Cigarette smoking, STAT4 and TNFRSF1B polymorphisms, and systemic lupus erythematosus in a Japanese population

Chikako Kiyohara, Masakazu Washio, Takahiko Horiuchi, Yoshifumi Tada, Toyoko Asami, Saburo Ide, Tatsuya Atsumi, Gen Kobashi, Hiroki Takahashi, Hiroko Kodama, Koichi Akashi, Mine Harada, Hiroshi Tsukamoto, Takao Hotokebuchi, Kohei Nagasawa, Osamu Ushiyama, Mitsuru Mori, Asae Oura, Yasuhisa Sinomura, Hiromu SuzukiMotohisa Yamamoto, Tetsuya Horita, Takao Koike, Takashi Abe, Hisato Tanaka, Norihiko Nogami, Kazushi Okamoto, Naomasa Sakamoto, Satoshi Sasaki, Yoshihiro Miyake, Tetsuji Yokoyama, Yoshio Hirota, Yutaka Inaba, Masaki Nagai

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Abstract

Objective. Recent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. Similarly, tumor necrosis factor receptor superfamily, member 1B (TNFRSF1B) has been reported to be associated with SLE risk in Japanese populations. Along with environmental factors such as smoking, both polymorphisms may modulate an individual's susceptibility to SLE. We investigated these relationships in a case-control study to evaluate risk factors for SLE among Japanese women. Methods. We investigated the relationship of the STAT4 rs7574865 and TNFRSF1B rs1061622 polymorphisms to SLE risk with special reference to their combination and interaction with cigarette smoking among 152 SLE cases and 427 controls. Results. The TT genotype of STAT4 rs7574865 was significantly associated with increased risk of SLE (OR 2.21, 95% CI 1.10-4.68). Subjects with at least one G allele of TNFRSF1B rs1061622 had an increased risk of SLE (OR 1.56, 95% CI 0.99-2.47). The attributable proportion due to the interaction between the TNFRSF1B rs1061622 genotypes and smoking was estimated to be 0.49 (95% CI 0.07-0.92), indicating that 49% of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction. A lack of significant associations of STAT4 with smoking was observed. No significant gene-gene interactions were found among polymorphisms of STAT4 and TNFRSF1B. Conclusion. Our findings suggest that the association between cigarette smoking and SLE could be differentiated by the TNFRSF1B rs1061622 T allele among female Japanese subjects. This preliminary exploratory result should be confirmed in a larger study. The Journal of Rheumatology

Original languageEnglish
Pages (from-to)2195-2203
Number of pages9
JournalJournal of Rheumatology
Volume36
Issue number10
DOIs
Publication statusPublished - Oct 1 2009

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STAT4 Transcription Factor
Receptors, Tumor Necrosis Factor, Type II
Systemic Lupus Erythematosus
Smoking
Population
Alleles
Genotype
Genes
Rheumatology
Case-Control Studies

All Science Journal Classification (ASJC) codes

  • Rheumatology
  • Immunology and Allergy
  • Immunology

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Cigarette smoking, STAT4 and TNFRSF1B polymorphisms, and systemic lupus erythematosus in a Japanese population. / Kiyohara, Chikako; Washio, Masakazu; Horiuchi, Takahiko; Tada, Yoshifumi; Asami, Toyoko; Ide, Saburo; Atsumi, Tatsuya; Kobashi, Gen; Takahashi, Hiroki; Kodama, Hiroko; Akashi, Koichi; Harada, Mine; Tsukamoto, Hiroshi; Hotokebuchi, Takao; Nagasawa, Kohei; Ushiyama, Osamu; Mori, Mitsuru; Oura, Asae; Sinomura, Yasuhisa; Suzuki, Hiromu; Yamamoto, Motohisa; Horita, Tetsuya; Koike, Takao; Abe, Takashi; Tanaka, Hisato; Nogami, Norihiko; Okamoto, Kazushi; Sakamoto, Naomasa; Sasaki, Satoshi; Miyake, Yoshihiro; Yokoyama, Tetsuji; Hirota, Yoshio; Inaba, Yutaka; Nagai, Masaki.

In: Journal of Rheumatology, Vol. 36, No. 10, 01.10.2009, p. 2195-2203.

Research output: Contribution to journalArticle

Kiyohara, C, Washio, M, Horiuchi, T, Tada, Y, Asami, T, Ide, S, Atsumi, T, Kobashi, G, Takahashi, H, Kodama, H, Akashi, K, Harada, M, Tsukamoto, H, Hotokebuchi, T, Nagasawa, K, Ushiyama, O, Mori, M, Oura, A, Sinomura, Y, Suzuki, H, Yamamoto, M, Horita, T, Koike, T, Abe, T, Tanaka, H, Nogami, N, Okamoto, K, Sakamoto, N, Sasaki, S, Miyake, Y, Yokoyama, T, Hirota, Y, Inaba, Y & Nagai, M 2009, 'Cigarette smoking, STAT4 and TNFRSF1B polymorphisms, and systemic lupus erythematosus in a Japanese population', Journal of Rheumatology, vol. 36, no. 10, pp. 2195-2203. https://doi.org/10.3899/jrheum.090181
Kiyohara, Chikako ; Washio, Masakazu ; Horiuchi, Takahiko ; Tada, Yoshifumi ; Asami, Toyoko ; Ide, Saburo ; Atsumi, Tatsuya ; Kobashi, Gen ; Takahashi, Hiroki ; Kodama, Hiroko ; Akashi, Koichi ; Harada, Mine ; Tsukamoto, Hiroshi ; Hotokebuchi, Takao ; Nagasawa, Kohei ; Ushiyama, Osamu ; Mori, Mitsuru ; Oura, Asae ; Sinomura, Yasuhisa ; Suzuki, Hiromu ; Yamamoto, Motohisa ; Horita, Tetsuya ; Koike, Takao ; Abe, Takashi ; Tanaka, Hisato ; Nogami, Norihiko ; Okamoto, Kazushi ; Sakamoto, Naomasa ; Sasaki, Satoshi ; Miyake, Yoshihiro ; Yokoyama, Tetsuji ; Hirota, Yoshio ; Inaba, Yutaka ; Nagai, Masaki. / Cigarette smoking, STAT4 and TNFRSF1B polymorphisms, and systemic lupus erythematosus in a Japanese population. In: Journal of Rheumatology. 2009 ; Vol. 36, No. 10. pp. 2195-2203.
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abstract = "Objective. Recent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. Similarly, tumor necrosis factor receptor superfamily, member 1B (TNFRSF1B) has been reported to be associated with SLE risk in Japanese populations. Along with environmental factors such as smoking, both polymorphisms may modulate an individual's susceptibility to SLE. We investigated these relationships in a case-control study to evaluate risk factors for SLE among Japanese women. Methods. We investigated the relationship of the STAT4 rs7574865 and TNFRSF1B rs1061622 polymorphisms to SLE risk with special reference to their combination and interaction with cigarette smoking among 152 SLE cases and 427 controls. Results. The TT genotype of STAT4 rs7574865 was significantly associated with increased risk of SLE (OR 2.21, 95{\%} CI 1.10-4.68). Subjects with at least one G allele of TNFRSF1B rs1061622 had an increased risk of SLE (OR 1.56, 95{\%} CI 0.99-2.47). The attributable proportion due to the interaction between the TNFRSF1B rs1061622 genotypes and smoking was estimated to be 0.49 (95{\%} CI 0.07-0.92), indicating that 49{\%} of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction. A lack of significant associations of STAT4 with smoking was observed. No significant gene-gene interactions were found among polymorphisms of STAT4 and TNFRSF1B. Conclusion. Our findings suggest that the association between cigarette smoking and SLE could be differentiated by the TNFRSF1B rs1061622 T allele among female Japanese subjects. This preliminary exploratory result should be confirmed in a larger study. The Journal of Rheumatology",
author = "Chikako Kiyohara and Masakazu Washio and Takahiko Horiuchi and Yoshifumi Tada and Toyoko Asami and Saburo Ide and Tatsuya Atsumi and Gen Kobashi and Hiroki Takahashi and Hiroko Kodama and Koichi Akashi and Mine Harada and Hiroshi Tsukamoto and Takao Hotokebuchi and Kohei Nagasawa and Osamu Ushiyama and Mitsuru Mori and Asae Oura and Yasuhisa Sinomura and Hiromu Suzuki and Motohisa Yamamoto and Tetsuya Horita and Takao Koike and Takashi Abe and Hisato Tanaka and Norihiko Nogami and Kazushi Okamoto and Naomasa Sakamoto and Satoshi Sasaki and Yoshihiro Miyake and Tetsuji Yokoyama and Yoshio Hirota and Yutaka Inaba and Masaki Nagai",
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T1 - Cigarette smoking, STAT4 and TNFRSF1B polymorphisms, and systemic lupus erythematosus in a Japanese population

AU - Kiyohara, Chikako

AU - Washio, Masakazu

AU - Horiuchi, Takahiko

AU - Tada, Yoshifumi

AU - Asami, Toyoko

AU - Ide, Saburo

AU - Atsumi, Tatsuya

AU - Kobashi, Gen

AU - Takahashi, Hiroki

AU - Kodama, Hiroko

AU - Akashi, Koichi

AU - Harada, Mine

AU - Tsukamoto, Hiroshi

AU - Hotokebuchi, Takao

AU - Nagasawa, Kohei

AU - Ushiyama, Osamu

AU - Mori, Mitsuru

AU - Oura, Asae

AU - Sinomura, Yasuhisa

AU - Suzuki, Hiromu

AU - Yamamoto, Motohisa

AU - Horita, Tetsuya

AU - Koike, Takao

AU - Abe, Takashi

AU - Tanaka, Hisato

AU - Nogami, Norihiko

AU - Okamoto, Kazushi

AU - Sakamoto, Naomasa

AU - Sasaki, Satoshi

AU - Miyake, Yoshihiro

AU - Yokoyama, Tetsuji

AU - Hirota, Yoshio

AU - Inaba, Yutaka

AU - Nagai, Masaki

PY - 2009/10/1

Y1 - 2009/10/1

N2 - Objective. Recent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. Similarly, tumor necrosis factor receptor superfamily, member 1B (TNFRSF1B) has been reported to be associated with SLE risk in Japanese populations. Along with environmental factors such as smoking, both polymorphisms may modulate an individual's susceptibility to SLE. We investigated these relationships in a case-control study to evaluate risk factors for SLE among Japanese women. Methods. We investigated the relationship of the STAT4 rs7574865 and TNFRSF1B rs1061622 polymorphisms to SLE risk with special reference to their combination and interaction with cigarette smoking among 152 SLE cases and 427 controls. Results. The TT genotype of STAT4 rs7574865 was significantly associated with increased risk of SLE (OR 2.21, 95% CI 1.10-4.68). Subjects with at least one G allele of TNFRSF1B rs1061622 had an increased risk of SLE (OR 1.56, 95% CI 0.99-2.47). The attributable proportion due to the interaction between the TNFRSF1B rs1061622 genotypes and smoking was estimated to be 0.49 (95% CI 0.07-0.92), indicating that 49% of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction. A lack of significant associations of STAT4 with smoking was observed. No significant gene-gene interactions were found among polymorphisms of STAT4 and TNFRSF1B. Conclusion. Our findings suggest that the association between cigarette smoking and SLE could be differentiated by the TNFRSF1B rs1061622 T allele among female Japanese subjects. This preliminary exploratory result should be confirmed in a larger study. The Journal of Rheumatology

AB - Objective. Recent studies have identified signal transducer and activator of transcription 4 (STAT4) as a susceptibility gene for systemic lupus erythematosus (SLE) in different populations. Similarly, tumor necrosis factor receptor superfamily, member 1B (TNFRSF1B) has been reported to be associated with SLE risk in Japanese populations. Along with environmental factors such as smoking, both polymorphisms may modulate an individual's susceptibility to SLE. We investigated these relationships in a case-control study to evaluate risk factors for SLE among Japanese women. Methods. We investigated the relationship of the STAT4 rs7574865 and TNFRSF1B rs1061622 polymorphisms to SLE risk with special reference to their combination and interaction with cigarette smoking among 152 SLE cases and 427 controls. Results. The TT genotype of STAT4 rs7574865 was significantly associated with increased risk of SLE (OR 2.21, 95% CI 1.10-4.68). Subjects with at least one G allele of TNFRSF1B rs1061622 had an increased risk of SLE (OR 1.56, 95% CI 0.99-2.47). The attributable proportion due to the interaction between the TNFRSF1B rs1061622 genotypes and smoking was estimated to be 0.49 (95% CI 0.07-0.92), indicating that 49% of the excess risk for SLE in smokers with at least one G allele was due to an additive interaction. A lack of significant associations of STAT4 with smoking was observed. No significant gene-gene interactions were found among polymorphisms of STAT4 and TNFRSF1B. Conclusion. Our findings suggest that the association between cigarette smoking and SLE could be differentiated by the TNFRSF1B rs1061622 T allele among female Japanese subjects. This preliminary exploratory result should be confirmed in a larger study. The Journal of Rheumatology

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