Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 정승준 | - |
dc.date.accessioned | 2020-11-23T07:08:47Z | - |
dc.date.available | 2020-11-23T07:08:47Z | - |
dc.date.issued | 2019-12 | - |
dc.identifier.citation | IMMUNE NETWORK, v. 19, no. 6, article no. e44 | en_US |
dc.identifier.issn | 1598-2629 | - |
dc.identifier.issn | 2092-6685 | - |
dc.identifier.uri | https://immunenetwork.org/DOIx.php?id=10.4110/in.2019.19.e44 | - |
dc.identifier.uri | https://repository.hanyang.ac.kr/handle/20.500.11754/155697 | - |
dc.description.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 beta-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 IgG(1)), 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. | en_US |
dc.description.sponsorship | We thank Drs. Shimon Sakaguchi and Youngnim Choi for providing SKG breeders and experimental resources. We also thank the Analytical Instrumental Center (Seoul) of Hanyang University for technical support. This work was supported by a grant funded by the Korean Health Technology R&D Project, Ministry of Health & Welfare, Korea (HI17C1103). | en_US |
dc.language.iso | en | en_US |
dc.publisher | KOREA ASSOC IMMUNOLOGISTS | en_US |
dc.subject | Sjogren's Syndrome | en_US |
dc.subject | Xerostomia | en_US |
dc.subject | Autoantibodies | en_US |
dc.title | Autoantibody-Mediated Dysfunction of Salivary Glands Leads to Xerostomia in SKG Mice | en_US |
dc.type | Article | en_US |
dc.relation.no | 6 | - |
dc.relation.volume | 19 | - |
dc.identifier.doi | 10.4110/in.2019.19.e44 | - |
dc.relation.page | 1-11 | - |
dc.relation.journal | IMMUNE NETWORK | - |
dc.contributor.googleauthor | Choi, Suk San | - |
dc.contributor.googleauthor | Jang, Eunkyeong | - |
dc.contributor.googleauthor | Jang, Kiseok | - |
dc.contributor.googleauthor | Jung, Sung Jun | - |
dc.contributor.googleauthor | Hwang, Kyung-Gyun | - |
dc.contributor.googleauthor | Youn, Jeehee | - |
dc.relation.code | 2019040308 | - |
dc.sector.campus | S | - |
dc.sector.daehak | COLLEGE OF MEDICINE[S] | - |
dc.sector.department | DEPARTMENT OF MEDICINE | - |
dc.identifier.pid | eurijj | - |
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.