Evidence map›Paper›PMID 10469239›Full record

ArticleImmunology1999

Sulfasalazine prevents T-helper 1 immune response by suppressing interleukin-12 production in macrophages.

B Y Kang, S W Chung, S Y Im, Y K Choe, T S Kim

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.7field-weighted citation impact, top 33% 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

11 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
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  9. The role of the T cell in autoimmune inflammation.Arthritis research & therapy · 2005
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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

5 authors at 2 institutions in 1 country.

B Y KangCollege of Pharmacy, Chonnam National University, Kwangju, Republic of Korea.
S W Chung
S Y Im
Y K Choe
T S Kim
Chonnam National University · KRKorea Research Institute of Bioscience and Biotechnology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin-12 (IL-12) plays a pivotal role in the development of T-helper 1 (Th1) immune response, which may be involved in the pathogenesis of chronic inflammatory autoimmune disorders. In this study we investigated the effects of sulfasalazine, a drug for treating inflammatory bowel disease and rheumatoid arthritis, on the production of IL-12 from mouse macrophages stimulated with lipopolysaccharide (LPS). Sulfasalazine potently inhibited the production of IL-12 in a dose-dependent manner, in part through the down-regulation of nuclear factor kappaB (NFkappaB) activation in IL-12 p40 gene. Activation of macrophages by LPS resulted in markedly enhanced binding activities to the kappaB site, which significantly decreased upon addition of sulfasalazine as demonstrated by an electrophoretic gel shift assay. Importantly, macrophages pretreated with sulfasalazine either in vitro or in vivo reduced their ability to induce interferon-gamma (IFN-gamma) and increased the ability to induce IL-4 in antigen-primed CD4+ T cells. From these results, sulfasalazine may induce the Th2 cytokine profile in CD4+ T cells by suppressing IL-12 production in macrophages, and sulfasalazine-induced inhibition of IL-12 production in macrophages may explain some of the known biological effects of sulfasalazine.

Indexed as

AnimalsAnti-Bacterial AgentsCD4-Positive T-LymphocytesCells, CulturedFemaleInterleukin-12LipopolysaccharidesListeria monocytogenesListeriosisMacrophagesMiceMice, Inbred DBASulfasalazineTh1 CellsAnti-Bacterial AgentsInterleukin-12LipopolysaccharidesSulfasalazine

Identifiers

PMID10469239
PMCPMC2326895
OpenAlexW2044633373

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.