title: Association of the polymorphisms of chemokine genes (IL8, RANTES, MIG, IP10, MCP1 and IL16) with the pathogenesis of autoimmune thyroid diseases.
abstract: Chemokines induce leukocyte chemotaxis and contribute to chronic inflammation. To clarify the association between functional polymorphisms in genes encoding some chemokines and the pathogenesis of Autoimmune thyroid disease (AITD), we genotyped IL8 -251T/A, Regulated upon Activation, Normal T cell Expressed and presumably Secreted (RANTES) - 403G/A, -28C/G, MIG rs2276886G/A, IP10 -1596C/T, Monocyte Chemoattractant Protein1 (MCP1) - 2518G/A and IL16 -295T/C polymorphisms. We genotyped these polymorphisms using the PCR-RFLP method in 149 Graves' disease (GD) patients, including 59 patients with intractable GD and 53 patients with GD in remission, as well as 131 Hashimoto's disease (HD) patients, including 54 patients with severe HD, 46 patients with mild HD and 99 healthy controls. The IL8 -251TT genotype and MIG rs2276886 A allele were more frequent in patients with AITD (p = 0.0139 and p = 0.0005, respectively). The RANTES - 403AA and -28GG genotypes were less frequent in patients with AITD (p = 0.0164 and p = 0.0221, respectively). The MCP1 -2518GG genotype was more frequent in HD patients (p = 0.0323). The MIG rs2276886 AG genotype was less frequent in patients with intractable GD (p = 0.0051). Interestingly, the age of onset in GD patients with the RANTES - 28CC genotype was younger than in those with -28CG and GG genotypes (p = 0.0028). In this study, we first reported that the polymorphisms in IL8, RANTES and MIG genes are associated with the development of AITD, and that the MIG rs2276886 AG genotype is associated with the intractability of GD. The RANTES - 28CC genotype is associated with young onset of GD.
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Maiko
authors.initials: M
authors.lastname: Akahane
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Mikio
authors.initials: M
authors.lastname: Watanabe
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Naoya
authors.initials: N
authors.lastname: Inoue
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Yumi
authors.initials: Y
authors.lastname: Miyahara
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Yuya
authors.initials: Y
authors.lastname: Arakawa
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Yuka
authors.initials: Y
authors.lastname: Inoue
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Yuka
authors.initials: Y
authors.lastname: Katsumata
authors.affiliation: b Laboratory for Clinical Investigation , Osaka University Hospital , Osaka , Japan.
authors.forename: Yoh
authors.initials: Y
authors.lastname: Hidaka
authors.affiliation: a Department of Biomedical Informatics , Division of Health Sciences, Osaka University Graduate School of Medicine , Osaka , Japan and.
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Iwatani
mesh_terms: D000328:Adult; D000368:Aged; D000483:Alleles; D001323:Autoantibodies / Q000097:blood / Q000276:immunology; D001327:Autoimmune Diseases / Q000175:diagnosis / Q000235:genetics*; D015415:Biomarkers; D016022:Case-Control Studies; D018932:Chemokine CCL2 / Q000235:genetics; D018946:Chemokine CCL5 / Q000235:genetics; D054370:Chemokine CXCL9 / Q000235:genetics; D018925:Chemokines / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D056726:Genetic Association Studies; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006111:Graves Disease / Q000235:genetics; D050031:Hashimoto Disease / Q000235:genetics; D006801:Humans; D019410:Interleukin-16 / Q000235:genetics; D016209:Interleukin-8 / Q000235:genetics; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D020641:Polymorphism, Single Nucleotide; D018121:Receptors, Cytokine / Q000235:genetics; D013959:Thyroid Diseases / Q000175:diagnosis / Q000235:genetics* / Q000276:immunology / Q000628:therapy
chemical_list: D001323:Autoantibodies; D015415:Biomarkers; C111835:CCL2 protein, human; C483024:CCL5 protein, human; C080810:CXCL9 protein, human; D018932:Chemokine CCL2; D018946:Chemokine CCL5; D054370:Chemokine CXCL9; D018925:Chemokines; C104577:IP10-Mig receptor; D019410:Interleukin-16; D016209:Interleukin-8; D018121:Receptors, Cytokine
keywords: Autoimmune thyroid disease; chemokine; intractability; severity; single nucleotide polymorphism