Evidence map›Paper›PMID 26780034›Full record

ReviewClinical reviews in allergy & immunology2017

The Immune Response and the Pathogenesis of Idiopathic Inflammatory Myositis: a Critical Review.

Angela Ceribelli, Maria De Santis, Natasa Isailovic, M Eric Gershwin, Carlo Selmi

Abstract readReview
PubMed Publisher
In one paragraph

Review in Clinical reviews in allergy & immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
4.1field-weighted citation impact, top 6% 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

28 citing papers in PubMed, 61 citations in OpenAlex.

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  8. [Significance of anti-Jo-1 antibody's clinical stratification in idiopathic inflammatory myopathy and disease spectrum].Beijing da xue xue bao. Yi xue ban = Journal of Peking University. Health sciences · 2023
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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 3 institutions in 2 countries.

Angela CeribelliDivision of Rheumatology and Clinical Immunology, Humanitas Research Hospital, via A. Manzoni 56, 20089, Rozzano, MI, Italy.
Maria De SantisDivision of Rheumatology and Clinical Immunology, Humanitas Research Hospital, via A. Manzoni 56, 20089, Rozzano, MI, Italy.
Natasa IsailovicDivision of Rheumatology and Clinical Immunology, Humanitas Research Hospital, via A. Manzoni 56, 20089, Rozzano, MI, Italy.
M Eric GershwinDivision of Rheumatology, Allergy, and Clinical Immunology, University of California Davis, Davis, CA, USA.
Carlo SelmiDivision of Rheumatology and Clinical Immunology, Humanitas Research Hospital, via A. Manzoni 56, 20089, Rozzano, MI, Italy. carlo.selmi@unimi.it.
IRCCS Humanitas Research Hospital · ITUniversity of Milan · ITUniversity of California, Davis · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The pathogenesis of idiopathic inflammatory myositis (IIMs, including polymyositis and dermatomyositis) remains largely enigmatic, despite advances in the study of the role played by innate immunity, adaptive immunity, genetic predisposition, and environmental factors in an orchestrated response. Several factors are involved in the inflammatory state that characterizes the different forms of IIMs which share features and mechanisms but are clearly different with respect to the involved sites and characteristics of the inflammation. Cellular and non-cellular mechanisms of both the immune and non-immune systems have been identified as key regulators of inflammation in polymyositis/dermatomyositis, particularly at different stages of disease, leading to the fibrotic state that characterizes the end stage. Among these, a special role is played by an interferon signature and complement cascade with different mechanisms in polymyositis and dermatomyositis; these differences can be identified also histologically in muscle biopsies. Numerous cellular components of the adaptive and innate immune response are present in the site of tissue inflammation, and the complexity of idiopathic inflammatory myositis is further supported by the involvement of non-immune mechanisms such as hypoxia and autophagy. The aim of this comprehensive review is to describe the major pathogenic mechanisms involved in the onset of idiopathic inflammatory myositis and to report on the major working hypothesis with therapeutic implications.

Indexed as

HumansMusclesMyositisCancerDermatomyositisInflammationMuscle biopsyPolymyositis

Identifiers

PMID26780034
OpenAlexW2254989075

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.