infection, to investigate relationships between NKT cell levels and clinical parameters, and to determine the mechanism responsible for the poor response to α-galactosylceramide (α-GalCer). NKT cell levels were significantly lower in the peripheral blood of pulmonary tuberculosis and extrapulmonary tuberculosis patients, and the proliferative responses of NKT cells to α-GalCer were also lower in patients, whereas NKT cell levels and responses were comparable in latent tuberculosis infection subjects and healthy controls. Furthermore, this NKT cell deficiency was found to be correlated with serum C-reactive protein levels. In addition, the poor response to α-GalCer in M. tuberculosis-infected patients was found to be due to increased NKT cell apoptosis, reduced CD1d expression, and a defect in NKT cells. Notably, M. tuberculosis infection was associated with an elevated expression of the inhibitory programmed death-1 (PD-1) receptor on NKT cells, and blockade of PD-1 signaling enhanced the response to α-GalCer. This study shows that NKT cell levels and functions are reduced in M. tuberculosis-infected patients and these deficiencies were found to reflect the presence of active tuberculosis.

Indexed as

AdultAgedAnimalsCase-Control StudiesCell DeathCell ProliferationCohort StudiesFemaleGalactosylceramidesGene Expression RegulationHumansMaleMiceMiddle AgedNatural Killer T-CellsProgrammed Cell Death 1 Receptoralpha-galactosylceramideGalactosylceramidesPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID22409933
PMCPMC3370582
OpenAlexW2161930955

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.