Evidence map›Paper›PMID 27014276›Full record

ReviewFrontiers in immunology2016

Silica, Silicosis, and Autoimmunity.

Kenneth Michael Pollard

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 195 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
195citing papers in PubMed, 3 pooled it
24.3field-weighted citation impact, top 1% 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

195 citing papers in PubMed, 3 syntheses or guidelines pooled it, 422 citations in OpenAlex.

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135 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

1 author at 1 institution in 1 country.

Kenneth Michael PollardDepartment of Molecular and Experimental Medicine, The Scripps Research Institute , La Jolla, CA , USA.
Scripps Research Institute · US

Funding

Influence of Innate Immunity on Xenobiotic-Induced Systemic AutoimmunityR01ES021464 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2013 to 2017
$3.4M
Xenobiotic-Induced Type 1 Interferon-Independent AutoimmunityR01ES022625 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2014 to 2018
$2.1M
The Diversity Outbred Mouse as a Model of Silica-induced AutoimmunityR21ES024485 · NIEHS · SCRIPPS RESEARCH INSTITUTE, THE · PI POLLARD, KENNETH MICHAEL · 2014 to 2015
$521k
NIEHS NIH HHS R01 ES021464NIEHS NIH HHS R01 ES022625NIEHS NIH HHS R21 ES024485
6 · The paper itself

Abstract

Inhalation of dust containing crystalline silica is associated with a number of acute and chronic diseases including systemic autoimmune diseases. Evidence for the link with autoimmune disease comes from epidemiological studies linking occupational exposure to crystalline silica dust with the systemic autoimmune diseases systemic lupus erythematosus, systemic sclerosis, and rheumatoid arthritis. Although little is known regarding the mechanism by which silica exposure leads to systemic autoimmune disease, there is a voluminous literature on silica exposure and silicosis that may help identify immune processes that precede development of autoimmunity. The pathophysiology of silicosis consists of deposition of silica particles in the alveoli of the lung. Ingestion of these particles by macrophages initiates an inflammatory response, which stimulates fibroblasts to proliferate and produce collagen. Silica particles are encased by collagen leading to fibrosis and the nodular lesions characteristic of the disease. The steps in the development of silicosis, including acute and chronic inflammation and fibrosis, have different molecular and cellular requirements, suggesting that silica-induced inflammation and fibrosis may be mechanistically separate. Significantly, it is unclear whether silica-induced inflammation and fibrosis contribute similarly to the development of autoimmunity. Nonetheless, the findings from human and animal model studies are consistent with an autoimmune pathogenesis that begins with activation of the innate immune system leading to proinflammatory cytokine production, pulmonary inflammation leading to activation of adaptive immunity, breaking of tolerance, and autoantibodies and tissue damage. The variable frequency of these immunological features following silica exposure suggests substantial genetic involvement and gene/environment interaction in silica-induced autoimmunity. However, numerous questions remain unanswered.

Indexed as

animal modelautoimmunityhumansilicasilicosis

Identifiers

PMID27014276
PMCPMC4786551
OpenAlexW2332243084

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.