Evidence map›Paper›PMID 26565900›Full record

ArticleCell reports2015

A Role for IFITM Proteins in Restriction of Mycobacterium tuberculosis Infection.

Shahin Ranjbar, Viraga Haridas, Luke D Jasenosky, James V Falvo, Anne E Goldfeld

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed, 1 pooled it
2.2field-weighted citation impact, top 12% 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

56 citing papers in PubMed, 1 synthesis or guideline pooled it, 95 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Article
  4. Article
  5. Review
  6. Article
  7. CAPRIN1 specifically mediates mCommunications biology · 2025
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  12. Viperin inhibits interferon-γ production to promote Mycobacterium tuberculosis survival by disrupting TBK1-IKKε-IRF3-axis and JAK-STAT signaling.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024
    Article
  13. Article
  14. Article
  15. Cytometry in High-Containment Laboratories.Methods in molecular biology (Clifton, N.J.) · 2024
    Review
  16. Article
  17. Article
  18. Article
  19. Gene Expression in Cord Blood and Tuberculosis in Early Childhood: A Nested Case-Control Study in a South African Birth Cohort.Clinical infectious diseases : an official publication of the Infectious Diseases Society of America · 2023
    Article
  20. 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

5 authors at 1 institution in 1 country.

Shahin RanjbarProgram in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, MA 02115, USA. Electronic address: shahin.ranjbar@childrens.harvard.edu.
Viraga HaridasProgram in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, MA 02115, USA.
Luke D JasenoskyProgram in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, MA 02115, USA.
James V FalvoProgram in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, MA 02115, USA.
Anne E GoldfeldProgram in Cellular and Molecular Medicine, Children's Hospital Boston, Boston, MA 02115, USA. Electronic address: anne.goldfeld@childrens.harvard.edu.
Boston Children's Hospital · US

Funding

Immune control mechanisms of TB latency in the setting of HIV co-infectionR01AI117929 · NIAID · BOSTON CHILDREN'S HOSPITAL · PI GOLDFELD, ANNE · 2016 to 2019
$1.8M
Host factors, inflammation, and HIV associated TBR56HL128154 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI GOLDFELD, ANNE · 2015 to 2015
$813k
NHLBI NIH HHS R56 HL128154NIAID NIH HHS R01 AI117929PHS HHS R56128154
6 · The paper itself

Abstract

The interferon (IFN)-induced transmembrane (IFITM) proteins are critical mediators of the host antiviral response. Here, we expand the role of IFITM proteins to host defense against intracellular bacterial infection by demonstrating that they restrict Mycobacterium tuberculosis (MTb) intracellular growth. Simultaneous knockdown of IFITM1, IFITM2, and IFITM3 by RNAi significantly enhances MTb growth in human monocytic and alveolar/epithelial cells, whereas individual overexpression of each IFITM impairs MTb growth in these cell types. Furthermore, MTb infection, Toll-like receptor 2 and 4 ligands, and several proinflammatory cytokines induce IFITM1-3 gene expression in human myeloid cells. We find that IFITM3 co-localizes with early and, in particular, late MTb phagosomes, and overexpression of IFITM3 enhances endosomal acidification in MTb-infected monocytic cells. These findings provide evidence that the antiviral IFITMs participate in the restriction of mycobacterial growth, and they implicate IFITM-mediated endosomal maturation in its antimycobacterial activity.

Indexed as

Antigens, DifferentiationCells, CulturedEndosomesEpithelial CellsHEK293 CellsHumansMembrane ProteinsMonocytesMycobacterium tuberculosisPhagocytosisProtein TransportRNA-Binding ProteinsSignal TransductionToll-Like Receptor 2Toll-Like Receptor 4Antigens, DifferentiationIFITM2 protein, humanIFITM3 protein, humanleu-13 antigenMembrane ProteinsRNA-Binding ProteinsTLR2 protein, humanTLR4 protein, humanToll-Like Receptor 2Toll-Like Receptor 4

Identifiers

PMID26565900
PMCPMC4916766
OpenAlexW2191007893

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.