Journal article
Decrease in multiple complement proteins associated with development of islet autoimmunity and type 1 diabetes
iScience, Vol.27(2), p.108769
02/16/2024
DOI: 10.1016/j.isci.2023.108769
PMCID: PMC10831269
PMID: 38303689
Abstract
Type 1 diabetes (T1D) is a chronic condition caused by autoimmune destruction of the insulin-producing pancreatic β cells. While it is known that gene-environment interactions play a key role in triggering the autoimmune process leading to T1D, the pathogenic mechanism leading to the appearance of islet autoantibodies—biomarkers of autoimmunity—is poorly understood. Here we show that disruption of the complement system precedes the detection of islet autoantibodies and persists through disease onset. Our results suggest that children who exhibit islet autoimmunity and progress to clinical T1D have lower complement protein levels relative to those who do not progress within a similar time frame. Thus, the complement pathway, an understudied mechanistic and therapeutic target in T1D, merits increased attention for use as protein biomarkers of prediction and potentially prevention of T1D.
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•The complement pathway is a possible target to predict onset of type 1 diabetes•Complement proteins are lower relative to controls prior to islet autoimmunity•The disruption of the complement system persists through type 1 diabetes onset
Immunology; Diabetology; Proteomics
Details
- Title: Subtitle
- Decrease in multiple complement proteins associated with development of islet autoimmunity and type 1 diabetes
- Creators
- Bobbie-Jo M. Webb-Robertson - Pacific Northwest National LaboratoryErnesto S. Nakayasu - Pacific Northwest National LaboratoryFran Dong - University of Colorado Anschutz Medical CampusKathy C. Waugh - University of Colorado Anschutz Medical CampusJavier E. Flores - Pacific Northwest National LaboratoryLisa M. Bramer - Pacific Northwest National LaboratoryAthena A. Schepmoes - Pacific Northwest National LaboratoryYuqian Gao - Pacific Northwest National LaboratoryThomas L. Fillmore - Pacific Northwest National LaboratorySuna Onengut-Gumuscu - University of VirginiaAshley Frazer-Abel - University of Colorado Anschutz Medical CampusStephen S. Rich - University of VirginiaV. Michael Holers - University of Colorado Anschutz Medical CampusThomas O. Metz - Pacific Northwest National LaboratoryMarian J. Rewers - University of Colorado Anschutz Medical Campus
- Resource Type
- Journal article
- Publication Details
- iScience, Vol.27(2), p.108769
- DOI
- 10.1016/j.isci.2023.108769
- PMID
- 38303689
- PMCID
- PMC10831269
- NLM abbreviation
- iScience
- ISSN
- 2589-0042
- eISSN
- 2589-0042
- Publisher
- Elsevier Inc
- Language
- English
- Date published
- 02/16/2024
- Academic Unit
- Biostatistics
- Record Identifier
- 9985113181902771
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