title: Cytotoxic T-lymphocyte antigen-4 gene polymorphisms and human T-cell lymphotrophic virus-1 infection: their associations with Hashimoto's thyroiditis in Japanese patients.
abstract: Cytotoxic T-lymphocyte antigen-4 (CTLA-4) decreases the immune response of T cells by inactivating the signal that occurs with interaction between CD28 on T cells and B7 on antigen-presenting cells. Gene polymorphisms involving CTLA-4 promoter (-318 C/T), exon 1 (49 A/G), and exon 4 (microsatellite (AT)n) have been linked to Hashimoto's thyroiditis (HT) and other autoimmune diseases. HT also has a reported association with human T-cell lymphotrophic virus-1 (HTLV-1) infection. We investigated the occurrence of CTLA-4 polymorphisms in Japanese patients with HT with and without anti-HTLV-1 antibodies (HTLV-1 Ab). DNA samples from 143 patients with HT and 199 controls were subjected to polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) analysis using the restriction enzymes, Bbv 1, Tse 1, and Mse 1. In the HTLV-1 Ab-positive group the exon 1 G allele was more frequent in patients with HT than in controls (67% vs. 53%, p = 0.0377), and in HTLV-1 Ab-negative group it was also frequent in patients with HT than in controls (68% vs. 53%, p = 0.0041). Frequency of the G allele in HT with HTLV-1 Ab was comparable to those without HTLV-1 Ab. Frequency of polymorphism in the promoter did not differ between patients with HT and controls, nor between controls with and without HTLV-1 Ab. HTLV-1 infection is not associated with CTLA-4 polymorphisms in either HT or controls. HTLV-1 infection is not regulated by genetic factor such as CTLA-4, and may affect occurrence of HT as an independent purely environmental factor.
authors.affiliation: Second Department of Internal Medicine, University of the Ryukyus School of Medicine, Nishihara, Okinawa, Japan. ttomoyos@estate.ocn.ne.jp
authors.forename: Takeaki
authors.initials: T
authors.lastname: Tomoyose
authors.forename: Ichiro
authors.initials: I
authors.lastname: Komiya
authors.forename: Masaki
authors.initials: M
authors.lastname: Takara
authors.forename: Kouichi
authors.initials: K
authors.lastname: Yabiku
authors.forename: Yoshino
authors.initials: Y
authors.lastname: Kinjo
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Shimajiri
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Yogi
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Kouki
authors.forename: Masato
authors.initials: M
authors.lastname: Masuda
authors.forename: Nobuyuki
authors.initials: N
authors.lastname: Takasu
mesh_terms: D000069594:Abatacept; D015703:Antigens, CD; D000943:Antigens, Differentiation / Q000235:genetics*; D060908:CTLA-4 Antigen; D006800:Deltaretrovirus Infections / Q000276:immunology*; D005091:Exons; D005260:Female; D020022:Genetic Predisposition to Disease; D015368:Human T-lymphotropic virus 1; D006801:Humans; D018796:Immunoconjugates; D007564:Japan; D008297:Male; D011110:Polymorphism, Genetic; D011401:Promoter Regions, Genetic / Q000235:genetics; D013967:Thyroiditis, Autoimmune / Q000235:genetics* / Q000276:immunology / Q000821:virology*
chemical_list: D015703:Antigens, CD; D000943:Antigens, Differentiation; D060908:CTLA-4 Antigen; C556706:CTLA4 protein, human; D018796:Immunoconjugates; D000069594:Abatacept