甲状腺滤泡状癌（FTC）与腺瘤的术前诊断一直是悬而未决的临床难题之一。本课题组前期工作发现FTC分泌高水平的CCL15招募肿瘤相关巨噬细胞（TAM）浸润，并且能够调控巨噬细胞向M2型分化，提示CCL15可能通过调控巨噬细胞M2型极化促进FTC的发生。本研究拟利用细胞模型、裸鼠模型和全身性基因敲除小鼠模型，探讨CCL15对TAM的极化作用，系统分析其对FTC增殖、转移等肿瘤生物学活性的影响与分子机制，并分析相关分子的临床意义，以提高FTC的早期诊断，降低甲状腺结节的过度治疗。

The preoperative diagnosis of follicular thyroid carcinoma (FTC) and benign follicular adenoma (FA) has been a clinical challenge due to their similar histological features. We found that the FTC could induce tumor-associated macrophages (TAMs) infiltration by producing CCL15 and FTC harbored a significantly higher density of M2 TAMs compared with FA, suggesting CCL15 might play an important role in FTC progress by regulating TAM polarization. We plan to systematically explore the role of CCL15 in TAM polarization and tumor growth, invasion and metastasis in the use of cell lines and mouse models, and analyze its clinical significance based on clinical data. Our project may bring new insights into the early diagnosis of FTC and provide potential target for its future intervention.