Evidence map›Paper›PMID 31333589›Full record

SynthesisFrontiers in endocrinology2019

Type 2 Diabetes: How Much of an Autoimmune Disease?

Paola de Candia, Francesco Prattichizzo, Silvia Garavelli, Veronica De Rosa, Mario Galgani, Francesca Di Rella, Maria Immacolata Spagnuolo, Alessandra Colamatteo, Clorinda Fusco, Teresa Micillo and 4 more

Abstract readSystematic Review
In one paragraph

Synthesis in Frontiers in endocrinology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
–field-weighted citation impact
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

69 citing papers in PubMed.

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9 more citing papers are in PubMed but not listed here.

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

14 authors.

Paola de CandiaIRCCS MultiMedica, Milan, Italy.
Francesco PrattichizzoIRCCS MultiMedica, Milan, Italy.
Silvia GaravelliLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.
Veronica De RosaLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.
Mario GalganiLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.
Francesca Di RellaDipartimento di Senologia, Oncologia Medica, IRCCS-Fondazione G. Pascale, Naples, Italy.
Maria Immacolata SpagnuoloDipartimento di Scienze Mediche Traslazionali, Università Degli Studi di Napoli "Federico II", Naples, Italy.
Alessandra ColamatteoTreg Cell Laboratory, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Degli Studi di Napoli "Federico II", Naples, Italy.
Clorinda FuscoTreg Cell Laboratory, Dipartimento di Medicina Molecolare e Biotecnologie Mediche, Università Degli Studi di Napoli "Federico II", Naples, Italy.
Teresa MicilloDipartimento di Biologia, Università Degli Studi di Napoli "Federico II", Naples, Italy.
Sara BruzzanitiLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.
Antonio CerielloIRCCS MultiMedica, Milan, Italy.
Annibale A PucaIRCCS MultiMedica, Milan, Italy.
Giuseppe MatareseLaboratorio di Immunologia, Istituto di Endocrinologia e Oncologia Sperimentale, Consiglio Nazionale Delle Ricerche (IEOS-CNR), Naples, Italy.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 2 diabetes (T2D) is characterized by a progressive status of chronic, low-grade inflammation (LGI) that accompanies the whole trajectory of the disease, from its inception to complication development. Accumulating evidence is disclosing a long list of possible "triggers" of inflammatory responses, many of which are promoted by unhealthy lifestyle choices and advanced age. Diabetic patients show an altered number and function of immune cells, of both innate and acquired immunity. Reactive autoantibodies against islet antigens can be detected in a subpopulation of patients, while emerging data are also suggesting an altered function of specific T lymphocyte populations, including T regulatory (Treg) cells. These observations led to the hypothesis that part of the inflammatory response mounting in T2D is attributable to an autoimmune phenomenon. Here, we review recent data supporting this framework, with a specific focus on both tissue resident and circulating Treg populations. We also propose that selective interception (or expansion) of T cell subsets could be an alternative avenue to dampen inappropriate inflammatory responses without compromising immune responses.

Indexed as

autoimmunitydiabetesimmunometabolisminflammationT cells

Identifiers

PMID31333589
PMCPMC6620611

What OpenQuestion holds

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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.