Evidence map›Paper›PMID 16418805›Full record

ArticleJournal of clinical immunology2006

COX-2 inhibitors modulate IL-12 signaling through JAK-STAT pathway leading to Th1 response in experimental allergic encephalomyelitis.

Gladson Muthian, Himanshu P Raikwar, Caroline Johnson, Johnson Rajasingh, Amit Kalgutkar, Lawrence J Marnett, John J Bright

Abstract read
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In one paragraph

Article in Journal of clinical immunology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.9field-weighted citation impact, top 9% 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, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.

  1. Pooled it
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  13. Involvement of the janus kinase/signal transducer and activator of transcription signaling pathway in multiple sclerosis and the animal model of experimental autoimmune encephalomyelitis.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2014
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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

7 authors at 1 institution in 1 country.

Gladson MuthianDepartment of Neurology, Vanderbilt University Medical Center, Nashville, Tennessee, USA.
Himanshu P Raikwar
Caroline Johnson
Johnson Rajasingh
Amit Kalgutkar
Lawrence J Marnett
John J Bright
Vanderbilt University Medical Center · US

Funding

FUNCTIONAL ANALYSIS OF CYCLOOXYGENASE 2R01CA089450 · NCI · VANDERBILT UNIVERSITY · PI MARNETT, LAWRENCE J. · 2001 to 2016
$6.3M
PPAR-gamma regulation of IL-12 in CNS demyelinationR01NS042257 · NINDS · VANDERBILT UNIVERSITY · PI BRIGHT, JOHN J · 2003 to 2005
$675k
NCI NIH HHS CA89450NINDS NIH HHS R01 NS42257-01A1
6 · The paper itself

Abstract

Experimental allergic encephalomyelitis (EAE) is a Th1 cell-mediated autoimmune disease model of multiple sclerosis (MS). IL-12 plays a crucial role in the pathogenesis of EAE/MS and inhibition of IL-12 production or IL-12 signaling was effective in preventing EAE. Cyclooxygenase (COX-2) is a key enzyme promoting inflammation in rheumatoid arthritis and tumor induced angiogenesis. Recent studies have shown that COX-2 inhibitors prevent EAE, however, their mechanism of action is not fully understood. In this study, we show that in vivo treatment (i.p.) with 100 mug COX-2 selective inhibitors (LM01, LM08, LM11, and NS398), on every other day from day 0 to 30, significantly reduced the incidence and severity of EAE in SJL/J and C57BL/6 mice. Further analyses showed that the COX-2 inhibitors reduced neural antigen-induced IL-12 production, T cell proliferation and Th1 differentiation ex vivo and in vitro. The COX-2 inhibitors also decreased IL-12-induced T cell responses through blocking tyrosine phosphorylation of JAK2, TYK2, STAT3, and STAT4 proteins in T cells. These results demonstrate that COX-2 inhibitors ameliorate EAE in association with the modulation of IL-12 signaling through JAK-STAT pathway leading to Th1 differentiation and suggest their use in the treatment of MS and other Th1 cell-mediated autoimmune diseases.

Indexed as

AnimalsCell ProliferationCyclooxygenase 2 InhibitorsDemyelinating DiseasesEncephalomyelitis, Autoimmune, ExperimentalInflammationInterferon-gammaInterleukin-12Janus Kinase 2MiceMice, Inbred C57BLMultiple Sclerosis, Chronic ProgressiveMultiple Sclerosis, Relapsing-RemittingPhosphorylationProtein-Tyrosine KinasesProto-Oncogene ProteinsCyclooxygenase 2 InhibitorsInterferon-gammaInterleukin-12Jak2 protein, mouseJanus Kinase 2Protein-Tyrosine KinasesProto-Oncogene ProteinsSTAT3 Transcription FactorSTAT4 Transcription Factor

Identifiers

PMID16418805
OpenAlexW2005897699

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.