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Dive into the research topics where Tanel Traks is active.

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Featured researches published by Tanel Traks.


BMC Medical Genetics | 2008

Polymorphisms in the interleukin-10 gene cluster are possibly involved in the increased risk for major depressive disorder

Tanel Traks; Kati Koido; Triin Eller; Eduard Maron; Külli Kingo; Veiko Vasar; Eero Vasar; Sulev Kõks

BackgroundInnate immune inflammatory response is suggested to have a role in the pathogenesis of major depressive disorder (MDD). Interleukin (IL)-10 family cytokines IL-10, IL-19, IL-20, and IL-24 are all implicated in the inflammatory processes and polymorphisms in respective genes have been associated with various immunopathological conditions. This study was carried out to investigate whether single-nucleotide polymorphisms (SNPs) in these genes are also associated with MDD.MethodsCase-control association study was performed with seven SNPs from the IL10 gene cluster. 153 patients with MDD and 277 healthy control individuals were recruited.ResultsNone of the selected SNPs were individually associated with MDD. The linkage disequilibrium (LD) analysis indicated the existence of two recombination sites in the IL10 gene cluster, thus confirming the formerly established LD pattern of this genomic region. This also created two haplotype blocks, both consisting of three SNPs. Additionally, the haplotype analysis detected a significantly higher frequency of block 2 (IL20 and IL24 genes) haplotype TGC in the patients group compared to healthy control individuals (P = 0.0097).ConclusionOur study established increased risk for MDD related to the IL20 and IL24 haplotype and suggests that cytokines may contribute to the pathogenesis of MDD. Since none of the block 2 SNPs were individually associated with MDD, it is possible that other polymorphisms linked to them contribute to the disease susceptibility. Future studies are needed to confirm the results and to find the possible functional explanation.


Translational Psychiatry | 2012

Associations between LSAMP gene polymorphisms and major depressive disorder and panic disorder.

Kati Koido; Tanel Traks; Roman Balõtšev; Triin Eller; Aviva Must; Sulev Kõks; Eduard Maron; Innar Tõru; Jakov Shlik; Veiko Vasar; Eero Vasar

The purpose of this case–control genetic association study was to explore potential relationships between polymorphisms in the limbic system-associated membrane protein (LSAMP) gene and mood and anxiety disorders. A total of 21 single-nucleotide polymorphisms (SNPs) from the LSAMP gene were analyzed in 591 unrelated patients with the diagnoses of major depressive disorder (MDD) or panic disorder (PD) and in 384 healthy control subjects. The results showed a strong association between LSAMP SNPs and MDD, and a suggestive association between LSAMP SNPs and PD. This is the first evidence of a possible role of LSAMP gene in mood and anxiety disorders in humans.


Acta Dermato-venereologica | 2012

Polymorphisms in the ATG16L1 gene are associated with psoriasis vulgaris.

Konstantinos Douroudis; Külli Kingo; Tanel Traks; Ene Reimann; Kristi Raud; Ranno Rätsep; Rotraut Mössner; Helgi Silm; Eero Vasar; Sulev Kõks

Psoriasis is an immune-mediated inflammatory disorder of the skin with a complex pathogenesis and a strong genetic component (1). Several regions in the genome, including the psoriasis susceptibility locus 1 (PSORl), have been identified as conferring susceptibility to psoriasis (2—4). However, the complete genetic background of psoriasis remains to be established. Autophagy is a fundamental biological process that is involved in cell growth and plays a role in innate and adaptive immunity. In particular, autophagy-selective responses contribute to inflammatory bowel disease (IBD) (5, 6), neurodegeneration (7), and cancer (8). The ATG16L1 protein, which is encoded by the ATG16L1 gene (2q37), is a key component of a large protein complex essential for autophagy (9), and polymorphisms within this gene have been reported to be associated with Crohns disease (5). Taking into consideration that genes in the autophagy pathway play an important role in inflammation and immunity, and as a part of our ongoing research on the impact of genetic variants to the risk of psoriasis vulgaris, the aim of the present study was to assess whether polymorphisms in ATG16L1 gene might also contribute to the risk of psoriasis.


Psychiatry Research-neuroimaging | 2014

Associations between polymorphisms of LSAMP gene and schizophrenia

Kati Koido; Sven Janno; Tanel Traks; Madis Parksepp; Ülle Ljubajev; Peeter Veiksaar; Anne Must; Jakov Shlik; Veiko Vasar; Eero Vasar

The purpose of this study was to explore relationships between single-nucleotide polymorphisms (SNPs) in the limbic system-associated membrane protein (LSAMP) gene and schizophrenia. Twenty-two SNPs were analysed in 127 unrelated schizophrenic patients and in 171 healthy controls. The results showed significant allelic and haplotypic associations between LSAMP gene and schizophrenia.


Human Immunology | 2013

Copy number variations in IL22 gene are associated with Psoriasis vulgaris.

Ele Prans; Külli Kingo; Tanel Traks; Helgi Silm; Eero Vasar; Sulev Kõks

Psoriasis vulgaris (PsV) is a frequent, chronically relapsing, immune-mediated systemic disease with characteristic skin changes. IL22 is a cytokine of IL10 family, with significant proliferative effect on different cell lines. Copy number variations (CNV) have been discovered to have phenotypic consequences and are associated with various types of diseases. In the work presented here we analyzed the copy number variations in IL22 gene of exon1 and exon5. Our results showed that the IL22 gene exon1 was significantly associated with psoriasis severity (P<0.0001). However, the association between IL22 gene exon5 copy numbers and psoriasis was not detected.


Journal of Dermatological Science | 2010

The CD226 Gly307Ser gene polymorphism is associated with severity of psoriasis

Konstantinos Douroudis; Külli Kingo; Helgi Silm; Ene Reimann; Tanel Traks; Eero Vasar; Sulev Kõks

Psoriasis is a chronic inflammatory T-cell mediated disease of the skin with a complex pathogenesis involving both genetic and environmental factors [1]. Several regions in the genome including the major histocompatibility complex (MHC) [2], [3] have been reported to confer susceptibility to psoriasis risk; however, the genetic background of psoriasis is yet to be established...


Journal of Psychiatric Research | 2010

Interleukin 10 family gene polymorphisms are not associated with major depressive disorder and panic disorder phenotypes

Kati Koido; Triin Eller; Külli Kingo; Sulev Kõks; Tanel Traks; Jakov Shlik; Veiko Vasar; Eero Vasar; Eduard Maron

Genetic regulation of immune system and inflammatory response may be related to the pathogenesis and manifestations of mood and anxiety disorders. In the present study we examined a range of single-nucleotide polymorphisms (SNP) in chromosomal region 1q32, the locus of interleukin 10 (IL10) gene, in patients with major depressive disorder (n=312) and panic disorder (n=210), and matched healthy controls (n=356). We found no significant associations of the SNPs in IL10 family genes with either diagnostic group. Haplotype analysis revealed seven haplotype blocks, but their frequencies did not differ between patients and controls. Significant associations were detected for SNP rs1539243 in IKBKE (inhibitor of kappa light polypeptide gene enhancer in B-cells, kinase epsilon) gene showing different allelic and genotypic distributions in the total as well as in separate diagnostic groups as compared to controls. IKBKE emerged as a candidate for further studies of genetic factors associated with panic disorder and major depressive disorder.


Journal of Dermatological Science | 2010

Further association analysis of chr 6q22-24 suggests a role of IL-20RA polymorphisms in psoriasis

Külli Kingo; Rotraut Mössner; Tanel Traks; Ranno Rätsep; Kristi Raud; Ene Reimann; Ullrich Krüger; Helgi Silm; Eero Vasar; Kristian Reich; Sulev Kõks

In our previous studies we obtained evidence that the interleukin-19 (IL19) gene cluster and interleukin-20 receptor alpha (IL20RA) gene may represent susceptibility regions for psoriasis [1], [2], [3]. The aim of the present study was to scan an additional set of single nucleotide polymorphisms (SNPs) in the chromosomal region 6q22-24, which contains IL20RA, the genes for interleukin-22 receptor alpha 2 (IL22RA2) and interferon-gamma receptor 1 (IFNGR1) for association with psoriasis...


Journal of Dermatological Science | 2012

Analysis of genetic variants of class II cytokine and their receptor genes in psoriasis patients of two ethnic groups from the Volga-Ural region of Russia

Elvira Galimova; V. L. Akhmetova; Boris Latipov; Külli Kingo; Ranno Rätsep; Tanel Traks; Sulev Kõks; Elza Khusnutdinova

BACKGROUND The molecular basis of pathogenesis of psoriasis remains unclear, but one unifying hypothesis of disease aetiology is the cytokine network model. The class II cytokines (CF2) and their receptors (CRF2) are all involved in the inflammatory processes and single nucleotide polymorphisms (SNPs) in respective genes have been associated with psoriasis in a previous study of the Estonian population. OBJECTIVE We performed a replication study of 47 SNPs in CF2 and CRF2 genes in independent cohorts of psoriasis patients of two ethnic groups (Russians and Bashkirs) from the Volga-Ural region of Russia. METHODS DNA was obtained from 395 psoriasis patients of two ethnic groups from the Volga-Ural region of Russia and 476 ethnically matched controls. 47 SNPs in the loci of the genes encoding Class II cytokines and their receptors were selected by SNPbrowser version 3.5. Genotyping was performed using the SNPlex™ (Applied Biosystems) platform. RESULTS The genetic variant rs30461 previously associated in original case-control study in Estonians, was also associated in Russians (corrected P-value (Pc=0.008, OR=0.44), but did not reach statistical significance in the Bashkir population. Additionally, the haplotype analysis provided that CC haplotype formed by the SNPs rs30461 and rs955155 had a protective effect in Russians (Pc=0.0024, OR=0.44), supporting the involvement of this locus in the protection against psoriasis. Combined meta-analysis of three populations, including 943 psoriasis patients and 812 healthy controls, showed that the IL29 rs30461 C-allele was not associated with decreased risk of psoriasis (P=0.165, OR=0.68). Moreover, stratification of studies by ethnicity revealed a significant association in the European cohort (P=9.506E-006, OR=0.53). CONCLUSION Therefore, there is no overall evidence of association between psoriasis and SNP rs30461 of the IL29 gene, but there is some evidence to suggest that an association exists in Europeans. However, this current concept should be considered as preliminary and the results need to be confirmed in future independent studies.


Human Immunology | 2011

ATG16L1 gene polymorphisms are associated with palmoplantar pustulosis

Konstantinos Douroudis; Külli Kingo; Tanel Traks; Ranno Rätsep; Helgi Silm; Eero Vasar; Sulev Kõks

Genes in autophagy pathway play an important role in innate and adaptive immunity. The aim of the study was to assess the impact of ATG16L1 gene on susceptibility of palmoplantar pustulosis. Four single nucleotide polymorphisms (SNPs) within the ATG16L1 region (rs2241880, rs2241879, rs7587633, and rs13005285) were genotyped in 241 control subjects and 38 palmoplantar pustulosis (PPP) patients of Estonian descent. The data analysis revealed a significantly higher frequency distribution of the rs2241880 G (odds ratio [OR] = 1.88, p = 0.0073) and rs2241879 A (OR = 1.87, p = 0.0079) allele in the PPP group when compared with the control group. The frequency distribution of the GACG haplotype was significantly higher (OR = 1.82, p = 0.016) in the PPP group when compared with the control group. The current study provides evidence of an association of the ATG16L1 gene in susceptibility to palmoplantar pustulosis, and supports the notion that the ATG16L1 gene as a member of the autophagy pathway most likely plays an important role in immune response.

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Külli Kingo

Tartu University Hospital

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