| First Author | Choi M | Year | 2019 |
| Journal | Scand J Immunol | Volume | 89 |
| Issue | 6 | Pages | e12764 |
| PubMed ID | 30892738 | Mgi Jnum | J:293586 |
| Mgi Id | MGI:6442327 | Doi | 10.1111/sji.12764 |
| Citation | Choi M, et al. (2019) Hepatic serum amyloid A1 upregulates interleukin-17 (IL-17) in gammadelta T cells through Toll-like receptor 2 and is associated with psoriatic symptoms in transgenic mice. Scand J Immunol 89(6):e12764 |
| abstractText | 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 gammadelta T cells. gammadelta 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 gammadelta 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 gammadelta T cells through TLR2. In vitro studies have confirmed that SAA1 increased IL-17 secretion in gammadelta 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 gammadelta 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 gammadelta T cells increased by SAA1. Our study confirmed that SAA1 was a prominent protein that increased IL-17 levels through TLR2 in gammadelta T cells, confirming the possibility that SAA1 may exacerbate inflammatory diseases through gammadelta T cells. |
