Evidence map›Paper›PMID 19912253›Full record

ArticleClinical and experimental immunology2010

Gene expression profiles for the human pancreas and purified islets in type 1 diabetes: new findings at clinical onset and in long-standing diabetes.

R Planas, J Carrillo, A Sanchez, M C Ruiz de Villa, F Nuñez, J Verdaguer, R F L James, R Pujol-Borrell, M Vives-Pi

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In one paragraph

Article in Clinical and experimental immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.3field-weighted citation impact, top 8% 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

47 citing papers in PubMed, 95 citations in OpenAlex.

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  14. Immune cell trafficking to the islets during type 1 diabetes.Clinical and experimental immunology · 2019
    Review
  15. Dimorphism of HLA-E and its Disease Association.International journal of molecular sciences · 2019
    Review
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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

9 authors at 7 institutions in 3 countries.

R PlanasLaboratory of Immunobiology for Research and Applications to Diagnosis (LIRAD), Research Institute Germans Trias i Pujol, Badalona, Spain.
J Carrillo
A Sanchez
M C Ruiz de Villa
F Nuñez
J Verdaguer
R F L James
R Pujol-Borrell
M Vives-Pi
Universitat Autònoma de Barcelona · ESBanc de Sang i Teixits · ESBiomedical Research Institute of Lleida · ESHebron University · PSUniversitat de Barcelona · ESUniversity of Leicester · GBVall d'Hebron Institut de Recerca · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is caused by the selective destruction of the insulin-producing beta cells of the pancreas by an autoimmune response. Due to ethical and practical difficulties, the features of the destructive process are known from a small number of observations, and transcriptomic data are remarkably missing. Here we report whole genome transcript analysis validated by quantitative reverse transcription-polymerase chain reaction (qRT-PCR) and correlated with immunohistological observations for four T1D pancreases (collected 5 days, 9 months, 8 and 10 years after diagnosis) and for purified islets from two of them. Collectively, the expression profile of immune response and inflammatory genes confirmed the current views on the immunopathogenesis of diabetes and showed similarities with other autoimmune diseases; for example, an interferon signature was detected. The data also supported the concept that the autoimmune process is maintained and balanced partially by regeneration and regulatory pathway activation, e.g. non-classical class I human leucocyte antigen and leucocyte immunoglobulin-like receptor, subfamily B1 (LILRB1). Changes in gene expression in islets were confined mainly to endocrine and neural genes, some of which are T1D autoantigens. By contrast, these islets showed only a few overexpressed immune system genes, among which bioinformatic analysis pointed to chemokine (C-C motif) receptor 5 (CCR5) and chemokine (CXC motif) receptor 4) (CXCR4) chemokine pathway activation. Remarkably, the expression of genes of innate immunity, complement, chemokines, immunoglobulin and regeneration genes was maintained or even increased in the long-standing cases. Transcriptomic data favour the view that T1D is caused by a chronic inflammatory process with a strong participation of innate immunity that progresses in spite of the regulatory and regenerative mechanisms.

Indexed as

Gene Expression ProfilingAdolescentAdultAntigens, CDAntigens, NeoplasmBiomarkers, TumorCell CountC-Reactive ProteinDiabetes Mellitus, Type 1Down-RegulationFemaleGene ExpressionGlucagon-Secreting CellsHistocompatibility Antigens Class IHLA AntigensHLA-E AntigensAntigens, CDAntigens, NeoplasmBiomarkers, TumorC-Reactive ProteinHistocompatibility Antigens Class IHLA AntigensHLA-E AntigensLectins, C-TypePancreatitis-Associated ProteinsREG3A protein, human

Identifiers

PMID19912253
PMCPMC2802692
OpenAlexW2039773800

What OpenQuestion holds

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Registered trials

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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.