IL‐10 Promoter −1082 Polymorphism is Associated with Elevated IL‐10 Levels in Control Subjects but Does not Explain Elevated Plasma IL‐10 Observed in Sjögren's Syndrome in a Hungarian Cohort
The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 (IL‐10) gene and the soluble IL‐10 levels in Hungarian primary Sjögren's syndrome (SS) patients. Ninety‐nine SS patients and 135 healthy volunteers were examined. Samples were analysed by the...
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Published in | Scandinavian journal of immunology Vol. 62; no. 5; pp. 474 - 480 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
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Oxford, UK; Malden, USA
Blackwell Science Ltd
01.11.2005
Wiley Subscription Services, Inc |
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Abstract | The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 (IL‐10) gene and the soluble IL‐10 levels in Hungarian primary Sjögren's syndrome (SS) patients. Ninety‐nine SS patients and 135 healthy volunteers were examined. Samples were analysed by the PCR restriction fragment length polymorphism method, and IL‐10 plasma levels were assesed by a commercial enzyme‐linked immunosorbent assay. IL‐10 plasma levels were higher in the primary SS patients (36.4 ± 57.5 pg/ml, n = 99) compared with the healthy subjects (9.9 ± 20.3 pg/ml, n = 135, P = 10−6). The elevated IL‐10 phenotype of SS patients was not associated with increased G allele frequency as reported earlier, while in the control group, we found higher IL‐10 levels among the subjects who were carriers of the GG genotype (17.7 ± 23.2 pg/ml) as compared with the other two genotype carriers (AA 8.98 ± 16.5 and GA 8.5 ± 21.1 pg/ml, P = 0.01). Our data do not support previous observations indicating an association between deregulated IL‐10 secretion in SS and higher G allele frequency. However, the results clearly demonstrate that GG homozygosity is associated with elevated IL‐10 levels in apparently healthy subjects, but this cannot account for the IL‐10‐related specific disease features observed in SS. Thus, other genetic factors contribute to the clinical spectrum of this heterogeneous disease at least in the Hungarian population. |
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AbstractList | The aim of this study was to investigate the frequency of the -1082 polymorphism of the interleukin-10 (IL-10) gene and the soluble IL-10 levels in Hungarian primary Sjögren's syndrome (SS) patients. Ninety-nine SS patients and 135 healthy volunteers were examined. Samples were analysed by the PCR restriction fragment length polymorphism method, and IL-10 plasma levels were assessed by a commercial enzyme-linked immunosorbent assay. IL-10 plasma levels were higher in the primary SS patients (36.4 +/- 57.5 pg/ml, n = 99) compared with the healthy subjects (9.9 +/- 20.3 pg/ml, n = 135, P = 10(-6)). The elevated IL-10 phenotype of SS patients was not associated with increased G allele frequency as reported earlier, while in the control group, we found higher IL-10 levels among the subjects who were carriers of the GG genotype (17.7 +/- 23.2 pg/ml) as compared with the other two genotype carriers (AA 8.98 +/- 16.5 and GA 8.5 +/- 21.1 pg/ml, P = 0.01). Our data do not support previous observations indicating an association between deregulated IL-10 secretion in SS and higher G allele frequency. However, the results clearly demonstrate that GG homozygosity is associated with elevated IL-10 levels in apparently healthy subjects, but this cannot account for the IL-10-related specific disease features observed in SS. Thus, other genetic factors contribute to the clinical spectrum of this heterogeneous disease at least in the Hungarian population. Abstract The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 ( IL‐10 ) gene and the soluble IL‐10 levels in Hungarian primary Sjögren's syndrome (SS) patients. Ninety‐nine SS patients and 135 healthy volunteers were examined. Samples were analysed by the PCR restriction fragment length polymorphism method, and IL‐10 plasma levels were assesed by a commercial enzyme‐linked immunosorbent assay. IL‐10 plasma levels were higher in the primary SS patients (36.4 ± 57.5 pg/ml, n = 99) compared with the healthy subjects (9.9 ± 20.3 pg/ml, n = 135, P = 10 −6 ). The elevated IL‐10 phenotype of SS patients was not associated with increased G allele frequency as reported earlier, while in the control group, we found higher IL‐10 levels among the subjects who were carriers of the GG genotype (17.7 ± 23.2 pg/ml) as compared with the other two genotype carriers (AA 8.98 ± 16.5 and GA 8.5 ± 21.1 pg/ml, P = 0.01). Our data do not support previous observations indicating an association between deregulated IL‐10 secretion in SS and higher G allele frequency. However, the results clearly demonstrate that GG homozygosity is associated with elevated IL‐10 levels in apparently healthy subjects, but this cannot account for the IL‐10‐related specific disease features observed in SS. Thus, other genetic factors contribute to the clinical spectrum of this heterogeneous disease at least in the Hungarian population. The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 (IL‐10) gene and the soluble IL‐10 levels in Hungarian primary Sjögren's syndrome (SS) patients. Ninety‐nine SS patients and 135 healthy volunteers were examined. Samples were analysed by the PCR restriction fragment length polymorphism method, and IL‐10 plasma levels were assesed by a commercial enzyme‐linked immunosorbent assay. IL‐10 plasma levels were higher in the primary SS patients (36.4 ± 57.5 pg/ml, n = 99) compared with the healthy subjects (9.9 ± 20.3 pg/ml, n = 135, P = 10−6). The elevated IL‐10 phenotype of SS patients was not associated with increased G allele frequency as reported earlier, while in the control group, we found higher IL‐10 levels among the subjects who were carriers of the GG genotype (17.7 ± 23.2 pg/ml) as compared with the other two genotype carriers (AA 8.98 ± 16.5 and GA 8.5 ± 21.1 pg/ml, P = 0.01). Our data do not support previous observations indicating an association between deregulated IL‐10 secretion in SS and higher G allele frequency. However, the results clearly demonstrate that GG homozygosity is associated with elevated IL‐10 levels in apparently healthy subjects, but this cannot account for the IL‐10‐related specific disease features observed in SS. Thus, other genetic factors contribute to the clinical spectrum of this heterogeneous disease at least in the Hungarian population. |
Author | Bessenyei, B. Semsei, I. Zeher, M. Márka, M. |
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BackLink | https://www.ncbi.nlm.nih.gov/pubmed/16305644$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_1080_03009740801910353 crossref_primary_10_1128_CVI_00314_09 crossref_primary_10_1371_journal_pone_0063401 crossref_primary_10_1080_03009740701606010 crossref_primary_10_1080_03009740801910361 crossref_primary_10_1902_jop_2008_070299 crossref_primary_10_1186_1479_5876_6_6 crossref_primary_10_1016_j_humimm_2015_06_009 crossref_primary_10_1111_jop_12149 |
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Snippet | The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 (IL‐10) gene and the soluble IL‐10 levels in Hungarian... The aim of this study was to investigate the frequency of the -1082 polymorphism of the interleukin-10 (IL-10) gene and the soluble IL-10 levels in Hungarian... Abstract The aim of this study was to investigate the frequency of the −1082 polymorphism of the interleukin‐10 ( IL‐10 ) gene and the soluble IL‐10 levels in... |
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SubjectTerms | Adult Aged Cohort Studies Female Gene Frequency Genotype Heterozygote Homozygote Humans Hungary Interleukin-10 - blood Interleukin-10 - genetics Male Middle Aged Polymorphism, Single Nucleotide - genetics Promoter Regions, Genetic - genetics Sjogren's Syndrome - blood Sjogren's Syndrome - genetics |
Title | IL‐10 Promoter −1082 Polymorphism is Associated with Elevated IL‐10 Levels in Control Subjects but Does not Explain Elevated Plasma IL‐10 Observed in Sjögren's Syndrome in a Hungarian Cohort |
URI | https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1365-3083.2005.01675.x https://www.ncbi.nlm.nih.gov/pubmed/16305644 https://www.proquest.com/docview/198199228 https://search.proquest.com/docview/68827642 |
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