Lack of correlation between the levels of soluble cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and the CT-60 gen
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BioMed Central
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Lack of correlation between the levels of soluble cytotoxic T-lymphocyte associated antigen-4 (CTLA-4) and the CT-60 genotypes Sharad Purohit†1, Robert Podolsky†1, Christin Collins1, Weipeng Zheng1, Desmond Schatz2, Andy Muir1, Diane Hopkins1, Yi-Hua Huang1 and JinXiong She*1 Address: 1Center for Biotechnology and Genomic Medicine, Medical College of Georgia, CA4095 Augusta, GA 30912 and 2Department of Pediatrics, University of Florida, Gainesville FL 32607, USA Email: Sharad Purohit - [email protected]; Robert Podolsky - [email protected]; Christin Collins - [email protected]; Weipeng Zheng - [email protected]; Desmond Schatz - [email protected]; Andy Muir - [email protected]; Diane Hopkins - [email protected]; Yi-Hua Huang - [email protected]; Jin-Xiong She* - [email protected] * Corresponding author †Equal contributors
Published: 31 October 2005 Journal of Autoimmune Diseases 2005, 2:8
doi:10.1186/1740-2557-2-8
Received: 16 August 2005 Accepted: 31 October 2005
This article is available from: http://www.jautoimdis.com/content/2/1/8 © 2005 Purohit et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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.
Background Effective T cell activation requires a 'costimulation' signal that is mediated through CD28 interacting with B7 family
members on antigen presenting
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