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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
- 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
- Choi, Minjee; Kim, Myoung Ok; Lee, Jinhee; Jeong, Jain; Sung, Yonghun; Park, Song; Kwon, Wookbong; Jang, Soyoung; Park, Si Jun; Kim, Hyeng‐Soo; Jang, Woo Young; Kim, Sung Hyun; Lee, Sanggyu; Choi, Seong-Kyoon; Ryoo, Zae Young
- DGIST Authors
- Choi, Seong-Kyoon
- Issue Date
- Scandinavian Journal of Immunology, 89(6)
- Article Type
- Author Keyword
- acute phase reactants; cytokines; experimental animals; inflammation; skin
- NECROSIS-FACTOR-ALPHA; NF-KAPPA-B; ARTHRITIS; DISEASE
- 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
- Blackwell Publishing Inc.
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