Immunohistochemical Analysis of Toll-Like Receptors, MyD88, and TRIF in Human Papillary Thyroid Carcinoma and Anaplastic Thyroid Carcinoma.

IF 1.7 Q4 ENDOCRINOLOGY & METABOLISM Journal of Thyroid Research Pub Date : 2021-07-01 eCollection Date: 2021-01-01 DOI:10.1155/2021/4226491

Yasuhiro Nihon-Yanagi, Megumi Wakayama, Naobumi Tochigi, Fumi Saito, Hideaki Ogata, Kazutoshi Shibuya

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引用次数: 3

Abstract

Purpose: We hypothesized that innate immune response pathways might be involved in thyroid carcinogenesis. To investigate this hypothesis, we aimed at analyzing the expression of several receptors and molecules in the innate immune system in papillary thyroid carcinoma (PTC) and anaplastic thyroid carcinoma (ATC) tissues.

Methods: Of the surgically resected specimens, 11 ATC tissues, 25 PTC tissues, and 8 nodular hyperplasia (NH) tissues were selected and examined for the expression of toll-like receptor (TLR) 2, TLR3, TLR4, TLR5, TLR7, TLR9, the myeloid differentiation primary response gene 88 (MyD88), and toll-interleukin-1 receptor domain-containing adaptor inducing INF-β (TRIF) by immunohistochemistry (IHC).

Results: Several TLRs were expressed in each tissue. TLR3 was strongly expressed in all tissues. In contrast, TLR4 was not detected in any tissues. While TLR5 was moderately expressed in NH but significantly reduced in PTC and ATC, TLR9 was absent in NH tissue but moderately expressed in both PTC and ATC. On MyD88 expression, no significant difference was found between PTC and ATC. TRIF was significantly upregulated in PTC and ATC compared to NH. Surprisingly, PTC and ATC tissues exhibited similar expression patterns of TLRs, MyD88, and TRIF.

Conclusion: These data suggest the involvement of the innate immune system in both PTC and ATC. Specifically, TLR3-mediated TRIF activation was confirmed in PTC and ATC. This provides new insight into thyroid carcinogenesis.

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人甲状腺乳头状癌和间变性甲状腺癌中toll样受体、MyD88和TRIF的免疫组织化学分析。

目的:我们假设先天免疫反应途径可能参与甲状腺癌的发生。为了验证这一假设，我们旨在分析先天性免疫系统中几种受体和分子在甲状腺乳头状癌(PTC)和间变性甲状腺癌(ATC)组织中的表达。方法:采用免疫组化(IHC)方法检测11例ATC组织、25例PTC组织和8例结节性增生(NH)组织中toll样受体(TLR) 2、TLR3、TLR4、TLR5、TLR7、TLR9、髓样分化主要反应基因88 (MyD88)和toll-白细胞介素-1受体结构域内接头诱导INF-β (TRIF)的表达。结果:各组织中均有多个tlr表达。TLR3在所有组织中均有强烈表达。相比之下，在任何组织中均未检测到TLR4。TLR5在NH组织中中度表达，但在PTC和ATC组织中显著表达减少，而TLR9在NH组织中不存在，但在PTC和ATC组织中均有中度表达。在MyD88的表达上，PTC与ATC无显著差异。与NH相比，PTC和ATC中TRIF显著上调。令人惊讶的是，PTC和ATC组织中TLRs、MyD88和TRIF的表达模式相似。结论:这些数据提示先天免疫系统参与了PTC和ATC。具体来说，在PTC和ATC中证实了tlr3介导的TRIF激活。这为甲状腺癌的发生提供了新的认识。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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