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논문 기본 정보

자료유형
학술저널
저자정보
Suk San Choi (Hanyang University College of Medicine) Eunkyeong Jang (Hanyang University College of Medicine) Kiseok Jang (Hanyang University College of Medicine) Sung Jun Jung (Hanyang University College of Medicine) Kyung-Gyun Hwang (Hanyang University College of Medicine) Jeehee Youn (Hanyang University College of Medicine)
저널정보
대한면역학회 Immune Network Immune Network Vol.19 No.6
발행연도
2019.12
수록면
104 - 114 (11page)

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초록· 키워드

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Sjögren"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 curdlaninjected SKG mice contained elevated titers of IgG (predominantly IgG₁), autoantibody to the muscarinic type 3 receptor (M3R) and inhibited carbachol-induced Ca<SUP>2+</SUP> 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.

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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS AND DISCUSSION
REFERENCES

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