局部复发和远端转移对甲状腺乳头状癌（PTC）患者的生存和生活质量产生负面影响。因此，识别 PTC 的潜在生物标志物和治疗靶点在临床上至关重要。在这项研究中，我们进行了多组学分析，确定了 PTC 肿瘤微环境中的 CD36 促炎巨噬细胞子集。 CD36 巨噬细胞向癌前区域的募集与 PTC 的不良结果密切相关，并且肿瘤浸润 CD36 巨噬细胞的存在被确定为复发的危险因素。 CD36 巨噬细胞表现出与代谢活跃的 ZCCHC12 肿瘤细胞的相互作用。通过分泌SPP1，CD36巨噬细胞激活PI3K-AKT信号通路，从而促进癌细胞增殖。碘代谢失调与巨噬细胞促炎表型的获得密切相关。补碘可抑制促炎信号传导的激活，并通过增强 DUSP2 表达来阻碍 CD36 巨噬细胞的发育。总的来说，我们的研究结果揭示了 CD36 巨噬细胞和 ZCCHC12 肿瘤细胞之间复杂的串扰，为 PTC 的治疗和预后提供了宝贵的见解。

Local recurrence and distal metastasis negatively impact the survival and quality of life in patients with papillary thyroid cancer (PTC). Therefore, identifying potential biomarkers and therapeutic targets for PTC is clinically crucial. In this study, we performed a multi-omics analysis that identified a subset of CD36+ pro-inflammatory macrophages within the tumor microenvironment of PTC. The recruitment of CD36+ macrophages to pre-malignant regions strongly correlated with unfavorable outcomes in PTC and the presence of tumor-infiltrating CD36+ macrophages was determined to be a risk factor for recurrence. The CD36+ macrophages exhibited interactions with metabolically active ZCCHC12+ tumor cells. By secreting SPP1, the CD36+ macrophages activated the PI3K-AKT signaling pathway, thereby promoting proliferation of the cancer cells. Dysregulation of iodine metabolism was closely related to the acquisition of the pro-inflammatory phenotype in macrophages. Iodine supplementation inhibited the activation of pro-inflammatory signaling and impeded the development of CD36+ macrophages by enhancing DUSP2 expression. Overall, our findings shed light on the intricate crosstalk between CD36+ macrophages and ZCCHC12+ tumor cells, providing valuable insights for the treatment and prognosis of PTC.