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MyD88 signaling causes autoimmune sialadenitis through formation of high endothelial venules and upregulation of LT beta receptor-mediated signaling

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Title: MyD88 signaling causes autoimmune sialadenitis through formation of high endothelial venules and upregulation of LT beta receptor-mediated signaling
Authors: Into, Takeshi Browse this author →KAKEN DB
Niida, Shumpei Browse this author →KAKEN DB
Shibata, Ken-ichiro Browse this author →KAKEN DB
Issue Date: 24-Sep-2018
Publisher: Nature Publishing Group
Journal Title: Scientific reports
Volume: 8
Start Page: 14272
Publisher DOI: 10.1038/s41598-018-32690-x
Abstract: Autoimmune sialadenitis (AS), chronic inflammation of the salivary glands (SGs) with focal lymphocyte infiltration, appears in autoimmune diseases such as Sjogren's syndrome. The pathological role of MyD88-dependent innate immune signaling in autoimmune diseases including AS has been studied using mouse models, such as NOD mice. Although AS development in NOD mice was reported to be suppressed by Myd88 deficiency, its specific role remains unclear. Here, we determined the potent suppressive effects of Myd88 deficiency on AS development in lupus-prone B6/lpr mice, which have lymphoproliferation abnormalities, and also in NOD mice, which have no lymphoproliferation abnormalities. This indicates that MyD88 signaling triggers AS through both lymphoproliferation-dependent and -independent mechanisms. To address the MyD88-dependent lymphoproliferation-independent AS manifestation, SGs from C57BL/6 mice were analyzed. Remarkable upregulation of Glycam1 and high endothelial venule (HEV)-associated changes were unexpectedly found in Myd88(+/+) mice, compared with Myd88(-/-) mice. MyD88-dependent HEV-associated changes were also observed in NOD mice. Additionally, Lta, Ltb, and Ltbr in SGs of NOD mice were lowered by Myd88 deficiency. Interestingly, LT beta R-induced HEV-associated gene expression in cultured cells was impaired by Myd88 deficiency. Our findings highlight novel roles for MyD88 in AS development, which imply the existence of MyD88-dependent HEV formation in ectopic lymphoid neogenesis.
Rights: http://creativecommons.org/licenses/by/4.0/
Type: article
URI: http://hdl.handle.net/2115/71748
Appears in Collections:歯学院・歯学研究院 (Graduate School of Dental Medicine / Faculty of Dental Medicine) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 柴田 健一郎

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