Wu Y Z, Hong J H, Huang H H, Dougherty G J, McBride W H, Chiang C S
Department of Atomic Science, Tsing Hua University, Hsinchu, Taiwan.
J Leukoc Biol. 2000 Dec;68(6):890-6.
IL-3 gene expression within tumors leads to host-cell infiltration, particularly by macrophages, slower tumor growth, and enhanced immunogenicity. Surprisingly, tumor-associated macrophages (TAMs) from within FSAN-JmIL3 tumors had decreased expression of TNF-alpha and iNOS. On short-term culture, TAMs from FSAN-JmIL3 tumors regained their capacity to produce TNF-alpha and NO, indicating that they were primed in vivo. In vitro experiments were unable to demonstrate differences between FSAN-JmIL3 and FSAN tumor cells in their ability to stimulate TNF-alpha production by TAMs. In the absence of evidence that TAM activation was responsible for the slower growth of FSAN-JmIL3 tumors, the response of tumor cells to these effector molecules was studied. TNF-alpha and NO were cytotoxic for FSAN-JmIL3 cells but growth stimulatory for FSAN. These tumor-related phenotypic changes may contribute as much if not more than functional changes in host infiltrating cells to the slower growth of FSAN-JmIL3 tumors in vivo.
肿瘤内白细胞介素-3基因表达会导致宿主细胞浸润，尤其是巨噬细胞浸润，肿瘤生长减缓，并增强免疫原性。令人惊讶的是，FSAN-JmIL3肿瘤内的肿瘤相关巨噬细胞（TAM）肿瘤坏死因子-α（TNF-α）和诱导型一氧化氮合酶（iNOS）的表达降低。短期培养时，FSAN-JmIL3肿瘤的TAM恢复了产生TNF-α和一氧化氮（NO）的能力，表明它们在体内已被启动。体外实验未能证明FSAN-JmIL3和FSAN肿瘤细胞在刺激TAM产生TNF-α的能力上存在差异。在没有证据表明TAM激活是FSAN-JmIL3肿瘤生长缓慢的原因的情况下，研究了肿瘤细胞对这些效应分子的反应。TNF-α和NO对FSAN-JmIL3细胞具有细胞毒性，但对FSAN具有生长刺激作用。这些与肿瘤相关的表型变化在体内对FSAN-JmIL3肿瘤生长缓慢的贡献可能与宿主浸润细胞的功能变化一样多，甚至更多。
