Evidence map›Paper›PMID 22042558›Full record

ArticleEuropean journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology2012

Characterization of Th1- and Th2-type immune response in human multidrug-resistant tuberculosis.

Q Tan, W P Xie, R Min, G Q Dai, C-C Xu, H Q Pan, C D Miao, Z Yang, W G Xu, H Wang

Abstract readMulticenter Study
PubMed Publisher
In one paragraph

Article in European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology, 2012. 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
0.6field-weighted citation impact, top 34% 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, 35 citations in OpenAlex.

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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

10 authors at 6 institutions in 2 countries.

Q TanDepartment of Respiratory Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, 210029, China.
W P Xie
R Min
G Q Dai
C-C Xu
H Q Pan
C D Miao
Z Yang
W G Xu
H Wang
Jiangsu Province Hospital · CNNanjing Medical University · CNCenters for Disease Control and Prevention · USJiangsu Provincial Center for Disease Control and Prevention · CNJiangsu University · CNNanjing Jiangning Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multidrug-resistant tuberculosis (MDR-TB) has become a lethal global threat. Insights into the immune regulation of MDR-TB are urgently needed for the development of new treatments; however, the T cell response to an MDR-TB infection in human remains unclear. In the present study, the proportion of Th1 and Th2 cell subsets and the level of related T cell subset cytokines in peripheral blood were investigated. We detected that an MDR-TB infection resulted in suppressed Th1 and Th2 cell activation, which was more remarkable in patients with MDR-TB than that in drug-sensitive tuberculosis (DS-TB) sufferers when compared to healthy controls (HCs). In addition, MDR-TB infection down-regulated the expression of IFN-γ, IL-2, and IL-10, and up-regulated IL-4, IL-6, and TNF-α expression. Our data suggest that the disturbance between protective and pathogenic effects induced by the immunosuppression of Th1- and Th2-type responses is a substantial characteristic of MDR-TB infections.

Indexed as

AdolescentAdultAgedBloodCytokinesFemaleHumansImmune ToleranceMaleMiddle AgedTh1 CellsTh2 CellsT-Lymphocyte SubsetsTuberculosis, Multidrug-ResistantYoung AdultCytokines

Identifiers

PMID22042558
OpenAlexW2009374284

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.