Myeloid CD11c+ S100+ dendritic cells express indoleamine 2,3-dioxygenase at the inflammatory border to invasive lower lip squamous cell carcinoma

Myeloid CD11c+ S100+ dendritic cells express indoleamine 2,3-dioxygenase at the inflammatory border to invasive lower lip squamous cell carcinoma
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DOI:
10.14670/hh-26.997
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发表时间:
2011-08-01
影响因子:
2
通讯作者:
von Bubnoff, Dagmar
von Bubnoff, Dagmar
中科院分区:
生物学4区
文献类型:
--
作者:
Kuales, Melanie Alice;Wenzel, Joerg;von Bubnoff, Dagmar

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下唇鳞状细胞癌(SCC-LL)的患病率在全世界范围内不断增加。由抗原呈递细胞和/或肿瘤细胞表达吲哚胺2,3-双加氧酶(IDO)通过抑制T细胞介导的排斥反应导致肿瘤逃逸。本研究的目的是确定IDO在SCC-LL中的表达。通过免疫组织化学和免疫荧光分析,分析了47例SCC-LL中IDO表达,以及T细胞(CD 3)、髓样DC(S100,CD 11 c)、巨噬细胞(CD 68,CD 11 c)、朗格汉斯细胞(CD 1a,Langerin(CD 207))、浆细胞样DC(CD 123)和调节性T细胞(Foxp 3)标志物的表达。47个LLSCC中的12个标本含有表达IDO的细胞。IDO阳性与癌症相关浸润的强度密切相关(P=0.0007)。IDO阳性细胞正好沿着发展中的肿瘤和炎性浸润之间的边界。免疫荧光染色显示,SCC-LL中CD 11 c(+)S100(+)CD 68(-)树突状细胞(DCs)表达IDO。LL-SCC中的IDO表达可能有助于免疫逃逸和慢性炎症,从而促进癌症进展。抑制IDO可能是增强SCC-LL抗肿瘤免疫应答的治疗策略。
The prevalence of squamous cell carcinoma of the lower lip (SCC-LL) is increasing worlwide. The expression of the enzyme indoleamine 2,3-dioxygenase (IDO) by antigen-presenting cells and/or tumor cells leads to tumor escape by inhibiting T cell-mediated rejection responses. The aim of this study was to determine the expression of IDO in SCC-LL. IDO-expression was analyzed in 47 SCC-LL, together with the expression of markers of T-cells (CD3), myeloid DCs (S100, CD11c), macrophages (CD68, CD11c), Langerhans cells (CD1a, Langerin (CD207)), plasmacytoid DCs (CD123), and regulatory T cells (Foxp3) by immunohistochemistry and immunofluorescence analysis. Twelve specimens out of 47 LLSCCs contained cells that expressed IDO. IDO-positivity was strongly associated with the intensity of the cancer-associated infiltrate (P=0.0007). IDO-positive cells are located right along the border between the developing tumor and the inflammatory infiltrate. Immunofluorescence stainings showed that CD11c(+)S100(+)CD68(-) dendritic cells (DCs) express IDO in SCC-LL. IDO expression in LL-SCC may aid immune escape and chronic inflammation to promote cancer progression. Inhibition of IDO might be a therapeutic strategy to increase the anti-tumor immune response in SCC-LL.