Johnson Sara D, Levingston Corinne, Young M Rita I
Research Service (151) Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, U.S.A. Department of Pathology and Laboratory Medicine, Medical University of South Carolina, Charleston, SC, U.S.A. Department of Otolaryngology-Head and Neck Surgery, Medical University of South Carolina, Charleston, SC, U.S.A.
Research Service (151) Ralph H. Johnson Veterans Affairs Medical Center, Charleston, SC, U.S.A.
Anticancer Res. 2016 Jul;36(7):3261-70.
Head and neck squamous cell carcinomas (HNSCC) are known to evade the host immune response. How premalignant oral lesions modulate the immune response, however, has yet to be elucidated.
A mouse model of oral carcinogenesis was used to determine how mediators from premalignant oral lesion cells vs. HNSCC cells impact on immune cytokine production and activation.
Media conditioned by premalignant lesion cells elicited an increased production of T cell-associated cytokines and proinflammatory mediators from cervical lymph node cells compared to media conditioned by HNSCC cells or media alone. In the presence of premalignant lesion cell-conditioned media, CD4(+) T cell expression of the IL-2 receptor CD25 and CD8(+) T cell expression of the activation marker CD69 was greater, compared to what was induced in HNSCC cell-conditioned media or media alone.
Premalignant lesion cells promote a proinflammatory environment and induce immune changes before HNSCC tumors are established.
已知头颈部鳞状细胞癌(HNSCC)会逃避宿主免疫反应。然而,癌前口腔病变如何调节免疫反应尚待阐明。
使用口腔致癌小鼠模型来确定来自癌前口腔病变细胞与HNSCC细胞的介质如何影响免疫细胞因子的产生和激活。
与HNSCC细胞条件培养基或单独培养基相比,癌前病变细胞条件培养基能诱导颈淋巴结细胞产生更多的T细胞相关细胞因子和促炎介质。与HNSCC细胞条件培养基或单独培养基相比,在癌前病变细胞条件培养基存在的情况下,IL-2受体CD25在CD4(+) T细胞中的表达以及激活标志物CD69在CD8(+) T细胞中的表达更高。
癌前病变细胞在HNSCC肿瘤形成之前促进促炎环境并诱导免疫变化。