Evidence map›Paper›PMID 27175635›Full record

ArticleMedicine2016

Transcriptome Analysis of Peripheral Blood in Chronic Inflammatory Demyelinating Polyradiculoneuropathy Patients Identifies TNFR1 and TLR Pathways in the IVIg Response.

Alexandra Richard, Jean-Christophe Corvol, Rabab Debs, Pauline Reach, Khadija Tahiri, Wassila Carpentier, Justine Gueguen, Vincent Guillemot, Céline Labeyrie, David Adams and 2 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Medicine, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
1.1field-weighted citation impact, top 22% 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

4 citing papers in PubMed, 11 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
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

12 authors at 3 institutions in 2 countries.

Alexandra RichardFrom the Sorbonne Universités (AR, J-CC, KT), UPMC Univ Paris 06, INSERM UMRS_1127, CIC_1422, CNRS UMR_7225, AP-HP, and ICM, Hôpital Pitié-Salpêtrière, Département des maladies du système nerveux; Hôpital Pitié Salpêtrière (RD, PR, KV), Département de Neurophysiologie Clinique; Plateforme Post-génomique P3S (WC), UPMC, Site Pitié Salpêtrière; IHU-A-ICM Bioinformatics/Biostatistics Core Facility (JG, VG), Paris; Hôpital de Bicêtre (CL, DA), Centre de Référence des Neuropathies Amyloïdes et autres Neuropathies Périphériques Rares, Le Kremlin-Bicêtre; and AP-HP, Hôpital Pitié Salpêtrière, Service de Médecine Interne, Institut E3M, Centre National de Référence Maladies auto-immunes Systémiques Rares, et Université Paris VI Pierre et Marie Curie, Sorbonnes Université, Paris, France (FCA).
Jean-Christophe Corvol
Rabab Debs
Pauline Reach
Khadija Tahiri
Wassila Carpentier
Justine Gueguen
Vincent Guillemot
Céline Labeyrie
David Adams
Karine Viala
Fleur Cohen Aubart
Nerve Centre · GBPitié-Salpêtrière Hospital · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We have studied the response to intravenous immunoglobulins (IVIg) by a transcriptomic approach in 11 chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) patients (CIDP duration = 6 [0.83-6.5] years). RNA was extracted from cells in whole blood collected before and 3 weeks after IVIg treatment, and hybridized on Illumina chips. After RNA quality controls, gene expression was analyzed using statistical tests fitted for microarrays (R software, limma package), and a pathway analysis was performed using DAVID software. We identified 52 genes with expression that varied significantly after IVIg (fold change [FC] > 1.2, P < 0.001, false discovery rate [FDR] <0.05). Among these 52 genes, 7 were related to immunity, 3 were related to the tumor necrosis factor (TNF)-α receptor 1 (TNFR1) pathway (inhibitor of caspase-activated DNase (ICAD): FC = 1.8, P = 1.7E-7, FDR = 0.004; p21 protein-activated kinase 2 [PAK2]: FC = 1.66, P = 2.6E-5, FDR = 0.03; TNF-α-induced protein 8-like protein 1 [TNFAIP8L1]: P = 1.00E-05, FDR = 0.026), and 2 were related to Toll-like receptors (TLRs), especially TLRs 7 and 9, and were implicated in autoimmunity. These genes were UNC93B1 (FC = 1.6, P = 2E-5, FDR = 0.03), which transports TLRs 7 and 9 to the endolysosomes, and RNF216 (FC = 1.5, P = 1E-05, FDR = 0.03), which promotes TLR 9 degradation. Pathway analysis showed that the TNFR1 pathway was significantly lessened by IVIg (enrichment score = 24, Fischer exact test = 0.003). TNF-α gene expression was higher in responder patients than in nonresponders; however, it decreased after IVIg in responders (P = 0.04), but remained stable in nonresponders. Our data suggest the actions of IVIg on the TNFR1 pathway and an original mechanism involving innate immunity through TLRs in CIDP pathophysiology and the response to IVIg. We conclude that responder patients have stronger inflammatory activity that is lessened by IVIg.

Indexed as

Gene Expression ProfilingAgedAntibody FormationFemaleHumansImmunoglobulins, IntravenousMaleMiddle AgedPharmacogeneticsPolyradiculoneuropathy, Chronic Inflammatory DemyelinatingReceptors, Tumor Necrosis Factor, Type ISignal TransductionToll-Like ReceptorsTumor Necrosis Factor-alphaImmunoglobulins, IntravenousReceptors, Tumor Necrosis Factor, Type ITNF protein, humanTNFRSF1A protein, humanToll-Like ReceptorsTumor Necrosis Factor-alpha

Identifiers

PMID27175635
PMCPMC4902477
OpenAlexW2372224646

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.