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Decrease in multiple complement proteins associated with development of islet autoimmunity and type 1 diabetes.

iScience | 2024

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.

Pubmed ID: 38303689 RIS Download

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Associated grants

  • Agency: NIDDK NIH HHS, United States
    Id: HHSN267200700014C
  • Agency: NIDDK NIH HHS, United States
    Id: R01 DK032493
  • Agency: NCATS NIH HHS, United States
    Id: UL1 TR002535

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