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Autoantibody-Mediated Dysfunction of Salivary Glands Leads to Xerostomia in SKG Mice

Immune Network 2019년 19권 6호 p.44 ~ 44
최석산 ( Choi Suk-San ) - Hanyang University College of Medicine Department of Anatomy and Cell Biology

장은경 ( Jang Eun-Kyeong ) - Hanyang University College of Medicine Department of Anatomy and Cell Biology
장기석 ( Jang Ki-Seok ) - Hanyang University College of Medicine Department of Pathology
정성준 ( Jung Sung-Jun ) - Hanyang University College of Medicine Department of Physiology
황경균 ( Hwang Kyung-Gyun ) - Hanyang University College of Medicine Department of Dentistry
윤지희 ( Youn Jee-Hee ) - Hanyang University College of Medicine Department of Anatomy and Cell Biology

Abstract


Sjogren's syndrome (SS) is a chronic heterogeneous disease that mainly affects exocrine glands, leading to sicca syndromes such as xerostomia. Despite the second highest prevalence rate among systemic autoimmune diseases, its pathophysiology remains largely unknown. Here we report that SKG mice, a cardinal model of Th17 cell-mediated arthritis, also develop a secondary form of SS-like disorder upon systemic exposure to purified curdlan, a type of β-glucan. The reduced production of saliva was not caused by focal immune cell infiltrates but was associated with IgG deposits in salivary glands. Sera from curdlan-injected SKG mice contained elevated titers of IgG (predominantly IgG1), autoantibody to the muscarinic type 3 receptor (M3R) and inhibited carbachol-induced Ca2+ signaling in salivary acinar cells. These results suggest that the Th17 cells that are elicited in SKG mice promote the production of salivary gland-specific autoantibodies including anti-M3R IgG; the antibodies are then deposited on acinar cells and inhibit M3R-mediated signaling required for salivation, finally leading to hypofunction of the salivary glands. This type II hypersensitivity reaction may explain the origin of secondary SS occurring without focal leukocyte infiltrates.

키워드

Sjogren's Syndrome; Xerostomia; Autoantibodies
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