High GAD65 autoantibody levels in nondiabetic adults are associated with HLA but not with CTLA-4 or INS VNTR.
(2003) In Journal of Internal Medicine 253(4). p.447-453- Abstract
- OBJECTIVES: To explore the relationship between genetic background and antibody levels in a nondiabetic population. We evaluated if high levels of autoantibodies against the 65 kDa isoform of glutamic acid decarboxylase (GAD65Ab), were associated with high-risk genes, i.e. HLA, CTLA-4 and INS VNTR genes. DESIGN AND SUBJECTS: Seventy-five (M/F 39/36) subjects exceeding the 95th percentile of GAD65 autoantibody index and 75 age and sex matched subjects below the 95th percentile, randomly selected amongst participants in the Västerbotten Intervention Programme. METHODS: The GAD65 Ab were measured in a radioligand-binding assay. HLA class II typing was performed by an oligoblot hybridization method. CTLA-4 repeat length was analysed and... (More)
- OBJECTIVES: To explore the relationship between genetic background and antibody levels in a nondiabetic population. We evaluated if high levels of autoantibodies against the 65 kDa isoform of glutamic acid decarboxylase (GAD65Ab), were associated with high-risk genes, i.e. HLA, CTLA-4 and INS VNTR genes. DESIGN AND SUBJECTS: Seventy-five (M/F 39/36) subjects exceeding the 95th percentile of GAD65 autoantibody index and 75 age and sex matched subjects below the 95th percentile, randomly selected amongst participants in the Västerbotten Intervention Programme. METHODS: The GAD65 Ab were measured in a radioligand-binding assay. HLA class II typing was performed by an oligoblot hybridization method. CTLA-4 repeat length was analysed and divided into short forms and long forms. Class I and class III alleles of INS VNTR were detected. Differences in distribution were tested by Pearson chi-square with Yates correction. Odds ratios (OR) were used to compare groups calculated with Cochran's and (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/1127430
- author
- Rolandsson, O ; Hägg, E ; Janer, M ; Rutledge, E ; Gaur, L K ; Nilsson, M ; Hallmans, G and Lernmark, Åke LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- Journal of Internal Medicine
- volume
- 253
- issue
- 4
- pages
- 447 - 453
- publisher
- Wiley-Blackwell
- external identifiers
-
- scopus:0345701218
- ISSN
- 1365-2796
- DOI
- 10.1046/j.1365-2796.2003.01115.x
- language
- English
- LU publication?
- yes
- id
- 199d256e-5936-4c79-ae26-b0245d402fe4 (old id 1127430)
- date added to LUP
- 2016-04-04 10:18:45
- date last changed
- 2022-04-16 01:39:49
@article{199d256e-5936-4c79-ae26-b0245d402fe4, abstract = {{OBJECTIVES: To explore the relationship between genetic background and antibody levels in a nondiabetic population. We evaluated if high levels of autoantibodies against the 65 kDa isoform of glutamic acid decarboxylase (GAD65Ab), were associated with high-risk genes, i.e. HLA, CTLA-4 and INS VNTR genes. DESIGN AND SUBJECTS: Seventy-five (M/F 39/36) subjects exceeding the 95th percentile of GAD65 autoantibody index and 75 age and sex matched subjects below the 95th percentile, randomly selected amongst participants in the Västerbotten Intervention Programme. METHODS: The GAD65 Ab were measured in a radioligand-binding assay. HLA class II typing was performed by an oligoblot hybridization method. CTLA-4 repeat length was analysed and divided into short forms and long forms. Class I and class III alleles of INS VNTR were detected. Differences in distribution were tested by Pearson chi-square with Yates correction. Odds ratios (OR) were used to compare groups calculated with Cochran's and}}, author = {{Rolandsson, O and Hägg, E and Janer, M and Rutledge, E and Gaur, L K and Nilsson, M and Hallmans, G and Lernmark, Åke}}, issn = {{1365-2796}}, language = {{eng}}, number = {{4}}, pages = {{447--453}}, publisher = {{Wiley-Blackwell}}, series = {{Journal of Internal Medicine}}, title = {{High GAD65 autoantibody levels in nondiabetic adults are associated with HLA but not with CTLA-4 or INS VNTR.}}, url = {{http://dx.doi.org/10.1046/j.1365-2796.2003.01115.x}}, doi = {{10.1046/j.1365-2796.2003.01115.x}}, volume = {{253}}, year = {{2003}}, }