Rheumatology Advance Access originally published online on May 4, 2004
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Rheumatology 2004; 43: 858-862
Rheumatology Vol. 43 No. 7 © British Society for Rheumatology 2004; all rights reserved
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Spontaneous development of multiple glandular and extraglandular lesions in aged IQI/Jic mice: a model for primary Sjögren's syndrome
Laboratory of Molecular Medicine, Department of Veterinary Clinical Sciences and 1 Laboratory of Anatomy, Department of Biomedical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, Sapporo, 060-0818, Japan.
Correspondence to: M. Inaba, Laboratory of Molecular Medicine, Department of Veterinary Clinical Sciences, Graduate School of Veterinary Medicine, Hokkaido University, N18W9, Sapporo, Hokkaido 060-0818, Japan. E-mail: inazo{at}vetmed.hokudai.ac.jp
Objective. In primary Sjögren's syndrome (SS), systemic exocrine and non-exocrine organs are frequently affected, in addition to the major target tissues of the lacrimal and salivary glands. This study aimed to examine whether the IQI/Jic mouse, an animal model of SS whose autoimmune dacryoadenitis and sialoadenitis have been documented, develops inflammatory lesions in multiple organs as in primary SS.
Methods. Systemic histopathological analysis was performed on IQI/Jic mice at various ages. Phenotypes of infiltrated lymphocytes were determined using immunohistochemical techniques.
Results. Inflammatory lesions were observed not only in the lacrimal and salivary glands, but also in multiple organs, including the lung, pancreas and kidney at advanced ages, and were mainly composed of CD4+ T cells and B cells. The incidence and severity of the inflammatory lesions increased with age in all these organs. The histological appearance and spreading of lesions were similar to those in human primary SS.
Conclusions. IQI/Jic mice spontaneously develop inflammatory cellular infiltrates in multiple exocrine and non-exocrine organs. This characteristic distinguishes IQI/Jic mice from other murine models, making them favourable for studies on the pathogenesis of systemic involvement in primary SS.
KEY WORDS: IQI/Jic mouse, Primary Sjögren's syndrome, Autoimmune disease
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