目的:探讨瘢痕疙瘩成纤维细胞对M0型巨噬细胞极化、炎症因子表达的影响及可能机制，为瘢痕疙瘩治疗的新靶点提供理论依据。方法:2020年11月至2021年9月，中山大学附属第一医院整形外科手术患者瘢痕疙瘩5例或正常皮肤组织3例石蜡标本分离培养瘢痕疙瘩成纤维细胞及正常皮肤成纤维细胞，并与佛波酯诱导人急性单核细胞白血病细胞(THP-1)后形成的M0细胞共培养，检测巨噬细胞极化标记物及细胞因子表达情况。外源性加入肿瘤坏死因子(TNF-α)检测瘢痕疙瘩成纤维细胞增殖与细胞外基质表达情况。结果:瘢痕疙瘩组织中存在以CD163n +(M2)为主的巨噬细胞聚集，相比正常皮肤成纤维细胞，与瘢痕疙瘩成纤维细胞共培养的M0细胞表达更多TNF-α；流式细胞内染色阳性率分别为19.32%和29.52%。外源性TNF-α刺激下，瘢痕疙瘩成纤维细胞增殖及胞外基质(Ⅲ型胶原α3，COL3A1；纤维连接蛋白，fibronectin1，FN1)，波形蛋白表达增加，瘢痕疙瘩成纤维细胞与正常皮肤成纤维细胞对巨噬细胞极化表面标志CD86和CD163表达变化差异无统计学意义。n 结论:瘢痕疙瘩成纤维细胞促进巨噬细胞TNF-α表达，反过来促进自身细胞增殖、细胞外基质分泌。“,”Objective:To investigate the effect of keloid fibroblasts on the polarization and expression of inflammatory factors of M0 macrophages and possible mechanisms, and provide theoretical basis for new targets for keloid therapy.Methods:Keloids, normal skin tissues and paraffin specimens from patients undergoing plastic surgery in the First Affiliated Hospital of Sun Yat-sen University from November 2020 to September 2021 were collected, and fibroblasts of keloids and normal skins were isolated and co-cultured with M0 cells formed form THP-1 by phorbol ester (PMA)-stimulation to detect the expression of macrophage polarization markers and cytokines. Besides, keloid fibroblasts were treated with exogenous tumor necrosis factor-α(TNF-α) to detect its effect on the proliferation and extracellular matrix expression.Results:Macrophages were dominated by CD163n + (M2) in keloid tissues. Moreover, M0 cells expressed more TNF-α when co-cultured with keloid fibroblasts, compared with those with normal skin fibroblasts, in which, the positive staining rates of TNF-α were 19.32% and 29.52% respectively by flow cytometry. Furthermore, the proliferation was promoted and the expression of extracellular matrix proteins (COL3A1 and FN1)and Vimentin were upregulated in keloid fibroblasts under TNF-α stimulation. However, there was no significant difference in the expression of polarization surface markers CD86 and CD163 in macrophages, when co-cultured with keloid fibroblasts or normal skin fibroblasts.n Conclusions:Keloid fibroblasts promote the expression of TNF-α in macrophages, which in turn promotes the proliferation and extracellular matrix secretion of keloid fibroblasts.