Evidence map›Paper›PMID 19422095›Full record

ArticleThe Journal of clinical investigation2009

Anti-TNF immunotherapy and tuberculosis reactivation: another mechanism revealed.

Elizabeth A Miller, Joel D Ernst

Open access · bronzeAbstract readComment
In one paragraph

Article in The Journal of clinical investigation, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed, 1 pooled it
4.1field-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

43 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
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  9. Model systems to studyFrontiers in cellular and infection microbiology · 2025
    Review
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  14. Observational
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

Elizabeth A MillerDepartment of Medicine, New York University School of Medicine, New York, New York 10016, USA.
Joel D Ernst
New York University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Anti-TNF immunotherapy has revolutionized the treatment of some inflammatory diseases, such as RA. However, a major concern is that patients receiving this therapy have an increased risk of fungal and bacterial infection, particularly of reactivating latent tuberculosis (TB). In this issue of the JCI, in an effort to understand how anti-TNF immunotherapy affects host mechanisms required to control TB, Bruns and colleagues examined the effects of the anti-TNF therapeutic infliximab on Mycobacterium tuberculosis-specific human lymphocytes (see the related article beginning on page 1167). The authors report that a granulysin-expressing CD45RA+ subset of effector memory CD8+ T cells that contributes to the killing of intracellular M. tuberculosis is depleted in vivo by infliximab in patients with RA, and that these cells are susceptible to complement-mediated lysis in the presence of infliximab in vitro. The study provides insight into host defense mechanisms that act to control TB infection and how they are affected during anti-TNF immunotherapy for autoimmune disease.

Indexed as

AnimalsAntibodies, MonoclonalAntirheumatic AgentsAutoimmune DiseasesCD8-Positive T-LymphocytesComplement System ProteinsCytotoxicity, ImmunologicHumansImmunotherapyInfliximabLeukocytes, MononuclearMiceModels, ImmunologicalMonocytesMycobacterium tuberculosisPerforinAntibodies, MonoclonalAntirheumatic AgentsComplement System ProteinsInfliximabPerforinPore Forming Cytotoxic ProteinsPRF1 protein, humanSYTL4 protein, humanTumor Necrosis Factor-alphaVesicular Transport Proteins

Identifiers

PMID19422095
PMCPMC2673853
OpenAlexW2032537032

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.