Department of Immunology, Translational Medicine Institute, Shenyang Medical College, Shenyang, China.
Allergy and Clinical Immunology Research Centre, the First Affiliated Hospital of Jinzhou Medical University, Jinzhou, China.
Am J Rhinol Allergy. 2021 Nov;35(6):746-760. doi: 10.1177/1945892421993034. Epub 2021 Feb 8.
Recently, it has been reported that Toll-like receptor 7 (TLR7) agonists can improve allergic rhinitis (AR) symptoms by up-regulation of Th1 cytokine release and suppression of Th2 cell functions. However, little is known of the expression of TLR7 in basophils of AR.
To explore the expression of TLR7 in basophils of AR, and influence of allergens on TLR7 expression.
The expression levels of TLR7 in basophils of patients with AR were determined by flow cytometry, and the influence of allergens on TLR7 expression was examined by real time (q) PCR.
The percentages of TLR7CCR3 cells ( < 0.001 and = 0.011), TLR7CD123HLA-DR cells ( = 0 .016 and = 0.042) and TLR7CCR3CD123HLA-DR cells ( = 0.046 and = 0.035) in blood granulocyte and mononucleated cell populations of the patients with AR were increased, respectively compared with HC subjects. TLR7 MFI on CCR3 cells ( = 0.050 and = 0.043), CD123HLA-DR cells ( < 0.001 and = 0.002) and CCR3CD123HLA-DR cells ( < 0.001 and = 0.003) were enhanced compared with HC subjects. Allergens Der p1 and OVA provoked upregulation of TLR7 expression at both protein and mRNA levels and IL-13 production in KU812 cells. House Dust Mite extract (HDME), Artemisia sieversiana wild allergen extract (ASWE), IL-31, IL-33, IL-37, and TSLP provoked elevation of IL-6 release from KU812 cells following 2 h incubation period.
The percentage of TLR7 basophils and TLR7 expression intensity in a single basophil are both increased in the blood of patients with AR, indicating that basophils likely contribute to the pathogenesis of AR via TLR7.
最近有报道称,Toll 样受体 7(TLR7)激动剂可通过上调 Th1 细胞因子释放和抑制 Th2 细胞功能来改善变应性鼻炎(AR)症状。然而,关于 AR 患者嗜碱性粒细胞中 TLR7 的表达知之甚少。
探讨 TLR7 在 AR 嗜碱性粒细胞中的表达及其变应原对 TLR7 表达的影响。
采用流式细胞术检测 AR 患者嗜碱性粒细胞中 TLR7 的表达水平,实时(q)PCR 检测变应原对 TLR7 表达的影响。
与健康对照(HC)受试者相比,AR 患者血液粒细胞和单核细胞群体中 TLR7CCR3 细胞( < 0.001 和 = 0.011)、TLR7CD123HLA-DR 细胞( = 0.016 和 = 0.042)和 TLR7CCR3CD123HLA-DR 细胞( = 0.046 和 = 0.035)的百分比均增加。与 HC 受试者相比,CCR3 细胞上 TLR7 MFI( = 0.050 和 = 0.043)、CD123HLA-DR 细胞( < 0.001 和 = 0.002)和 CCR3CD123HLA-DR 细胞( < 0.001 和 = 0.003)的 TLR7 荧光强度均增强。Der p1 和 OVA 变应原在蛋白和 mRNA 水平均能诱导 KU812 细胞 TLR7 表达上调和 IL-13 产生。屋尘螨提取物(HDME)、蒿属野蒿变应原提取物(ASWE)、IL-31、IL-33、IL-37 和 TSLP 在孵育 2 小时后均可引起 KU812 细胞释放 IL-6 增加。
AR 患者血液中 TLR7 嗜碱性粒细胞的百分比和单个嗜碱性粒细胞中 TLR7 的表达强度均增加,提示嗜碱性粒细胞可能通过 TLR7 参与 AR 的发病机制。