Evidence map›Paper›PMID 17339358›Full record

ArticleInfection and immunity2007

Modulation of gamma interferon receptor 1 by Mycobacterium tuberculosis: a potential immune response evasive mechanism.

Amit Singhal, Anand Jaiswal, Virendra K Arora, Hanumanthappa K Prasad

Abstract read
In one paragraph

Article in Infection and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
2.1field-weighted citation impact, top 14% 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

27 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
  2. Cytokine Receptors-Regulators of Antimycobacterial Immune Response.International journal of molecular sciences · 2022
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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

4 authors at 2 institutions in 1 country.

Amit SinghalTB Immunology Laboratory, Department of Biotechnology, All India Institute of Medical Sciences, New Delhi 110029, India.
Anand Jaiswal
Virendra K Arora
Hanumanthappa K Prasad
All India Institute of Medical Sciences · INLRS Institute of Tuberculosis and Respiratory Diseases · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mycobacterium tuberculosis inhibits gamma interferon (IFN-gamma)-mediated antimycobacterial action by adopting diverse mechanisms. IFN-gamma binds to its receptor, IFN-gammaR, in order to initiate proper signaling. We have observed reduced surface expression levels of IFN-gamma receptor 1 (IFN-gammaR1) in untreated pulmonary tuberculosis patients compared to those in healthy individuals (P < 0.01). Following antitubercular therapy, the expression of IFN-gammaR1 was restored in these patients. To delineate the mechanism by which M. tuberculosis modulates IFN-gammaR1, in vitro experiments were designed, wherein the down modulation of IFN-gammaR1 surface expression was observed for CD14+ cells in peripheral blood mononuclear cells (PBMCs) cocultured with live M. tuberculosis compared to that for uninfected cells (P < 0.01). No modulation of IFN-gammaR1 expression was observed for CD14+ cells in PBMCs infected with Mycobacterium smegmatis. A time-dependent decrease in IFN-gammaR1 mRNA expression was observed for PBMCs infected with M. tuberculosis. Similar down modulation of IFN-gammaR1 protein and mRNA expression in phorbol myristate acetate-differentiated THP-1 cells (pdTHP-1) by M. tuberculosis was observed (P < 0.01). Using reporter gene analysis of 5' deletion constructs of the IFN-gammaR1 gene (IFNGR1) promoter, the decrease in IFN-gammaR1 mRNA in M. tuberculosis-infected pdTHP-1 cells was shown to be due to the decreased transcription of IFNGR1. By immunoblotting and electrophoretic mobility shift assays, the down regulation of stimulating protein 1 (Sp1) expression and its recruitment on the phorbol ester-responsive element of the IFNGR1 promoter in M. tuberculosis-infected pdTHP-1 cells was observed. This down regulation of Sp1 in pdTHP-1 cells cocultured with M. tuberculosis may be responsible for the down regulation of IFN-gammaR1 expression, thereby potentially altering its receptivity to IFN-gamma.

Indexed as

Down-RegulationCell LineCells, CulturedHumansInterferon gamma ReceptorLeukocytes, MononuclearLipopolysaccharide ReceptorsMycobacterium tuberculosisReceptors, InterferonTuberculosis, PulmonaryInterferon gamma ReceptorLipopolysaccharide ReceptorsReceptors, Interferon

Identifiers

PMID17339358
PMCPMC1865798
OpenAlexW2167239214

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.