Lack of correlation between the levels of soluble cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and the CT-60 genotypes
- ,
- Robert Podolsky,
- Christin Collins,
- Weipeng Zheng,
- Desmond Schatz,
- Andy Muir
- ,
- ,
- ,
- Medical College of Georgia,
- University of Florida,
Open access
Sustainable Development Goals
- SDG 3 Good Health and Well
Abstract
Background: Cytotoxic T lymphocyte-associated antigen-4 (CTLA-4) plays a critical role in downregulation of antigen-activated immune response and polymorphisms at the CTLA-4 gene have been shown to be associated with several autoimmune diseases including type-1 diabetes (T1D). The etiological mutation was mapped to the CT60-A/G single nucleotide polymorphism (SNP) that is believed to control the processing and production of soluble CTLA-4 (sCTLA-4). Methods: We therefore determined sCTLA-4 protein levels in the sera from 82 T1D patients and 19 autoantibody positive (AbP) subjects and 117 autoantibody negative (AbN) controls using ELISA. The CT-60 SNP was genotyped for these samples by using PCR and restriction enzyme digestion of a 268 bp DNA segment containing the SNP. Genotyping of CT-60 SNP was confirmed by dye terminating sequencing reaction. Results: Higher levels of sCTLA-4 were observed in T1D (2.24 ng/ml) and AbP (mean = 2.17 ng/ml) subjects compared to AbN controls (mean = 1.69 ng/ml) with the differences between these subjects becoming significant with age (p = 0.02). However, we found no correlation between sCTLA-4 levels and the CTLA-4 CT-60 SNP genotypes. Conclusion: Consistent with the higher serum sCTLA-4 levels observed in other autoimmune diseases, our results suggest that sCTLA-4 may be a risk factor for T1D. However, our results do not support the conclusion that the CT-60 SNP controls the expression of sCTLA-4.
Publication Information
Output type
Original language
English (US)Article number
8Journal (Volume, Issue Number)
Journal of Autoimmune Diseases (Volume 2)Publication milestones
- Published - 10/31/2005
Publication status
ISSN
1740-2557Publication IDs
- Scopus: 28444435565
- ORCID: /0000-0003-0385-3829/work/121881124
