CAJ | 학술논문

目的：研究Lewis肺癌细胞裂解物对小鼠树突状细胞（ DC）的免疫抑制作用。方法：反复冻融法制备Lewis肺癌细胞裂解物，骨髓冲洗提取C57／BL6小鼠DC，GM-CSF、IL-4体外诱导培养DC，ELISA检测肿瘤细胞裂解物（ TCL）中透明质酸（ HA）含量，ELISA检测DC 培养上清液中IL-12和IL-10水平。结果：经检测， Lewis 肺癌细胞 TCL 中含有HA，其含量为42 mg／ml。将这种TCL作用于C57／BL6小鼠DC，同对照组相比，DC的IL-12分泌水平显著下降（P＜0．01），而IL-10的分泌水平显著提高（P＜0．01），这符合免疫耐受DC细胞因子分泌特点。在用Pep-1抗体封闭DC表面的HA受体CD44后，DC的IL-12、IL-10分泌水平则恢复至同对照组相同的水平（P＞0．05）。结论：Lewis肺癌细胞裂解物中含有HA。通过这种物质，肺癌细胞裂解物可以诱生鼠源免疫耐受性DC，从而抑制DC的免疫活性。
목적：연구Lewis폐암세포렬해물대소서수돌상세포（ DC）적면역억제작용。방법：반복동융법제비Lewis폐암세포렬해물，골수충세제취C57／BL6소서DC，GM-CSF、IL-4체외유도배양DC，ELISA검측종류세포렬해물（ TCL）중투명질산（ HA）함량，ELISA검측DC 배양상청액중IL-12화IL-10수평。결과：경검측， Lewis 폐암세포 TCL 중함유HA，기함량위42 mg／ml。장저충TCL작용우C57／BL6소서DC，동대조조상비，DC적IL-12분비수평현저하강（P＜0．01），이IL-10적분비수평현저제고（P＜0．01），저부합면역내수DC세포인자분비특점。재용Pep-1항체봉폐DC표면적HA수체CD44후，DC적IL-12、IL-10분비수평칙회복지동대조조상동적수평（P＞0．05）。결론：Lewis폐암세포렬해물중함유HA。통과저충물질，폐암세포렬해물가이유생서원면역내수성DC，종이억제DC적면역활성。
Objective:To investigate the immunosuppressive effect of the lysates from Lewis lung cancer cells on mouse dendritic cells(DC).Methods:DCs were initially obtained from the C57/BL6 mouse marrow.The lysates of Lewis lung cancer cells were prepared with repeated freezing-thawing tech-nique,and in vitro cultured in granulocyte-macrophage colony-stimulating factor(GM-CSF) and interleukin-4(IL-4).ELISA was used to detect the con-centration of hyaluronan(HA) in the tumor cell lysates(TCL) as well as the level of IL-12 and IL-10 in the culture supernatant of DCs.Results:HA was detected in the TCL of Lewis lung cancer cells,and its concentration reached 42 mg/ml.Once the TCL was delivered into the DCs of C57/BL6 mice,whose IL-12 level in DCs was significantly decreased,whereas the IL-10 level was markedly increased as compared with the controls(P<0.01).These changes were complying with the immunological tolerance properties of DCs .However,IL-12 and IL-10 levels were restored equivalently to those of the control group after inhibition of the surface HA receptor CD44 in DCs using Pep-1 antibody (P>0.05).Conclusion:TCL of Lewis lung cancer contains a HA that is capable of inducing the immunogenic DC in mouse to eventually inhibit the immunocompetence of DCs .