Classification of idiopathic interstitial pneumonias using anti-myxovirus resistance-protein 1 autoantibody.

Hyota Takamatsu, Atsushi Kumanogoh, Yoshikazu Inoue, Noriyuki Tomiyama, Masanori Kitaichi, Takashi Kijima, Kenji Mizuguchi, Hiroyoshi Nishikawa, Masahide Mori, Yoshito Takeda, Izumi Nagatomo, Koji Inoue, Haruhiko Hirata, Toshiyuki Minami, Tomoyuki Otsuka, Yoshimasa Hamano, Yasuhiro Kato, Tetsuya Kimura, Yukihiro Yano, Toshimitsu Hamasaki, Masaki Hirose, Toru Arai, Lokesh P Tripathi, Osamu Honda, Ken Ueda, Masahiro Yanagawa, Akihiro Murakami, Shoichi Ihara, Hiroshi Kida

Journal: Scientific reports 2018;7():43201

PMID: 28230086

Abstract

Chronic fibrosing idiopathic interstitial pneumonia (IIP) can be divided into two main types: idiopathic pulmonary fibrosis (IPF), a steroid-resistant and progressive disease with a median survival of 2-3 years, and idiopathic non-specific interstitial pneumonia (INSIP), a steroid-sensitive and non-progressive autoimmune disease. Although the clinical courses of these two diseases differ, they may be difficult to distinguish at diagnosis. We performed a comprehensive analysis of serum autoantibodies from patients definitively diagnosed with IPF, INSIP, autoimmune pulmonary alveolar proteinosis, and sarcoidosis. We identified disease-specific autoantibodies and enriched KEGG pathways unique to each disease, and demonstrated that IPF and INSIP are serologically distinct. Furthermore, we discovered a new INSIP-specific autoantibody, anti-myxovirus resistance-1 (MX1) autoantibody. Patients positive for anti-MX1 autoantibody constituted 17.5% of all cases of chronic fibrosing IIPs. Notably, patients rarely simultaneously carried the anti-MX1 autoantibody and the anti-aminoacyl-transfer RNA synthetase autoantibody, which is common in chronic fibrosing IIPs. Because MX1 is one of the most important interferon-inducible anti-viral genes, we have not only identified a new diagnostic autoantibody of INSIP but also obtained new insight into the pathology of INSIP, which may be associated with viral infection and autoimmunity.

Address: Department of Respiratory Medicine, Allergy and Rheumatic Diseases, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita City, Osaka 565-0871, Japan.; AMED, CREST, Suita City, Osaka 565-0871, Japan.; Medical &Biological Laboratories Co., Ltd., Ina Laboratory, 1063-103 Terasawaoka, Ina City, Nagano 396-0002, Japan.; Department of Radiology, Osaka University Graduate School of Medicine, 2-2 Yamadaoka, Suita City, Osaka 565-0871, Japan.; National Institutes of Biomedical Innovation, Health and Nutrition, 7-6-8 Saitoasagi, Ibaraki City, Osaka 567-0085, Japan.; National Hospital Organization Kinki-Chuo Chest Medical Center, 1180 Nagasone-Cho, Kita-Ku, Sakai City, Osaka 591-8555, Japan.; Office of Biostatistics and Data Management, National Cerebral and Cardiovascular Center, 5-7-1 Fujishirodai, Suita City, Osaka 565-8565, Japan.; National Hospital Organization Toneyama National Hospital, 5-1-1 Toneyama, Toyonaka City, Osaka 560-8552, Japan.; Department of Immunopathology, WPI Immunology Frontier Research Center, Osaka University, Yamadaoka 3-1, Suita City, Osaka 565-0871, Japan.; Department of Experimental Immunology, WPI Immunology Frontier Research Center, Osaka University, Yamadaoka 3-1, Suita City, Osaka 565-0871, Japan.
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