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Autoantibodies in Diabetes Catherine Pihoker, Lisa K Autoantibodies in Diabetes Catherine Pihoker, Lisa K. Gilliam, Christiane S. Hampe, and Åke Lernmark Islet cell autoantibodies are strongly associated with the tation tests followed by a biochemical analysis of the development of type 1 diabetes. The appearance of auto- purified immune complexes should make it possible to antibodies to one or several of the autoantigens—GAD65, identify islet autoantigens recognized by immunoglobulin IA-2, or insulin—signals an autoimmune pathogenesis of in sera from newly diagnosed diabetic children. Early ␤-cell killing. A ␤-cell attack may be best reflected by the studies showed the presence of a 64K protein, later shown emergence of autoantibodies dependent on the genotype to have GAD activity and found to represent a hitherto risk factors, isotype, and subtype of the autoantibodies as well as their epitope specificity. It is speculated that unknown isoform, GAD65. Subsequently, it was demon- progression to ␤-cell loss and clinical onset of type 1 strated that many new-onset type 1 diabetic patients had diabetes is reflected in a developing pattern of epitope- insulin autoantibodies (IAAs), and further analysis of islet specific autoantibodies. Although the appearance of auto- autoantigens resulted in the discovery of the insulinoma- antibodies does not follow a distinct pattern, the presence antigen 2 (IA-2), which was co-precipitated with GAD65 in of multiple autoantibodies has the highest positive predic- many 64Kϩ patient sera. All three autoantigens are avail- tive value for type 1 diabetes. In the absence of reliable able as recombinant proteins that can be radioactively T-cell tests, dissection of autoantibody responses in sub- labeled either by in vitro transcription and translation or jects of genetic risk should prove useful in identifying triggers of islet autoimmunity by examining seroconver- by iodination. In this way, it has been possible to develop sion and maturation of the autoantibody response that may reproducible and precise autoantibody assays to detect mark time to onset of type 1 diabetes. The complexity of what are sometimes referred to as “biochemical antibod- the disease process is exemplified by multiple clinical ies,” referred to henceforth in this article as “diabetes phenotypes, including autoimmune diabetes masquerading autoantibodies” (DAAs). These DAAs have been or are in as type 2 diabetes in youth and adults. Autoantibodies may the process of being standardized worldwide through also provide prognostic information in clinically heteroge- serum exchange workshop exercises and proficiency test- neous patient populations when examined longitudinally. ing, using a World Health Organization standard as refer- Diabetes 54 (Suppl. 2):S52–S61, 2005 ence (rev. in 2). The ability to measure autoantibodies in type 1 diabetes using recombinant autoantigens has paved the way for the ISLET CELL AUTOANTIBODIES identification of several different autoantigens detected by Autoantibodies are created by the immune system when it autoantibodies in a large number of other autoimmune fails to distinguish between “self” and “nonself.” It is disorders. The utility of these autoantigen-specific—al- normally trained to recognize and ignore the body’s own though yet to be standardized—autoantibody assays has cells and to not overreact to nonthreatening substances in led to the notion that many autoimmune diseases can be the environment. At the same time, the immune system detected before the clinical diagnosis. The finding that ICA must be able to create antibodies that target and fight reactivity does not always correlate to reactivity toward specific foreign substances that do pose a threat. The bad defined autoantigens suggests that additional specific au- news is, when this highly regulated and efficient system is toantigens remain to be identified (3). However, the cur- turned onto self-antigens, target tissue damage ensues. rent tests for autoantibodies to these three autoantigens Autoantibodies that bind to specific proteins found in the are highly predictive of type 1 diabetes (rev. in 4). In the pancreatic islet cells were first described Ͼ30 years ago present article, we will discuss the mechanisms by which (1). The initial studies of islet cell antibodies (ICAs) were the autoantibodies to GAD65 (GAD65Ab), IA-2 (IA-2Ab), based on descriptive morphological tests aiming to local- and insulin (IAA) appear, pathways of formation, shift ize the site of antibody binding. The indirect immunofluo- between isotypes and subtypes, epitope recognition, and rescence test proved to be cumbersome and difficult to detection, as well as the potential usefulness of epitope- standardize. Because autoantibodies recognize unique au- specific autoantibody tests to improve prediction and toantigens, it was reasoned that standard immunoprecipi- classification of autoimmune diabetes. The human immune response to foreign antigens is often studied after vaccination or monitored using the From the Departments of Pediatrics and Medicine, University of Washington, Seattle, Washington. bacteriophage oX174 (5). The latter antigen is potent and Address correspondence and reprint requests to Dr. Catherine Pihoker, causes no recognized toxic effects in humans. It is used to Department of Pediatrics, University of Washington, Seattle, WA 98195. monitor antigen clearance as well as primary and second- E-mail: [email protected]. Received for publication 4 March 2005 and accepted in revised form 4 May ary antibody responses, including the sequence of anti- 2005. body class. In parallel with antigen clearance, IgM This article is based on a presentation at a symposium. The symposium and antibodies are produced and within a couple of days, the publication of this article were made possible by an unrestricted educa- followed by low-level IgG. A second injection of oX174 is tional grant from Servier. DAA, diabetes autoantibody; DAISY, Diabetes Autoimmunity Study in the followed by a marked IgG response and only a limited IgM Young; DASP, Diabetes Autoantibody Standardization Program; DPT-1, Dia- response. The series of events associated with the forma- betes Prevention Trial; GAD65Ab, GAD65 autoantibody; IA-2, insulinoma- tion of autoantibodies to islet autoantigens is not known. antigen 2; IA-2Ab, IA-2 autoantibody; IAA, insulin autoantibody; ICA, islet cell antibody; LADA, latent autoimmune diabetes in the adult. It is assumed that there is shedding of the autoantigen © 2005 by the American Diabetes Association. within the pancreatic islet, that the autoantigen is taken up S52 DIABETES, VOL. 54, SUPPLEMENT 2, DECEMBER 2005 C. PIHOKER AND ASSOCIATES by resident or circulating macrophages or dendritic cells, STANDARDIZATION OF DAAs TO IMPROVE UTILITY IN and that these cells then migrate to lymph nodes draining CLINICAL STUDIES the pancreas where the antigen presentation takes place In addition to the important information DAAs provide to (6). This series of events is poorly documented in sponta- further our understanding of the autoimmune disease neously diabetic laboratory rodents, such as the NOD process in type 1 diabetes, DAAs have great value in mouse or the BB rat, because neither animal has an studies of disease prediction. The usefulness of a test for autoantibody response of the character and magnitude prediction or diagnosis is evaluated by its sensitivity that is observed in human type 1 diabetes. In humans, (number of subjects with ϩDAAs who develop type 1 limited information about GAD65Ab isotypes at onset and diabetes/number of subjects who develop diabetes), spec- in the prodromal period is available (7,8). The common ificity (number of subjects with ϪDAA who do not de- assay used for the detection of autoantibodies is based on velop type 1 diabetes/number of subjects who do not immunoprecipitation using Protein A Sepharose. While develop diabetes), and positive predictive value. Because Protein A binds efficiently to the majority of human IgG, it of the relatively long prodrome between initial antibody binds only poorly to IgA, IgM, and the IgG3 subtype. These detection and clinical symptoms in type 1 diabetes, as isotypes or subtypes are therefore underrepresented in the well as their high positive predictive value, DAAs are a current detection method. Our present understanding is useful marker for prediction of disease. ICAs, and more limited to the early detection of islet autoantibodies to recently GAD65Abs, IA-2Abs, and IAAs, have been stud- insulin, GAD65, and IA-2 in children with genetic suscep- ied extensively in both the general population and in tibility to type 1 diabetes (9–11). However, in none of populations at increased risk, namely first-degree rela- these studies has the blood sampling occurred frequently tives of probands with type 1 diabetes. In fact, diabetes enough such that the IgM to IgG isotype shift has been has been the disorder in which the largest number of documented. Further studies are needed to carefully mon- studies have been conducted in the predictive value of itor the IgM, IgA, and IgG responses to autoantigen pre- antibodies for autoimmune diseases (4). Several interna- sentation in humans, and it will also be important to tional workshops (Immunology and Diabetes Workshop, monitor circulating autoantigens to relate autoantigen Immunology of Diabetes Society Workshop, and the first clearance to antibody formation. and second Diabetes Autoantibody Standardization Pro- gram [DASP]) have been conducted to develop thresholds AUTOANTIBODY EFFECTS ON ANTIGEN PRESENTATION
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