Evidence map›Paper›PMID 29037052›Full record

ReviewAntioxidants & redox signaling2018

Redox-Sensitive Innate Immune Pathways During Macrophage Activation in Type 1 Diabetes.

Ashley R Burg, Hubert M Tse

Abstract readReview
In one paragraph

Review in Antioxidants & redox signaling, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Article
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  15. The Impact of the CaBiomolecules · 2021
    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

2 authors at 1 institution in 1 country.

Ashley R BurgDepartment of Microbiology, Comprehensive Diabetes Center, University of Alabama at Birmingham , Birmingham, Alabama.
Hubert M TseDepartment of Microbiology, Comprehensive Diabetes Center, University of Alabama at Birmingham , Birmingham, Alabama.
University of Alabama at Birmingham · US

Funding

Zevalin Radioimmunotherapy Using a Modified TreatmentM01RR000032 · NCRR · UNIVERSITY OF SOUTHERN CALIFORNIA · PI RICH, ROBERT R. · 1985 to 2008
$23.6M
University of Alabama at Birmingham's Diabetes Research CenterP30DK079626 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Kirk Michael Habegger · 2013 to 2026
$19.5M
IMMUNOLOGIC DISEASES AND BASIC IMMUNOLOGYT32AI007051 · NIAID · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI Laurie Ellen Harrington · 1985 to 2026
$13.1M
NCRR NIH HHS M01 RR000032NIAID NIH HHS T32 AI007051NIDDK NIH HHS P30 DK079626
6 · The paper itself

Abstract

significanceType 1 diabetes (T1D) is an autoimmune disease resulting in β-cell destruction mediated by islet-infiltrating leukocytes. The role of oxidative stress in human and murine models of T1D is highly significant as these noxious molecules contribute to diabetic complications and β-cell lysis, but their direct impact on dysregulated autoimmune responses is highly understudied. Pro-inflammatory macrophages play a vital role in the initiation and effector phases of T1D by producing free radicals and pro-inflammatory cytokines to facilitate β-cell destruction and to present antigen to autoreactive T cells. Recent Advances: Redox modulation of macrophage functions may play critical roles in autoimmunity. These include enhancing pro-inflammatory innate immune signaling pathways in response to environmental triggers, enforcing an M1 macrophage differentiation program, controlling antigen processing, and altering peptide recognition by oxidative post-translational modification. Therefore, an oxidative environment may act on multiple macrophage functions to orchestrate T1D pathogenesis. CRITICAL ISSUES: Mechanisms involved in the initiation of T1D remain unclear, making preventive and early therapeutics difficult to develop. Although many of these advances in the redox regulation of macrophages are in their infancy, they provide insight into how oxidative stress aids in the precipitating event of autoimmune activation. FUTURE DIRECTIONS: Future studies should be aimed at mechanistically determining which redox-regulated macrophage functions are pertinent in T1D pathogenesis, as well as at investigating potential targetable therapeutics to halt and/or dampen innate immune activation in T1D.

Indexed as

AnimalsDiabetes Mellitus, Type 1HumansImmunity, InnateMacrophage ActivationMacrophagesOxidation-Reductioninnate immunitymacrophageNADPH oxidasereactive oxygen speciestype 1 diabetesvirus

Identifiers

PMID29037052
PMCPMC6166692
OpenAlexW2769772366

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.