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Hepatic serum amyloid A1 upregulates interleukin-17 (IL-17) in γδ T cells through Toll-like receptor 2 and is associated with psoriatic symptoms in transgenic mice

Title
Hepatic serum amyloid A1 upregulates interleukin-17 (IL-17) in γδ T cells through Toll-like receptor 2 and is associated with psoriatic symptoms in transgenic mice
Authors
Choi, MinjeeKim, Myoung OkLee, JinheeJeong, JainSung, YonghunPark, SongKwon, WookbongJang, SoyoungPark, Si JunKim, Hyeng‐SooJang, Woo YoungKim, Sung HyunLee, SanggyuChoi, Seong-KyoonRyoo, Zae Young
DGIST Authors
Choi, Seong-Kyoon
Issue Date
2019-06
Citation
Scandinavian Journal of Immunology, 89(6)
Type
Article
Article Type
Article
Author Keyword
acute phase reactants; cytokines; experimental animals; inflammation; skin
Keyword
NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; ARTHRITIS; DISEASE
ISSN
0300-9475
Abstract
Serum amyloid A (SAA) is an acute phase protein with pro-inflammatory cytokine-like properties. Recent studies have revealed that SAA promoted interleukin-17 (IL-17) production by various cells, including γδ T cells. γδ T cells are innate immune cells and express Toll-like receptor 2 (TLR2) on their surface, which is one of the SAA receptors. In this study, we investigated the relationship between γδ T cells and SAA1 through TLR2, by using hepatic SAA1-overexpressing transgenic (TG) mice. By injecting CU-CPT22, which is a TLR2 inhibitor, into the mice, we confirmed that SAA1 induced IL-17 in γδ T cells through TLR2. In vitro studies have confirmed that SAA1 increased IL-17 secretion in γδ T cells in combination with IL-23. We also observed a thickened epidermis layer and granulocyte penetration into the skin similar to the pathology of psoriasis in TG mice. In addition, strongly expressed SAA1 and penetration of γδ T cells in the skin of TG mice were detected. The exacerbation of psoriasis is associated with an increase in IL-17 levels. Therefore, these symptoms were induced by IL-17-producing γδ T cells increased by SAA1. Our study confirmed that SAA1 was a prominent protein that increased IL-17 levels through TLR2 in γδ T cells, confirming the possibility that SAA1 may exacerbate inflammatory diseases through γδ T cells. © 2019 The Foundation for the Scandinavian Journal of Immunology
URI
http://hdl.handle.net/20.500.11750/9821
DOI
10.1111/sji.12764
Publisher
Blackwell Publishing Inc.
Related Researcher
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Collection:
Core Protein Resources Center1. Journal Articles


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