IgG4-related disease in the Japanese population: a genome-wide association study

Chikashi Terao; Masao Ota; Takeshi Iwasaki; Masahiro Shiokawa; Shuji Kawaguchi; Katsutoshi Kuriyama; Takahisa Kawaguchi; Yuzo Kodama; Izumi Yamaguchi; Kazushige Uchida; Koichiro Higasa; Motohisa Yamamoto; Kensuke Kubota; Shujiro Yazumi; Kenji Hirano; Yasufumi Masaki; Hiroyuki Maguchi; Tomoki Origuchi; Shoko Matsui; Takahiro Nakazawa; Hideyuki Shiomi; Terumi Kamisawa; Osamu Hasebe; Eisuke Iwasaki; Kazuo Inui; Yoshiya Tanaka; Koh ichi Ohshima; Takashi Akamizu; Shigeo Nakamura; Seiji Nakamura; Takako Saeki; Hisanori Umehara; Tooru Shimosegawa; Nobumasa Mizuno; Mitsuhiro Kawano; Atsushi Azumi; Hiroki Takahashi; Tsuneyo Mimori; Yoichiro Kamatani; Kazuichi Okazaki; Tsutomu Chiba; Shigeyuki Kawa; Fumihiko Matsuda; Atsushi Kanno; Yoshihiro Okabe; Shinji Katsushima; Tetsuro Inokuma; Yukitaka Yamashita; Yoshitaka Nakai; Takayoshi Nishino; Kozo Kajimura; Mitsushige Shibatoge; Naoki Kanda; Akio Ido; Masaya Ohana; Ichiro Moriyama; Hiroshi Tatsuta; Kazuyoshi Matsumura; Keita Fujikawa; Norimoto Gotoh; Takanobu Tsutsumi; Masakazu Shimizu; Kazuya Setoh; Meiko Takahashi; Yasuharu Tabara; Jun Mimura; Takefumi Nakamura; Toshiyuki Kimura; Chiharu Kawanami

doi:10.1016/S2665-9913(19)30006-2

IgG4-related disease in the Japanese population: a genome-wide association study

Chikashi Terao, Masao Ota, Takeshi Iwasaki, Masahiro Shiokawa, Shuji Kawaguchi, Katsutoshi Kuriyama, Takahisa Kawaguchi, Yuzo Kodama, Izumi Yamaguchi, Kazushige Uchida, Koichiro Higasa, Motohisa Yamamoto, Kensuke Kubota, Shujiro Yazumi, Kenji Hirano, Yasufumi Masaki, Hiroyuki Maguchi, Tomoki Origuchi, Shoko Matsui, Takahiro NakazawaHideyuki Shiomi, Terumi Kamisawa, Osamu Hasebe, Eisuke Iwasaki, Kazuo Inui, Yoshiya Tanaka, Koh ichi Ohshima, Takashi Akamizu, Shigeo Nakamura, Seiji Nakamura, Takako Saeki, Hisanori Umehara, Tooru Shimosegawa, Nobumasa Mizuno, Mitsuhiro Kawano, Atsushi Azumi, Hiroki Takahashi, Tsuneyo Mimori, Yoichiro Kamatani, Kazuichi Okazaki, Tsutomu Chiba, Shigeyuki Kawa, Fumihiko Matsuda, Atsushi Kanno, Yoshihiro Okabe, Shinji Katsushima, Tetsuro Inokuma, Yukitaka Yamashita, Yoshitaka Nakai, Takayoshi Nishino, Kozo Kajimura, Mitsushige Shibatoge, Naoki Kanda, Akio Ido, Masaya Ohana, Ichiro Moriyama, Hiroshi Tatsuta, Kazuyoshi Matsumura, Keita Fujikawa, Norimoto Gotoh, Takanobu Tsutsumi, Masakazu Shimizu, Kazuya Setoh, Meiko Takahashi, Yasuharu Tabara, Jun Mimura, Takefumi Nakamura, Toshiyuki Kimura, Chiharu Kawanami

Department of Internal Medicine (Gastroenterology and Hepatology)

Research output: Contribution to journal › Article › peer-review

22 Citations (Scopus)

Abstract

Background: IgG4-related disease is a newly recognised immunopathological entity that includes autoimmune pancreatitis, IgG4-related sialadenitis, and IgG4-related kidney disease. To understand the genetic landscape of IgG4-related disease, we did a genome-wide association study. Methods: We did a genome-wide association study of Japanese individuals, initially screening 857 patients with IgG4-related disease at 50 Japanese research institutions and DNA samples from 2082 healthy control participants from the Nagahama Prospective Genome Cohort for the Comprehensive Human Bioscience. From Oct 27, 2008, to July 22, 2014, we enrolled 835 patients and used data from 1789 healthy participants. Only patients with confirmed diagnosis of IgG4-related disease according to the international diagnostic criteria were included. Genotyping was done with the Infinium HumanOmni5Exome, HumanOmni2.5Exome, or HumanOmni2.5 Illumina arrays, and genomic distributions were compared between case and control samples for 958 440 single nucleotide polymorphisms. The HLA region was extensively analysed using imputation of HLA alleles and aminoacid residues. Fine mapping of the FCGR2B region was also done. Associations between clinical manifestations of disease and the genetic variations identified in these two genes were examined. Findings: We identified the HLA-DRB1 (p=1·1×10⁻¹¹) and FCGR2B (p=2·0×10⁻⁸) regions as susceptibility loci for IgG4-related disease. We also identified crucial aminoacid residues in the β domain of the peptide-binding groove of HLA-DRB1, in which the seventh aminoacid residue showed the strongest association signal with IgG4-related disease (p=1·7×10⁻¹⁴), as has been reported with other autoimmune diseases. rs1340976 in FCGR2B showed an association with increased FCGR2B expression (p=2·7×10⁻¹⁰) and was in weak linkage disequilibrium with rs1050501, a missense variant of FCGR2B previously associated with systemic lupus erythematosus. Furthermore, rs1340976 was associated with the number of swollen organs at diagnosis (p=0·011) and IgG4 concentration at diagnosis (p=0·035). Interpretation: Two susceptibility loci for IgG4-related disease were identified. Both FCGR2B and HLA loci might have important roles in IgG4-related disease development. Common molecular mechanisms might underlie IgG4-related disease and other immune-related disorders Funding: The Japanese Ministry of Health, Labour, and Welfare, the Japanese Agency of Medical Research and Development, and Kyoto University Grant for Top Global University Japan Project.

Original language	English
Pages (from-to)	e14-e22
Journal	The Lancet Rheumatology
Volume	1
Issue number	1
DOIs	https://doi.org/10.1016/S2665-9913(19)30006-2
Publication status	Published - 2019 Sept

ASJC Scopus subject areas

Rheumatology
Immunology and Allergy
Immunology

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1016/S2665-9913(19)30006-2

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Terao, C., Ota, M., Iwasaki, T., Shiokawa, M., Kawaguchi, S., Kuriyama, K., Kawaguchi, T., Kodama, Y., Yamaguchi, I., Uchida, K., Higasa, K., Yamamoto, M., Kubota, K., Yazumi, S., Hirano, K., Masaki, Y., Maguchi, H., Origuchi, T., Matsui, S., ... Kawanami, C. (2019). IgG4-related disease in the Japanese population: a genome-wide association study. The Lancet Rheumatology, 1(1), e14-e22. https://doi.org/10.1016/S2665-9913(19)30006-2

Terao, C, Ota, M, Iwasaki, T, Shiokawa, M, Kawaguchi, S, Kuriyama, K, Kawaguchi, T, Kodama, Y, Yamaguchi, I, Uchida, K, Higasa, K, Yamamoto, M, Kubota, K, Yazumi, S, Hirano, K, Masaki, Y, Maguchi, H, Origuchi, T, Matsui, S, Nakazawa, T, Shiomi, H, Kamisawa, T, Hasebe, O, Iwasaki, E, Inui, K, Tanaka, Y, Ohshima, KI, Akamizu, T, Nakamura, S, Nakamura, S, Saeki, T, Umehara, H, Shimosegawa, T, Mizuno, N, Kawano, M, Azumi, A, Takahashi, H, Mimori, T, Kamatani, Y, Okazaki, K, Chiba, T, Kawa, S, Matsuda, F, Kanno, A, Okabe, Y, Katsushima, S, Inokuma, T, Yamashita, Y, Nakai, Y, Nishino, T, Kajimura, K, Shibatoge, M, Kanda, N, Ido, A, Ohana, M, Moriyama, I, Tatsuta, H, Matsumura, K, Fujikawa, K, Gotoh, N, Tsutsumi, T, Shimizu, M, Setoh, K, Takahashi, M, Tabara, Y, Mimura, J, Nakamura, T, Kimura, T & Kawanami, C 2019, 'IgG4-related disease in the Japanese population: a genome-wide association study', The Lancet Rheumatology, vol. 1, no. 1, pp. e14-e22. https://doi.org/10.1016/S2665-9913(19)30006-2

@article{e335dd717d2c43588aa108e0ae9e7cf8,

title = "IgG4-related disease in the Japanese population: a genome-wide association study",

abstract = "Background: IgG4-related disease is a newly recognised immunopathological entity that includes autoimmune pancreatitis, IgG4-related sialadenitis, and IgG4-related kidney disease. To understand the genetic landscape of IgG4-related disease, we did a genome-wide association study. Methods: We did a genome-wide association study of Japanese individuals, initially screening 857 patients with IgG4-related disease at 50 Japanese research institutions and DNA samples from 2082 healthy control participants from the Nagahama Prospective Genome Cohort for the Comprehensive Human Bioscience. From Oct 27, 2008, to July 22, 2014, we enrolled 835 patients and used data from 1789 healthy participants. Only patients with confirmed diagnosis of IgG4-related disease according to the international diagnostic criteria were included. Genotyping was done with the Infinium HumanOmni5Exome, HumanOmni2.5Exome, or HumanOmni2.5 Illumina arrays, and genomic distributions were compared between case and control samples for 958 440 single nucleotide polymorphisms. The HLA region was extensively analysed using imputation of HLA alleles and aminoacid residues. Fine mapping of the FCGR2B region was also done. Associations between clinical manifestations of disease and the genetic variations identified in these two genes were examined. Findings: We identified the HLA-DRB1 (p=1·1×10−11) and FCGR2B (p=2·0×10−8) regions as susceptibility loci for IgG4-related disease. We also identified crucial aminoacid residues in the β domain of the peptide-binding groove of HLA-DRB1, in which the seventh aminoacid residue showed the strongest association signal with IgG4-related disease (p=1·7×10−14), as has been reported with other autoimmune diseases. rs1340976 in FCGR2B showed an association with increased FCGR2B expression (p=2·7×10−10) and was in weak linkage disequilibrium with rs1050501, a missense variant of FCGR2B previously associated with systemic lupus erythematosus. Furthermore, rs1340976 was associated with the number of swollen organs at diagnosis (p=0·011) and IgG4 concentration at diagnosis (p=0·035). Interpretation: Two susceptibility loci for IgG4-related disease were identified. Both FCGR2B and HLA loci might have important roles in IgG4-related disease development. Common molecular mechanisms might underlie IgG4-related disease and other immune-related disorders Funding: The Japanese Ministry of Health, Labour, and Welfare, the Japanese Agency of Medical Research and Development, and Kyoto University Grant for Top Global University Japan Project.",

author = "Chikashi Terao and Masao Ota and Takeshi Iwasaki and Masahiro Shiokawa and Shuji Kawaguchi and Katsutoshi Kuriyama and Takahisa Kawaguchi and Yuzo Kodama and Izumi Yamaguchi and Kazushige Uchida and Koichiro Higasa and Motohisa Yamamoto and Kensuke Kubota and Shujiro Yazumi and Kenji Hirano and Yasufumi Masaki and Hiroyuki Maguchi and Tomoki Origuchi and Shoko Matsui and Takahiro Nakazawa and Hideyuki Shiomi and Terumi Kamisawa and Osamu Hasebe and Eisuke Iwasaki and Kazuo Inui and Yoshiya Tanaka and Ohshima, {Koh ichi} and Takashi Akamizu and Shigeo Nakamura and Seiji Nakamura and Takako Saeki and Hisanori Umehara and Tooru Shimosegawa and Nobumasa Mizuno and Mitsuhiro Kawano and Atsushi Azumi and Hiroki Takahashi and Tsuneyo Mimori and Yoichiro Kamatani and Kazuichi Okazaki and Tsutomu Chiba and Shigeyuki Kawa and Fumihiko Matsuda and Atsushi Kanno and Yoshihiro Okabe and Shinji Katsushima and Tetsuro Inokuma and Yukitaka Yamashita and Yoshitaka Nakai and Takayoshi Nishino and Kozo Kajimura and Mitsushige Shibatoge and Naoki Kanda and Akio Ido and Masaya Ohana and Ichiro Moriyama and Hiroshi Tatsuta and Kazuyoshi Matsumura and Keita Fujikawa and Norimoto Gotoh and Takanobu Tsutsumi and Masakazu Shimizu and Kazuya Setoh and Meiko Takahashi and Yasuharu Tabara and Jun Mimura and Takefumi Nakamura and Toshiyuki Kimura and Chiharu Kawanami",

note = "Funding Information: This study was supported by in part by the Japanese Ministry of Health, Labour, and Welfare ( grant number #H22-Nanchi-084 ), the Japanese Agency of Medical Research and Development (grant numbers JP16EK0109070 and JP18EK0109283 ), and Kyoto University Grant for Top Global University Japan Project. We are grateful to all of the patients for their invaluable contributions. Funding Information: YM reports grants from Kyowa Kirin Pharmaceutical Development, Astellas, Eisai, Ono, Pfizer, Asahi Kasei, MSD, Daiichi-Sankyo, Taisho, Taiho, Takeda, Chugai, Teijin, Nippon Kayaku, and Mochida outside the submitted work. YT reports non-financial support and honoraria or speakers fees funding from Astellas during the conduct of the study, grants from Mitsubishi-Tanabe, Bristol-Myers Squibb, Eisai, Chugai, Takeda, AbbVie, Astellas, Daiichi-Sankyo, Ono, MSD, and Taisho-Toyama, and honoraria or speakers fees funding from Daiichi-Sankyo, Astellas, Eli Lilly, Chugai, Sanofi, AbbVie, Pfizer, YL Biologics, Bristol-Myers Squibb, GlaxoSmithKline, UCB, Mitsubishi-Tanabe, Novartis, Eisai, Takeda, Janssen, and Asahi Kasei outside the submitted work. NM reports grants from Merck Serono, AstraZeneca, Zeria, NanoCarrier, Eisai, MSD, Dainippon Sumitomo, ASLAN, Incyte, and Pharma Valley Center, personal fees from Ono and Teijin, grants and personal fees from Yakult Honsha and Taiho, and grants, personal fees, and non-financial support from Novartis outside the submitted work. All other authors declare no conflicts. Funding Information: This study was supported by in part by the Japanese Ministry of Health, Labour, and Welfare (grant number #H22-Nanchi-084), the Japanese Agency of Medical Research and Development (grant numbers JP16EK0109070 and JP18EK0109283), and Kyoto University Grant for Top Global University Japan Project. We are grateful to all of the patients for their invaluable contributions. Publisher Copyright: {\textcopyright} 2019 Elsevier Ltd",

year = "2019",

month = sep,

doi = "10.1016/S2665-9913(19)30006-2",

language = "English",

volume = "1",

pages = "e14--e22",

journal = "The Lancet Rheumatology",

issn = "2665-9913",

publisher = "Lancet Publishing Group",

number = "1",

}

TY - JOUR

T1 - IgG4-related disease in the Japanese population

T2 - a genome-wide association study

AU - Terao, Chikashi

AU - Ota, Masao

AU - Iwasaki, Takeshi

AU - Shiokawa, Masahiro

AU - Kawaguchi, Shuji

AU - Kuriyama, Katsutoshi

AU - Kawaguchi, Takahisa

AU - Kodama, Yuzo

AU - Yamaguchi, Izumi

AU - Uchida, Kazushige

AU - Higasa, Koichiro

AU - Yamamoto, Motohisa

AU - Kubota, Kensuke

AU - Yazumi, Shujiro

AU - Hirano, Kenji

AU - Masaki, Yasufumi

AU - Maguchi, Hiroyuki

AU - Origuchi, Tomoki

AU - Matsui, Shoko

AU - Nakazawa, Takahiro

AU - Shiomi, Hideyuki

AU - Kamisawa, Terumi

AU - Hasebe, Osamu

AU - Iwasaki, Eisuke

AU - Inui, Kazuo

AU - Tanaka, Yoshiya

AU - Ohshima, Koh ichi

AU - Akamizu, Takashi

AU - Nakamura, Shigeo

AU - Nakamura, Seiji

AU - Saeki, Takako

AU - Umehara, Hisanori

AU - Shimosegawa, Tooru

AU - Mizuno, Nobumasa

AU - Kawano, Mitsuhiro

AU - Azumi, Atsushi

AU - Takahashi, Hiroki

AU - Mimori, Tsuneyo

AU - Kamatani, Yoichiro

AU - Okazaki, Kazuichi

AU - Chiba, Tsutomu

AU - Kawa, Shigeyuki

AU - Matsuda, Fumihiko

AU - Kanno, Atsushi

AU - Okabe, Yoshihiro

AU - Katsushima, Shinji

AU - Inokuma, Tetsuro

AU - Yamashita, Yukitaka

AU - Nakai, Yoshitaka

AU - Nishino, Takayoshi

AU - Kajimura, Kozo

AU - Shibatoge, Mitsushige

AU - Kanda, Naoki

AU - Ido, Akio

AU - Ohana, Masaya

AU - Moriyama, Ichiro

AU - Tatsuta, Hiroshi

AU - Matsumura, Kazuyoshi

AU - Fujikawa, Keita

AU - Gotoh, Norimoto

AU - Tsutsumi, Takanobu

AU - Shimizu, Masakazu

AU - Setoh, Kazuya

AU - Takahashi, Meiko

AU - Tabara, Yasuharu

AU - Mimura, Jun

AU - Nakamura, Takefumi

AU - Kimura, Toshiyuki

AU - Kawanami, Chiharu

N1 - Funding Information: This study was supported by in part by the Japanese Ministry of Health, Labour, and Welfare ( grant number #H22-Nanchi-084 ), the Japanese Agency of Medical Research and Development (grant numbers JP16EK0109070 and JP18EK0109283 ), and Kyoto University Grant for Top Global University Japan Project. We are grateful to all of the patients for their invaluable contributions. Funding Information: YM reports grants from Kyowa Kirin Pharmaceutical Development, Astellas, Eisai, Ono, Pfizer, Asahi Kasei, MSD, Daiichi-Sankyo, Taisho, Taiho, Takeda, Chugai, Teijin, Nippon Kayaku, and Mochida outside the submitted work. YT reports non-financial support and honoraria or speakers fees funding from Astellas during the conduct of the study, grants from Mitsubishi-Tanabe, Bristol-Myers Squibb, Eisai, Chugai, Takeda, AbbVie, Astellas, Daiichi-Sankyo, Ono, MSD, and Taisho-Toyama, and honoraria or speakers fees funding from Daiichi-Sankyo, Astellas, Eli Lilly, Chugai, Sanofi, AbbVie, Pfizer, YL Biologics, Bristol-Myers Squibb, GlaxoSmithKline, UCB, Mitsubishi-Tanabe, Novartis, Eisai, Takeda, Janssen, and Asahi Kasei outside the submitted work. NM reports grants from Merck Serono, AstraZeneca, Zeria, NanoCarrier, Eisai, MSD, Dainippon Sumitomo, ASLAN, Incyte, and Pharma Valley Center, personal fees from Ono and Teijin, grants and personal fees from Yakult Honsha and Taiho, and grants, personal fees, and non-financial support from Novartis outside the submitted work. All other authors declare no conflicts. Funding Information: This study was supported by in part by the Japanese Ministry of Health, Labour, and Welfare (grant number #H22-Nanchi-084), the Japanese Agency of Medical Research and Development (grant numbers JP16EK0109070 and JP18EK0109283), and Kyoto University Grant for Top Global University Japan Project. We are grateful to all of the patients for their invaluable contributions. Publisher Copyright: © 2019 Elsevier Ltd

PY - 2019/9

Y1 - 2019/9

N2 - Background: IgG4-related disease is a newly recognised immunopathological entity that includes autoimmune pancreatitis, IgG4-related sialadenitis, and IgG4-related kidney disease. To understand the genetic landscape of IgG4-related disease, we did a genome-wide association study. Methods: We did a genome-wide association study of Japanese individuals, initially screening 857 patients with IgG4-related disease at 50 Japanese research institutions and DNA samples from 2082 healthy control participants from the Nagahama Prospective Genome Cohort for the Comprehensive Human Bioscience. From Oct 27, 2008, to July 22, 2014, we enrolled 835 patients and used data from 1789 healthy participants. Only patients with confirmed diagnosis of IgG4-related disease according to the international diagnostic criteria were included. Genotyping was done with the Infinium HumanOmni5Exome, HumanOmni2.5Exome, or HumanOmni2.5 Illumina arrays, and genomic distributions were compared between case and control samples for 958 440 single nucleotide polymorphisms. The HLA region was extensively analysed using imputation of HLA alleles and aminoacid residues. Fine mapping of the FCGR2B region was also done. Associations between clinical manifestations of disease and the genetic variations identified in these two genes were examined. Findings: We identified the HLA-DRB1 (p=1·1×10−11) and FCGR2B (p=2·0×10−8) regions as susceptibility loci for IgG4-related disease. We also identified crucial aminoacid residues in the β domain of the peptide-binding groove of HLA-DRB1, in which the seventh aminoacid residue showed the strongest association signal with IgG4-related disease (p=1·7×10−14), as has been reported with other autoimmune diseases. rs1340976 in FCGR2B showed an association with increased FCGR2B expression (p=2·7×10−10) and was in weak linkage disequilibrium with rs1050501, a missense variant of FCGR2B previously associated with systemic lupus erythematosus. Furthermore, rs1340976 was associated with the number of swollen organs at diagnosis (p=0·011) and IgG4 concentration at diagnosis (p=0·035). Interpretation: Two susceptibility loci for IgG4-related disease were identified. Both FCGR2B and HLA loci might have important roles in IgG4-related disease development. Common molecular mechanisms might underlie IgG4-related disease and other immune-related disorders Funding: The Japanese Ministry of Health, Labour, and Welfare, the Japanese Agency of Medical Research and Development, and Kyoto University Grant for Top Global University Japan Project.

AB - Background: IgG4-related disease is a newly recognised immunopathological entity that includes autoimmune pancreatitis, IgG4-related sialadenitis, and IgG4-related kidney disease. To understand the genetic landscape of IgG4-related disease, we did a genome-wide association study. Methods: We did a genome-wide association study of Japanese individuals, initially screening 857 patients with IgG4-related disease at 50 Japanese research institutions and DNA samples from 2082 healthy control participants from the Nagahama Prospective Genome Cohort for the Comprehensive Human Bioscience. From Oct 27, 2008, to July 22, 2014, we enrolled 835 patients and used data from 1789 healthy participants. Only patients with confirmed diagnosis of IgG4-related disease according to the international diagnostic criteria were included. Genotyping was done with the Infinium HumanOmni5Exome, HumanOmni2.5Exome, or HumanOmni2.5 Illumina arrays, and genomic distributions were compared between case and control samples for 958 440 single nucleotide polymorphisms. The HLA region was extensively analysed using imputation of HLA alleles and aminoacid residues. Fine mapping of the FCGR2B region was also done. Associations between clinical manifestations of disease and the genetic variations identified in these two genes were examined. Findings: We identified the HLA-DRB1 (p=1·1×10−11) and FCGR2B (p=2·0×10−8) regions as susceptibility loci for IgG4-related disease. We also identified crucial aminoacid residues in the β domain of the peptide-binding groove of HLA-DRB1, in which the seventh aminoacid residue showed the strongest association signal with IgG4-related disease (p=1·7×10−14), as has been reported with other autoimmune diseases. rs1340976 in FCGR2B showed an association with increased FCGR2B expression (p=2·7×10−10) and was in weak linkage disequilibrium with rs1050501, a missense variant of FCGR2B previously associated with systemic lupus erythematosus. Furthermore, rs1340976 was associated with the number of swollen organs at diagnosis (p=0·011) and IgG4 concentration at diagnosis (p=0·035). Interpretation: Two susceptibility loci for IgG4-related disease were identified. Both FCGR2B and HLA loci might have important roles in IgG4-related disease development. Common molecular mechanisms might underlie IgG4-related disease and other immune-related disorders Funding: The Japanese Ministry of Health, Labour, and Welfare, the Japanese Agency of Medical Research and Development, and Kyoto University Grant for Top Global University Japan Project.

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UR - http://www.scopus.com/inward/citedby.url?scp=85071687187&partnerID=8YFLogxK

U2 - 10.1016/S2665-9913(19)30006-2

DO - 10.1016/S2665-9913(19)30006-2

M3 - Article

AN - SCOPUS:85071687187

SN - 2665-9913

VL - 1

SP - e14-e22

JO - The Lancet Rheumatology

JF - The Lancet Rheumatology

IS - 1

ER -

IgG4-related disease in the Japanese population: a genome-wide association study

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UN SDGs

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