Islet autoantibodies as precision diagnostic tools to characterize heterogeneity in type 1 diabetes: a systematic review.


Journal

Communications medicine
ISSN: 2730-664X
Titre abrégé: Commun Med (Lond)
Pays: England
ID NLM: 9918250414506676

Informations de publication

Date de publication:
06 Apr 2024
Historique:
received: 09 05 2023
accepted: 05 03 2024
medline: 7 4 2024
pubmed: 7 4 2024
entrez: 6 4 2024
Statut: epublish

Résumé

Islet autoantibodies form the foundation for type 1 diabetes (T1D) diagnosis and staging, but heterogeneity exists in T1D development and presentation. We hypothesized that autoantibodies can identify heterogeneity before, at, and after T1D diagnosis, and in response to disease-modifying therapies. We systematically reviewed PubMed and EMBASE databases (6/14/2022) assessing 10 years of original research examining relationships between autoantibodies and heterogeneity before, at, after diagnosis, and in response to disease-modifying therapies in individuals at-risk or within 1 year of T1D diagnosis. A critical appraisal checklist tool for cohort studies was modified and used for risk of bias assessment. Here we show that 152 studies that met extraction criteria most commonly characterized heterogeneity before diagnosis (91/152). Autoantibody type/target was most frequently examined, followed by autoantibody number. Recurring themes included correlations of autoantibody number, type, and titers with progression, differing phenotypes based on order of autoantibody seroconversion, and interactions with age and genetics. Only 44% specifically described autoantibody assay standardization program participation. Current evidence most strongly supports the application of autoantibody features to more precisely define T1D before diagnosis. Our findings support continued use of pre-clinical staging paradigms based on autoantibody number and suggest that additional autoantibody features, particularly in relation to age and genetic risk, could offer more precise stratification. To improve reproducibility and applicability of autoantibody-based precision medicine in T1D, we propose a methods checklist for islet autoantibody-based manuscripts which includes use of precision medicine MeSH terms and participation in autoantibody standardization workshops. Islet autoantibodies are markers found in the blood when insulin-producing cells in the pancreas become damaged and can be used to predict future development of type 1 diabetes. We evaluated published literature to determine whether characteristics of islet antibodies (type, levels, numbers) could improve prediction and help understand differences in how individuals with type 1 diabetes respond to treatments. We found existing evidence shows that islet autoantibody type and number are most useful to predict disease progression before diagnosis. In addition, the age when islet autoantibodies first appear strongly influences rate of progression. These findings provide important information for patients and care providers on how islet autoantibodies can be used to understand future type 1 diabetes development and to identify individuals who have the potential to benefit from intervention or prevention therapy.

Sections du résumé

BACKGROUND BACKGROUND
Islet autoantibodies form the foundation for type 1 diabetes (T1D) diagnosis and staging, but heterogeneity exists in T1D development and presentation. We hypothesized that autoantibodies can identify heterogeneity before, at, and after T1D diagnosis, and in response to disease-modifying therapies.
METHODS METHODS
We systematically reviewed PubMed and EMBASE databases (6/14/2022) assessing 10 years of original research examining relationships between autoantibodies and heterogeneity before, at, after diagnosis, and in response to disease-modifying therapies in individuals at-risk or within 1 year of T1D diagnosis. A critical appraisal checklist tool for cohort studies was modified and used for risk of bias assessment.
RESULTS RESULTS
Here we show that 152 studies that met extraction criteria most commonly characterized heterogeneity before diagnosis (91/152). Autoantibody type/target was most frequently examined, followed by autoantibody number. Recurring themes included correlations of autoantibody number, type, and titers with progression, differing phenotypes based on order of autoantibody seroconversion, and interactions with age and genetics. Only 44% specifically described autoantibody assay standardization program participation.
CONCLUSIONS CONCLUSIONS
Current evidence most strongly supports the application of autoantibody features to more precisely define T1D before diagnosis. Our findings support continued use of pre-clinical staging paradigms based on autoantibody number and suggest that additional autoantibody features, particularly in relation to age and genetic risk, could offer more precise stratification. To improve reproducibility and applicability of autoantibody-based precision medicine in T1D, we propose a methods checklist for islet autoantibody-based manuscripts which includes use of precision medicine MeSH terms and participation in autoantibody standardization workshops.
Islet autoantibodies are markers found in the blood when insulin-producing cells in the pancreas become damaged and can be used to predict future development of type 1 diabetes. We evaluated published literature to determine whether characteristics of islet antibodies (type, levels, numbers) could improve prediction and help understand differences in how individuals with type 1 diabetes respond to treatments. We found existing evidence shows that islet autoantibody type and number are most useful to predict disease progression before diagnosis. In addition, the age when islet autoantibodies first appear strongly influences rate of progression. These findings provide important information for patients and care providers on how islet autoantibodies can be used to understand future type 1 diabetes development and to identify individuals who have the potential to benefit from intervention or prevention therapy.

Autres résumés

Type: plain-language-summary (eng)
Islet autoantibodies are markers found in the blood when insulin-producing cells in the pancreas become damaged and can be used to predict future development of type 1 diabetes. We evaluated published literature to determine whether characteristics of islet antibodies (type, levels, numbers) could improve prediction and help understand differences in how individuals with type 1 diabetes respond to treatments. We found existing evidence shows that islet autoantibody type and number are most useful to predict disease progression before diagnosis. In addition, the age when islet autoantibodies first appear strongly influences rate of progression. These findings provide important information for patients and care providers on how islet autoantibodies can be used to understand future type 1 diabetes development and to identify individuals who have the potential to benefit from intervention or prevention therapy.

Identifiants

pubmed: 38582818
doi: 10.1038/s43856-024-00478-y
pii: 10.1038/s43856-024-00478-y
doi:

Types de publication

Journal Article

Langues

eng

Pagination

66

Investigateurs

Deirdre K Tobias (DK)
Jordi Merino (J)
Abrar Ahmad (A)
Catherine Aiken (C)
Jamie L Benham (JL)
Dhanasekaran Bodhini (D)
Amy L Clark (AL)
Kevin Colclough (K)
Rosa Corcoy (R)
Sara J Cromer (SJ)
Daisy Duan (D)
Jamie L Felton (JL)
Ellen C Francis (EC)
Pieter Gillard (P)
Véronique Gingras (V)
Romy Gaillard (R)
Eram Haider (E)
Alice Hughes (A)
Jennifer M Ikle (JM)
Laura M Jacobsen (LM)
Anna R Kahkoska (AR)
Jarno L T Kettunen (JLT)
Raymond J Kreienkamp (RJ)
Lee-Ling Lim (LL)
Jonna M E Männistö (JME)
Robert Massey (R)
Niamh-Maire Mclennan (NM)
Rachel G Miller (RG)
Mario Luca Morieri (ML)
Jasper Most (J)
Rochelle N Naylor (RN)
Bige Ozkan (B)
Kashyap Amratlal Patel (KA)
Scott J Pilla (SJ)
Katsiaryna Prystupa (K)
Sridharan Raghavan (S)
Mary R Rooney (MR)
Martin Schön (M)
Zhila Semnani-Azad (Z)
Magdalena Sevilla-Gonzalez (M)
Pernille Svalastoga (P)
Wubet Worku Takele (WW)
Claudia Ha-Ting Tam (CH)
Anne Cathrine B Thuesen (ACB)
Mustafa Tosur (M)
Amelia S Wallace (AS)
Caroline C Wang (CC)
Jessie J Wong (JJ)
Jennifer M Yamamoto (JM)
Katherine Young (K)
Chloé Amouyal (C)
Mette K Andersen (MK)
Maxine P Bonham (MP)
Mingling Chen (M)
Feifei Cheng (F)
Tinashe Chikowore (T)
Sian C Chivers (SC)
Christoffer Clemmensen (C)
Dana Dabelea (D)
Adem Y Dawed (AY)
Aaron J Deutsch (AJ)
Laura T Dickens (LT)
Linda A DiMeglio (LA)
Monika Dudenhöffer-Pfeifer (M)
Carmella Evans-Molina (C)
María Mercè Fernández-Balsells (MM)
Hugo Fitipaldi (H)
Stephanie L Fitzpatrick (SL)
Stephen E Gitelman (SE)
Mark O Goodarzi (MO)
Jessica A Grieger (JA)
Marta Guasch-Ferré (M)
Nahal Habibi (N)
Torben Hansen (T)
Chuiguo Huang (C)
Arianna Harris-Kawano (A)
Heba M Ismail (HM)
Benjamin Hoag (B)
Angus G Jones (AG)
Robert W Koivula (RW)
Aaron Leong (A)
Gloria K W Leung (GKW)
Ingrid M Libman (IM)
Kai Liu (K)
William L Lowe (WL)
Robert W Morton (RW)
Ayesha A Motala (AA)
Suna Onengut-Gumuscu (S)
James S Pankow (JS)
Maleesa Pathirana (M)
Sofia Pazmino (S)
Dianna Perez (D)
John R Petrie (JR)
Camille E Powe (CE)
Alejandra Quinteros (A)
Rashmi Jain (R)
Debashree Ray (D)
Mathias Ried-Larsen (M)
Zeb Saeed (Z)
Vanessa Santhakumar (V)
Sarah Kanbour (S)
Sudipa Sarkar (S)
Gabriela S F Monaco (GSF)
Denise M Scholtens (DM)
Elizabeth Selvin (E)
Wayne Huey-Herng Sheu (WH)
Maggie A Stanislawski (MA)
Nele Steenackers (N)
Andrea K Steck (AK)
Norbert Stefan (N)
Julie Støy (J)
Rachael Taylor (R)
Sok Cin Tye (SC)
Gebresilasea Gendisha Ukke (GG)
Marzhan Urazbayeva (M)
Bart Van der Schueren (B)
Camille Vatier (C)
Wesley Hannah (W)
Sara L White (SL)
Gechang Yu (G)
Yingchai Zhang (Y)
Shao J Zhou (SJ)
Jacques Beltrand (J)
Michel Polak (M)
Ingvild Aukrust (I)
Elisa de Franco (E)
Sarah E Flanagan (SE)
Kristin A Maloney (KA)
Andrew McGovern (A)
Janne Molnes (J)
Mariam Nakabuye (M)
Pål Rasmus Njølstad (PR)
Hugo Pomares-Millan (H)
Michele Provenzano (M)
Cécile Saint-Martin (C)
Cuilin Zhang (C)
Yeyi Zhu (Y)
Sungyoung Auh (S)
Russell de Souza (R)
Andrea J Fawcett (AJ)
Chandra Gruber (C)
Eskedar Getie Mekonnen (EG)
Emily Mixter (E)
Diana Sherifali (D)
Robert H Eckel (RH)
John J Nolan (JJ)
Louis H Philipson (LH)
Rebecca J Brown (RJ)
Liana K Billings (LK)
Kristen Boyle (K)
Tina Costacou (T)
John M Dennis (JM)
Jose C Florez (JC)
Anna L Gloyn (AL)
Maria F Gomez (MF)
Peter A Gottlieb (PA)
Siri Atma W Greeley (SAW)
Kurt Griffin (K)
Andrew T Hattersley (AT)
Irl B Hirsch (IB)
Marie-France Hivert (MF)
Korey K Hood (KK)
Jami L Josefson (JL)
Soo Heon Kwak (SH)
Lori M Laffel (LM)
Siew S Lim (SS)
Ruth J F Loos (RJF)
Ronald C W Ma (RCW)
Chantal Mathieu (C)
Nestoras Mathioudakis (N)
James B Meigs (JB)
Shivani Misra (S)
Viswanathan Mohan (V)
Rinki Murphy (R)
Richard Oram (R)
Katharine R Owen (KR)
Susan E Ozanne (SE)
Ewan R Pearson (ER)
Wei Perng (W)
Toni I Pollin (TI)
Rodica Pop-Busui (R)
Richard E Pratley (RE)
Leanne M Redman (LM)
Rebecca M Reynolds (RM)
Robert K Semple (RK)
Jennifer L Sherr (JL)
Emily K Sims (EK)
Arianne Sweeting (A)
Tiinamaija Tuomi (T)
Miriam S Udler (MS)
Kimberly K Vesco (KK)
Tina Vilsbøll (T)
Robert Wagner (R)
Stephen S Rich (SS)
Paul W Franks (PW)

Informations de copyright

© 2024. The Author(s).

Références

DiMeglio, L. A., Evans-Molina, C. & Oram, R. A. Type 1 diabetes. Lancet 391, 2449–2462 (2018).
pubmed: 29916386 pmcid: 6661119 doi: 10.1016/S0140-6736(18)31320-5
Insel, R. A. et al. Staging presymptomatic type 1 diabetes: a scientific statement of JDRF, the Endocrine Society, and the American Diabetes Association. Diabetes Care 38, 1964–1974 (2015).
pubmed: 26404926 pmcid: 5321245 doi: 10.2337/dc15-1419
Nolan, J. J. et al. ADA/EASD precision medicine in diabetes initiative: an international perspective and future vision for precision medicine in diabetes. Diabetes Care 45, 261–266 (2022).
pubmed: 35050364 pmcid: 8914425 doi: 10.2337/dc21-2216
Tobias, D. K. et al. Second international consensus report on gaps and opportunities for the clinical translation of precision diabetes medicine. Nat. Med. 29, 2438–2457 (2023).
pubmed: 37794253 pmcid: 10735053 doi: 10.1038/s41591-023-02502-5
Battaglia, M. et al. Introducing the endotype concept to address the challenge of disease heterogeneity in type 1 diabetes. Diabetes Care 43, 5–12 (2020).
pubmed: 31753960 doi: 10.2337/dc19-0880
Lampasona, V. et al. Islet Autoantibody Standardization Program 2018 Workshop: interlaboratory comparison of glutamic acid decarboxylase autoantibody assay performance. Clin. Chem. 65, 1141–1152 (2019).
pubmed: 31409598 pmcid: 8936135 doi: 10.1373/clinchem.2019.304196
Bonifacio, E. et al. Harmonization of glutamic acid decarboxylase and islet antigen-2 autoantibody assays for national institute of diabetes and digestive and kidney diseases consortia. J. Clin. Endocrinol. Metab. 95, 3360–3367 (2010).
pubmed: 20444913 pmcid: 2928900 doi: 10.1210/jc.2010-0293
Mire-Sluis, A. R., Gaines Das, R. & Lernmark, Å. The World Health Organization international collaborative study for islet cell antibodies. Diabetologia 43, 1282–1292 (2000).
pubmed: 11079747 doi: 10.1007/s001250051524
Bingley, P. J. & Williams, A. J. K. Validation of autoantibody assays in type 1 diabetes: workshop programme. Autoimmunity 37, 257–260 (2004).
pubmed: 15518037 doi: 10.1080/08916930410001710677
Marzinotto, I. et al. Islet autoantibody standardization program: interlaboratory comparison of insulin autoantibody assay performance in 2018 and 2020 workshops. Diabetologia 66, 897–912 (2023).
pubmed: 36759347 pmcid: 10036445 doi: 10.1007/s00125-023-05877-9
Ziegler, A. G. et al. Seroconversion to multiple islet autoantibodies and risk of progression to diabetes in children. J. Am. Med. Assoc. 309, 2473–2479 (2013).
doi: 10.1001/jama.2013.6285
Steck, A. K. et al. Predictors of progression from the appearance of islet autoantibodies to early childhood diabetes: The Environmental Determinants of Diabetes in the Young (TEDDY). Diabetes Care 38, 808–813 (2015).
pubmed: 25665818 pmcid: 4407751 doi: 10.2337/dc14-2426
Giannopoulou, E. Z. et al. Islet autoantibody phenotypes and incidence in children at increased risk for type 1 diabetes. Diabetologia 58, 2317–2323 (2015).
pubmed: 26138334 doi: 10.1007/s00125-015-3672-y
Vehik, K. et al. Reversion of β-cell autoimmunity changes risk of type 1 diabetes: TEDDY study. Diabetes Care 39, 1535–1542 (2016).
pubmed: 27311490 pmcid: 5001144 doi: 10.2337/dc16-0181
Gorus, F. K. et al. Twenty-year progression rate to clinical onset according to autoantibody profile, age, and HLA-DQ genotype in a registry-based group of children and adults with a first-degree relative with type 1 diabetes. Diabetes Care 40, 1065–1072 (2017).
pubmed: 28701370 doi: 10.2337/dc16-2228
Pöllänen, P. M. et al. Characterisation of rapid progressors to type 1 diabetes among children with HLA-conferred disease susceptibility. Diabetologia 60, 1284–1293 (2017).
pubmed: 28364254 doi: 10.1007/s00125-017-4258-7
Steck, A. K. et al. Predicting progression to diabetes in islet autoantibody positive children. J. Autoimmun. 90, 59–63 (2018).
pubmed: 29395739 pmcid: 5949243 doi: 10.1016/j.jaut.2018.01.006
Jacobsen, L. M. et al. Predicting progression to type 1 diabetes from ages 3 to 6 in islet autoantibody positive TEDDY children. Pediatr. Diabetes 20, 263–270 (2019).
pubmed: 30628751 pmcid: 6456374 doi: 10.1111/pedi.12812
Pöllänen, P. M. et al. Characteristics of slow progression to type 1 diabetes in children with increased HLA-conferred disease risk. J. Clin. Endocrinol. Metab. 104, 5585–5594 (2019).
pubmed: 31314077 doi: 10.1210/jc.2019-01069
Korneva, K. G. et al. Diagnostic capabilities of islet autoantibodies in children with new-onset type 1 diabetes mellitus and healthy siblings. Sovrem. Tekhnologii Med. 12, 29–35 (2021).
pubmed: 34796016 doi: 10.17691/stm2020.12.6.04
Steck, A. K. et al. Age of islet autoantibody appearance and mean levels of insulin, but not GAD or IA-2 autoantibodies, predict age of diagnosis of type 1 diabetes: diabetes autoimmunity study in the young. Diabetes Care 34, 1397–1399 (2011).
pubmed: 21562325 pmcid: 3114355 doi: 10.2337/dc10-2088
Vehik, K. et al. Development of autoantibodies in the TrialNet natural history study. Diabetes Care 34, 1897–1901 (2011).
pubmed: 21750277 pmcid: 3161292 doi: 10.2337/dc11-0560
Parikka, V. et al. Early seroconversion and rapidly increasing autoantibody concentrations predict prepubertal manifestation of type 1 diabetes in children at genetic risk. Diabetologia 55, 1926–1936 (2012).
pubmed: 22441569 doi: 10.1007/s00125-012-2523-3
Bonifacio, E. et al. An age-related exponential decline in the risk of multiple islet autoantibody seroconversion during childhood. Diabetes Care 44, 2260–2268 (2021).
pubmed: 33627366 pmcid: 8929192 doi: 10.2337/dc20-2122
Jacobsen, L. M. et al. The risk of progression to type 1 diabetes is highly variable in individuals with mulitple autoantibodies following screening. Diabetologia 63, 588–596 (2020).
pubmed: 31768570 doi: 10.1007/s00125-019-05047-w
Vehik, K. et al. Hierarchical order of distinct autoantibody spreading and progression to type 1 diabetes in the TEDDY study. Diabetes Care 43, 2066–2073 (2020).
pubmed: 32641373 pmcid: 7440899 doi: 10.2337/dc19-2547
Eising, S. et al. Danish children born with glutamic acid decarboxylase-65 and islet antigen-2 autoantibodies at birth had an increased risk to develop type 1 diabetes. Eur. J. Endocrinol. 164, 247 (2011).
pubmed: 21097569 pmcid: 3022336 doi: 10.1530/EJE-10-0792
Sosenko, J. M. et al. A longitudinal study of GAD65 and ICA512 autoantibodies during the progression to type 1 diabetes in diabetes prevention trial-type 1 (DPT-1) participants. Diabetes Care 34, 2435–2437 (2011).
pubmed: 21911777 pmcid: 3198298 doi: 10.2337/dc11-0981
Krause, S. et al. IA-2 autoantibody affinity in children at risk for type 1 diabetes. Clin. Immunol. 145, 224–229 (2012).
pubmed: 23110943 doi: 10.1016/j.clim.2012.09.010
Achenbach, P. et al. Characteristics of rapid vs slow progression to type 1 diabetes in multiple islet autoantibody-positive children. Diabetologia 56, 1615–1622 (2013).
pubmed: 23539116 doi: 10.1007/s00125-013-2896-y
Gorus, F. K. et al. Screening for insulinoma antigen 2 and zinc transporter 8 autoantibodies: a cost-effective and age-independent strategy to identify rapid progressors to clinical onset among relatives of type 1 diabetic patients. Clin. Exp. Immunol. 171, 82–90 (2013).
pubmed: 23199327 doi: 10.1111/j.1365-2249.2012.04675.x
Mbunwe, E. et al. In antibody-positive first-degree relatives of patients with type 1 diabetes, HLA-A*24 and HLA-B*18, but not HLA-B*39, are predictors of impending diabetes with distinct HLA-DQ interactions. Diabetologia 56, 1964–1970 (2013).
pubmed: 23712485 pmcid: 3918938 doi: 10.1007/s00125-013-2951-8
Xu, P. & Krischer, J. P. Prognostic classification factors associated with development of multiple autoantibodies, dysglycemia, and type 1 diabetes—a recursive partitioning analysis. Diabetes Care 39, 1036–1044 (2016).
pubmed: 27208341 pmcid: 4878220 doi: 10.2337/dc15-2292
Yu, L. et al. Zinc transporter-8 autoantibodies improve prediction of type 1 diabetes in relatives positive for the standard biochemical autoantibodies. Diabetes Care 35, 1213–1218 (2012).
pubmed: 22446173 pmcid: 3357246 doi: 10.2337/dc11-2081
Ilonen, J. et al. Patterns of β-cell autoantibody appearance and genetic associations during the first years of life. Diabetes 62, 3636–3640 (2013).
pubmed: 23835325 pmcid: 3781470 doi: 10.2337/db13-0300
Yu, L. et al. Proinsulin/insulin autoantibodies measured with electrochemiluminescent assay are the earliest indicator of prediabetic islet autoimmunity. Diabetes Care 36, 2266–2270 (2013).
pubmed: 23423694 pmcid: 3714529 doi: 10.2337/dc12-2245
Krischer, J. P. et al. Genetic and environmental interactions modify the risk of diabetes-related autoimmunity by 6 years of age: the TEDDY study. Diabetes Care 40, 1194–1202 (2017).
pubmed: 28646072 pmcid: 5566280 doi: 10.2337/dc17-0238
Bosi, E. et al. Impact of age and antibody type on progression from single to multiple autoantibodies in type 1 diabetes relatives. J. Clin. Endocrinol. Metab. 102, 2881–2886 (2017).
pubmed: 28531305 pmcid: 5546870 doi: 10.1210/jc.2017-00569
Redondo, M. J., Steck, A. K. & Pugliese, A. Genetics of type 1 diabetes. Pediatr. Diabetes 19, 346–353 (2018).
pubmed: 29094512 doi: 10.1111/pedi.12597
Lempainen, J. et al. Effect of the PTPN22 and INS risk genotypes on the progression to clinical type 1 diabetes after the initiation of β-cell autoimmunity. Diabetes 61, 963–966 (2012).
pubmed: 22357962 pmcid: 3314352 doi: 10.2337/db11-0386
Redondo, M. J. et al. A type 1 diabetes genetic risk score predicts progression of islet autoimmunity and development of type 1 diabetes in individuals at risk. Diabetes Care 41, 1887–1894 (2018).
pubmed: 30002199 pmcid: 6105323 doi: 10.2337/dc18-0087
Bender, C., Schlosser, M., Christen, U., Ziegler, A. G. & Achenbach, P. GAD autoantibody affinity in schoolchildren from the general population. Diabetologia 57, 1911–1918 (2014).
pubmed: 24939430 doi: 10.1007/s00125-014-3294-9
Siljander, H. T. et al. Insulin secretion and sensitivity in the prediction of type 1 diabetes in children with advanced β-cell autoimmunity. Eur. J. Endocrinol. 169, 479–485 (2013).
pubmed: 23904276 doi: 10.1530/EJE-13-0206
Xu, P. et al. Prognostic accuracy of immunologic and metabolic markers for type 1 diabetes in a high-risk population: receiver operating characteristic analysis. Diabetes Care 35, 1975–1980 (2012).
pubmed: 22787174 pmcid: 3447832 doi: 10.2337/dc12-0183
Fouts, A. et al. Do electrochemiluminescence assays improve prediction of time to type 1 diabetes in autoantibody-positive TrialNet subjects? Diabetes Care 39, 1738–1744 (2016).
pubmed: 27456836 pmcid: 5033080 doi: 10.2337/dc16-0302
Sosenko, J. M. et al. The use of electrochemiluminescence assays to predict autoantibody and glycemic progression toward type 1 diabetes in individuals with single autoantibodies. Diabetes Technol. Ther. 19, 183–187 (2017).
pubmed: 28177779 pmcid: 5359659 doi: 10.1089/dia.2016.0243
Jia, X. et al. High-affinity ZnT8 autoantibodies by electrochemiluminescence assay improve risk prediction for type 1 diabetes. J. Clin. Endocrinol. Metab. 106, 3455–3463 (2021).
pubmed: 34343303 pmcid: 8864749
Bollyky, J. B. et al. Heterogeneity in recent-onset type 1 diabetes—a clinical trial perspective. Diabetes Metab. Res. Rev. 31, 588–594 (2015).
pubmed: 25689602 pmcid: 4815427 doi: 10.1002/dmrr.2643
Luo, S. et al. Distinct two different ages associated with clinical profiles of acute onset type 1 diabetes in Chinese patients. Diabetes Metab. Res. Rev. 36, e3209 (2020).
pubmed: 31343818 doi: 10.1002/dmrr.3209
Leslie, R. D. et al. Adult-onset type 1 diabetes: current understanding and challenges. Diabetes Care 44, 2449–2456 (2021).
pubmed: 34670785 pmcid: 8546280 doi: 10.2337/dc21-0770
Vicinanza, A., Messaaoui, A., Tenoutasse, S. & Dorchy, H. Diabetic ketoacidosis in children newly diagnosed with type 1 diabetes mellitus: role of demographic, clinical, and biochemical features along with genetic and immunological markers as risk factors. A 20-year experience in a tertiary Belgian center. Pediatr. Diabetes 20, 584–593 (2019).
pubmed: 31038262
Hameed, S. et al. Persistently autoantibody negative (PAN) type 1 diabetes mellitus in children. Pediatr. Diabetes 12, 142–149 (2011).
pubmed: 21518407 doi: 10.1111/j.1399-5448.2010.00681.x
Stoupa, A. & Dorchy, H. HLA-DQ genotypes—but not immune markers—differ by ethnicity in patients with childhood onset type 1 diabetes residing in Belgium. Pediatr. Diabetes 17, 342–350 (2016).
pubmed: 26134450 doi: 10.1111/pedi.12293
Marino, K. R. et al. A predictive model for lack of partial clinical remission in new-onset pediatric type 1 diabetes. PLoS ONE 12, e0176860 (2017).
pubmed: 28459844 pmcid: 5411061 doi: 10.1371/journal.pone.0176860
Ludvigsson, J. et al. Decline of C-peptide during the first year after diagnosis of type 1 diabetes in children and adolescents. Diabetes Res. Clin. Pract. 100, 203–209 (2013).
pubmed: 23529064 doi: 10.1016/j.diabres.2013.03.003
Greenbaum, C. et al. Effect of oral insulin on prevention of diabetes in relatives of patients with type 1 diabetes: a randomized clinical trial. J. Am. Med. Assoc. 318, 1891–1902 (2017).
doi: 10.1001/jama.2017.17070
Wherrett, D. K. et al. Antigen-based therapy with glutamic acid decarboxylase (GAD) vaccine in patients with recent-onset type 1 diabetes: a randomised double-blind trial. Lancet 378, 319–327 (2011).
pubmed: 21714999 pmcid: 3580128 doi: 10.1016/S0140-6736(11)60895-7
Ludvigsson, J. et al. GAD65 antigen therapy in recently diagnosed type 1 diabetes mellitus. N. Engl. J. Med. 366, 433–442 (2012).
pubmed: 22296077 doi: 10.1056/NEJMoa1107096
Christie, M. R., Molvig, J., Hawkes, C. J., Carstensen, B. & Mandrup-Poulsen, T. IA-2 antibody-negative status predicts remission and recovery of C-peptide levels in type 1 diabetic patients treated with cyclosporin. Diabetes Care 25, 1192–1197 (2002).
pubmed: 12087018 doi: 10.2337/diacare.25.7.1192
Herold, K. C. et al. An anti-CD3 antibody, teplizumab, in relatives at risk for type 1 diabetes. N. Engl. J. Med. 381, 603–613 (2019).
pubmed: 31180194 pmcid: 6776880 doi: 10.1056/NEJMoa1902226
Pescovitz, M. D. et al. Rituximab, B-lymphocyte depletion, and preservation of beta-cell function. N. Engl. J. Med. 361, 2143–2152 (2009).
pubmed: 19940299 pmcid: 6410357 doi: 10.1056/NEJMoa0904452
Yu, L. et al. Rituximab selectively suppresses specific islet antibodies. Diabetes 60, 2560–2565 (2011).
pubmed: 21831969 pmcid: 3178300 doi: 10.2337/db11-0674
Elsayed, N. A. et al. 2. Classification and diagnosis of diabetes: standards of care in diabetes—2023. Diabetes Care 46, S19–S40 (2023).
pubmed: 36507649 doi: 10.2337/dc23-S002
So, M. et al. Advances in type 1 diabetes prediction using islet autoantibodies: beyond a simple count. Endocr. Rev. 42, 584–604 (2021).
pubmed: 33881515 doi: 10.1210/endrev/bnab013
So, M. et al. Characterising the age-dependent effects of risk factors on type 1 diabetes progression. Diabetologia 65, 684–694 (2022).
pubmed: 35041021 pmcid: 9928893 doi: 10.1007/s00125-021-05647-5
Arif, S. et al. Blood and islet phenotypes indicate immunological heterogeneity in type 1 diabetes. Diabetes 63, 3835–3845 (2014).
pubmed: 24939426 pmcid: 4207393 doi: 10.2337/db14-0365
Viisanen, T. et al. Circulating CXCR5+PD-1+ICOS+ follicular T helper cells are increased close to the diagnosis of type 1 diabetes in children with multiple autoantibodies. Diabetes 66, 437–447 (2017).
pubmed: 28108610 doi: 10.2337/db16-0714
Andrade Lima Gabbay, M., Sato, M. N., Duarte, A. J. S. & Dib, S. A. Serum titres of anti-glutamic acid decarboxylase-65 and anti-IA-2 autoantibodies are associated with different immunoregulatory milieu in newly diagnosed type 1 diabetes patients. Clin. Exp. Immunol. 168, 60–67 (2012).
pmcid: 3390495 doi: 10.1111/j.1365-2249.2011.04538.x
Spanier, J. A. et al. Increased effector memory insulin-specific CD4+ T cells correlate with insulin autoantibodies in patients with recent-onset type 1 diabetes. Diabetes 66, 3051–3060 (2017).
pubmed: 28842400 pmcid: 5697953 doi: 10.2337/db17-0666
Chen, Y. G. et al. Molecular signatures differentiate immune states in type 1 diabetic families. Diabetes 63, 3960–3973 (2014).
pubmed: 24760139 pmcid: 4207392 doi: 10.2337/db14-0214
Anand, V. et al. Islet autoimmunity and HLA markers of presymptomatic and clinical type 1 diabetes: Joint analyses of prospective cohort studies in Finland, Germany, Sweden, and the U.S. Diabetes Care 44, 2269 (2021).
pubmed: 34162665 pmcid: 8929180 doi: 10.2337/dc20-1836
Frohnert, B. I. et al. Late-onset islet autoimmunity in childhood: the Diabetes Autoimmunity Study in the Young (DAISY). Diabetologia 60, 998–1006 (2017).
pubmed: 28314946 pmcid: 5504909 doi: 10.1007/s00125-017-4256-9
Hanna, S. J. et al. Slow progressors to type 1 diabetes lose islet autoantibodies over time, have few islet antigen-specific CD8+ T cells and exhibit a distinct CD95hi B cell phenotype. Diabetologia 63, 1174–1185 (2020).
pubmed: 32157332 pmcid: 7228996 doi: 10.1007/s00125-020-05114-7
Pöllänen, P. M. et al. Dynamics of islet autoantibodies during prospective follow-up from birth to age 15 years. J. Clin. Endocrinol. Metab. 105, e4638–e4651 (2020).
pubmed: 32882033 pmcid: 7686032 doi: 10.1210/clinem/dgaa624
So, M., O’Rourke, C., Bahnson, H. T., Greenbaum, C. J. & Speake, C. Autoantibody reversion: changing risk categories in multiple-autoantibody-positive individuals. Diabetes Care 43, 913–917 (2020).
pubmed: 32019856 pmcid: 7085807 doi: 10.2337/dc19-1731
Chung, W. K. et al. Precision medicine in diabetes: a Consensus Report from the American Diabetes Association (ADA) and the European Association for the Study of Diabetes (EASD). Diabetologia 63, 1671–1693 (2020).
pubmed: 32556613 pmcid: 8185455 doi: 10.1007/s00125-020-05181-w
Bingley, P. J. & Williams, A. J. K. Validation of autoantibody assays in type 1 diabetes: workshop programme. Autoimmunity 37, 257–260 (2009).
Oram, R. A. et al. Utility of diabetes type-specific genetic risk scores for the classification of diabetes type among multiethnic youth. Diabetes Care 45, 1124–1131 (2022).
pubmed: 35312757 pmcid: 9174964 doi: 10.2337/dc20-2872
Tarn, A. C. et al. Predicting insulin-dependent diabetes. Lancet 1, 845–850 (1988).
pubmed: 2895363 doi: 10.1016/S0140-6736(88)91601-7
Bonifacio, E. & Achenbach, P. Birth and coming of age of islet autoantibodies. Clin. Exp. Immunol. 198, 294–305 (2019).
pubmed: 31397889 pmcid: 6857083 doi: 10.1111/cei.13360
Weiss, A. et al. Progression likelihood score identifies substages of presymptomatic type 1 diabetes in childhood public health screening. Diabetologia 65, 2121–2131 (2022).
pubmed: 36028774 pmcid: 9630406 doi: 10.1007/s00125-022-05780-9
Frohnert, B. I. et al. Refining the definition of stage 1 type 1 diabetes: an ontology-driven analysis of the heterogeneity of multiple islet autoimmunity. Diabetes Care https://doi.org/10.2337/dc22-1960 (2023).
Ghalwash, M. et al. Two-age islet-autoantibody screening for childhood type 1 diabetes: a prospective cohort study. lancet. Diabetes Endocrinol. 10, 589–596 (2022).
Kwon, B. C. et al. Progression of type 1 diabetes from latency to symptomatic disease is predicted by distinct autoimmune trajectories. Nat. Commun. 13, 1514 (2022).
pubmed: 35314671 pmcid: 8938551 doi: 10.1038/s41467-022-28909-1
Ng, K. et al. Islet autoantibody type-specific titer thresholds improve stratification of risk of progression to type 1 diabetes in children. Diabetes Care 45, 160–168 (2022).
pubmed: 34758977 doi: 10.2337/dc21-0878
Nielsen, L. B. et al. Relationship between ZnT8Ab, the SLC30A8 gene and disease progression in children with newly diagnosed type 1 diabetes. Autoimmunity 44, 616–623 (2011).
pubmed: 21604969 doi: 10.3109/08916934.2011.576724
Andersen, M. L. M. et al. Association between autoantibodies to the Arginine variant of the Zinc transporter 8 (ZnT8) and stimulated C-peptide levels in Danish children and adolescents with newly diagnosed type 1 diabetes. Pediatr. Diabetes 13, 454–462 (2012).
pubmed: 22686132 doi: 10.1111/j.1399-5448.2012.00857.x
Sorensen, J. S. et al. Islet autoantibodies and residual beta cell function in type 1 diabetes children followed for 3-6 years. Diabetes Res. Clin. Pract. 96, 204–210 (2012).
pubmed: 22251574 doi: 10.1016/j.diabres.2011.12.013
Chao, C. et al. Change of glutamic acid decarboxylase antibody and protein tyrosine phosphatase antibody in Chinese patients with acute-onset type 1 diabetes mellitus. Chin. Med. J. 126, 4006–4012 (2013).
pubmed: 24229665 doi: 10.3760/cma.j.issn.0366-6999.20130841
Pecheur, A. et al. Characteristics and determinants of partial remission in children with type 1 diabetes using the insulin-dose-adjusted A1C definition. J. Diabetes Res. 2014, 851378 (2014).
pubmed: 25254220 pmcid: 4164125 doi: 10.1155/2014/851378
Camilo, D. S. et al. Partial remission in Brazilian children and adolescents with type 1 diabetes. Association with a haplotype of class II human leukocyte antigen and synthesis of autoantibodies. Pediatr. Diabetes 21, 606–614 (2020).
pubmed: 32078220 doi: 10.1111/pedi.12999
Steck, A. K. et al. Factors associated with the decline of C-peptide in a cohort of young children diagnosed with type 1 diabetes. J. Clin. Endocrinol. Metab. 106, E1380–E1388 (2021).
pubmed: 33035311 doi: 10.1210/clinem/dgaa715
Gale, E. A. M., Bingley, P. J., Emmett, C. L. & Collier, T. European Nicotinamide Diabetes Intervention Trial (ENDIT): a randomised controlled trial of intervention before the onset of type 1 diabetes. Lancet 363, 925–931 (2004).
pubmed: 15043959 doi: 10.1016/S0140-6736(04)15786-3
JS, S. et al. Effects of oral insulin in relatives of patients with type 1 diabetes: the diabetes prevention trial-type 1. Diabetes Care 28, 1068–1076 (2005).
doi: 10.2337/diacare.28.5.1068
Näntö-Salonen, K. et al. Nasal insulin to prevent type 1 diabetes in children with HLA genotypes and autoantibodies conferring increased risk of disease: a double-blind, randomised controlled trial. Lancet 372, 1746–1755 (2008).
pubmed: 18814906 doi: 10.1016/S0140-6736(08)61309-4
Herold, K. C. et al. Teplizumab (Anti-CD3 mAb) treatment preserves C-peptide responses in patients with new-onset type 1 diabetes in a randomized controlled trial: metabolic and immunologic features at baseline identify a subgroup of responders. Diabetes 62, 3766–3774 (2013).
pubmed: 23835333 pmcid: 3806618 doi: 10.2337/db13-0345
Aronson, R. et al. Low-dose otelixizumab anti-CD3 monoclonal antibody DEFEND-1 study: results of the randomized phase III study in recent-onset human type 1 diabetes. Diabetes Care 37, 2746–2754 (2014).
pubmed: 25011949 pmcid: 4392937 doi: 10.2337/dc13-0327
Demeester, S. et al. Preexisting insulin autoantibodies predict efficacy of otelixizumab in preserving residual β-cell function in recent-onset type 1 diabetes. Diabetes Care 38, 644–651 (2015).
pubmed: 25583753 pmcid: 4370324 doi: 10.2337/dc14-1575
Krischer, J., Schatz, D., Bundy, B., Skyler, J. & Greenbaum, C. Effect of oral insulin on prevention of diabetes in relatives of patients with type 1 diabetes: a randomized clinical trial. JAMA 318, 1891–1902 (2017).
pubmed: 29164254 pmcid: 5798455 doi: 10.1001/jama.2017.17070

Auteurs

Jamie L Felton (JL)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Maria J Redondo (MJ)

Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
Division of Pediatric Diabetes and Endocrinology, Texas Children's Hospital, Houston, TX, USA.

Richard A Oram (RA)

NIHR Exeter Biomedical Research Centre (BRC), Academic Kidney Unit, University of Exeter, Exeter, UK.
Department of Clinical and Biomedical Sciences, University of Exeter Medical School, Exeter, UK.
Royal Devon University Healthcare NHS Foundation Trust, Exeter, UK.

Cate Speake (C)

Center for Interventional Immunology, Benaroya Research Institute, Seattle, WA, USA.

S Alice Long (SA)

Center for Translational Immunology, Benaroya Research Institute, Seattle, WA, USA.

Suna Onengut-Gumuscu (S)

Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA.

Stephen S Rich (SS)

Center for Public Health Genomics, University of Virginia, Charlottesville, VA, USA.

Gabriela S F Monaco (GSF)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Arianna Harris-Kawano (A)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.

Dianna Perez (D)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.

Zeb Saeed (Z)

Department of Endocrinology, Diabetes and Metabolism, Indiana University School of Medicine, Indianapolis, IN, USA.

Benjamin Hoag (B)

Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, SD, USA.

Rashmi Jain (R)

Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, SD, USA.

Carmella Evans-Molina (C)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.
Department of Endocrinology, Diabetes and Metabolism, Indiana University School of Medicine, Indianapolis, IN, USA.
Richard L. Roudebush VAMC, Indianapolis, IN, USA.

Linda A DiMeglio (LA)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Heba M Ismail (HM)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA.

Dana Dabelea (D)

Lifecourse Epidemiology of Adiposity and Diabetes (LEAD) Center, Aurora, CO, USA.

Randi K Johnson (RK)

Department of Biomedical Informatics, University of Colorado Anschutz Medical Campus, Aurora, CO, USA.
Department of Epidemiology, Colorado School of Public Health, Aurora, CO, USA.

Marzhan Urazbayeva (M)

Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.

John M Wentworth (JM)

Royal Melbourne Hospital Department of Diabetes and Endocrinology, Parkville, VIC, Australia.
Walter and Eliza Hall Institute, Parkville, VIC, Australia.
University of Melbourne Department of Medicine, Parkville, VIC, Australia.

Kurt J Griffin (KJ)

Department of Pediatrics, Sanford School of Medicine, University of South Dakota, Sioux Falls, SD, USA.
Sanford Research, Sioux Falls, SD, USA.

Emily K Sims (EK)

Department of Pediatrics, Center for Diabetes and Metabolic Diseases, Indianapolis, IN, USA. eksims@iu.edu.
Herman B Wells Center for Pediatric Research, Indiana University School of Medicine, Indianapolis, IN, USA. eksims@iu.edu.

Classifications MeSH