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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
Author(s) -
Choi Minjee,
Kim Myoung Ok,
Lee Jinhee,
Jeong Jain,
Sung Yonghun,
Park Song,
Kwon Wookbong,
Jang Soyoung,
Park Si Jun,
Kim HyengSoo,
Jang Woo Young,
Kim Sung Hyun,
Lee Sanggyu,
Choi SeongKyoon,
Ryoo Zae Young
Publication year - 2019
Publication title -
scandinavian journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.934
H-Index - 88
eISSN - 1365-3083
pISSN - 0300-9475
DOI - 10.1111/sji.12764
Subject(s) - tlr2 , cytokine , serum amyloid a , interleukin , chemistry , immunology , endocrinology , biology , medicine , immune system , inflammation , innate immune system
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.