scholarly journals Natural History of β-Cell Autoimmunity in Young Children with Increased Genetic Susceptibility to Type 1 Diabetes Recruited from the General Population

2002 ◽  
Vol 87 (10) ◽  
pp. 4572-4579 ◽  
Author(s):  
T. Kimpimäki ◽  
P. Kulmala ◽  
K. Savola ◽  
A. Kupila ◽  
S. Korhonen ◽  
...  
Diabetes ◽  
2015 ◽  
Vol 65 (3) ◽  
pp. 719-731 ◽  
Author(s):  
Martha Campbell-Thompson ◽  
Ann Fu ◽  
John S. Kaddis ◽  
Clive Wasserfall ◽  
Desmond A. Schatz ◽  
...  

2015 ◽  
Vol 11 (01) ◽  
pp. 10 ◽  
Author(s):  
Kimber M Simmons ◽  
Aaron W Michels ◽  
◽  

Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by destruction of insulin-producing β cells in the pancreas. The incidence of T1D is increasing dramatically, and the prevalence has doubled in the last 2 decades, further increasing the morbidity and mortality associated with the disease. T1D is now predictable with the measurement of antibodies directed against β cell proteins. Islet autoantibodies (IAs) are detectable from the peripheral blood months to years before clinical diagnosis. With the presence of two or more antibodies, the risk for developing T1D is nearly 100 % given enough time. Targeted screening for T1D risk has been carried out in first-degree relatives and those with a significant genetic risk. However, more than 85 % of individuals who are diagnosed with T1D do not have a family history. In light of the predictability of T1D and recent advances in IA measurement, general population screening is on the horizon. We provide an overview of the history of general population screening and discuss the rationale for and arguments against screening the general population for T1D risk.


2019 ◽  
Vol 15 (5) ◽  
pp. 256-257 ◽  
Author(s):  
Paolo Pozzilli ◽  
Alberto Signore

2012 ◽  
Vol 95 (2) ◽  
pp. 471-478 ◽  
Author(s):  
Suvi M Virtanen ◽  
Jaakko Nevalainen ◽  
Carina Kronberg-Kippilä ◽  
Suvi Ahonen ◽  
Heli Tapanainen ◽  
...  

1999 ◽  
Vol 44 ◽  
pp. S26
Author(s):  
S. Salardi ◽  
S. Zucchini ◽  
L. Ragni ◽  
B. Mainetti ◽  
E. Cacciari

2009 ◽  
Vol 25 (4) ◽  
pp. 325-328 ◽  
Author(s):  
Jerry P. Palmer

2006 ◽  
Vol 155 (4) ◽  
pp. 633-642 ◽  
Author(s):  
Matti S Ronkainen ◽  
Sanna Hoppu ◽  
Sari Korhonen ◽  
Satu Simell ◽  
Riitta Veijola ◽  
...  

Objective: The pattern of the humoral immunity to disease-associated autoantigens may reflect the severity of the autoimmune disease process. The purpose of this study was to delineate the maturation of the humoral immunity to one of the main autoantigens in type 1 diabetes (T1D), glutamic acid decarboxylase (GAD65). Design and methods: Serum samples were obtained for the detection of epitope- and isotype-specific antibodies sequentially with short intervals from 36 young children with HLA-conferred genetic susceptibility to T1D starting from the first appearance of GAD65Ab. During prospective observation, ten children developed T1D. Antibodies were analyzed using biotinylated anti-human immunoglobulin (Ig) antibodies and chimeric GAD molecules in radio-binding assays. Results: The immune response to GAD65 started as reactivity to the middle region and spread rapidly to the C-terminal region. IgG1 antibodies dominated among the isotypes from the first appearance of GAD65Ab, while other IgG subclasses were observed to a lesser extent. IgG4 antibodies emerged clearly as the last IgG subclass. A broad initial response comprising three to four IgG subclasses and the lack of an emerging IgG4 response during follow-up was associated with increased risk for progression to clinical diabetes (P<0.05). Conclusions: The humoral response to GAD65 epitope clusters is relatively uniform in young children, whereas there is conspicuous individual variation in IgG subclass responses except for IgG1. A narrow initial IgG subclass response to GAD65 and the emergence of IgG4 antibodies were characteristic of those who remained non-diabetic over the first few years of GAD65 autoimmunity.


2010 ◽  
Vol 39 (3) ◽  
pp. 513-525 ◽  
Author(s):  
Ezio Bonifacio ◽  
Anette G. Ziegler

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