Department of Pharmacology, Peking University Health Science Center, School of Basic Medical Sciences, Beijing, China.
J Drug Target. 2012 Aug;20(7):582-92. doi: 10.3109/1061186X.2012.697167. Epub 2012 Jun 14.
It is obvious that malignant cells evade from immune system in patients with manifest malignancy. Deficient major histocompatibility complex (MHC) class I and costimulatory molecules on malignant cells partially consist of evasion strategy since antigen bond MHC and costimulatory molecules provide two signals necessary for T cell activation. Therefore, enhancement of MHC-I and costimulatory molecules may favor restraint of the evasion. For this purpose, Ganoderma lucidum Polysaccharides (Gl-PS) was used on B16F10 melanoma cells in this study.
Immunocytochemistry and flowcytometry were used to determine the H-2K(b) and H-2D(b) (two prominent MHC class I molecules in C57BL mouse) as well as B7-1 and B7-2 (two prominent costimulatory molecules) expression on B16F10 cells after incubation with Gl-PS, while messenger ribonucleic acid (mRNA) of these molecules was detected by reverse transcription polymerase chain reaction (RT-PCR).
The H-2K(b) and H-2D(b), and B7-1 and B7-2 on B16F10 cells and mRNAs of these molecules were enhanced by Gl-PS, and more efficient antitumor cytotoxicity was induced by the Gl-PS treated cells.
The MHC class I molecules and costimulatory molecules may be enhanced by Gl-PS, and more efficient immune cell mediated cytotoxicity against these B16F10 cells may be induced, which may favor cancer therapy.
显然，恶性肿瘤患者体内的恶性细胞会逃避免疫系统的攻击。恶性细胞 MHC Ⅰ类主要组织相容性复合体（MHC）和共刺激分子的缺乏部分构成了逃避策略，因为抗原结合 MHC 和共刺激分子提供了 T 细胞激活所必需的两个信号。因此，增强 MHC-I 和共刺激分子可能有利于抑制这种逃避。为此，本研究采用灵芝多糖（Gl-PS）作用于 B16F10 黑色素瘤细胞。
采用免疫细胞化学和流式细胞术检测 Gl-PS 孵育后 B16F10 细胞上 H-2K(b)和 H-2D(b)（C57BL 小鼠中两种主要的 MHC Ⅰ类分子）以及 B7-1 和 B7-2（两种主要的共刺激分子）的表达，同时采用逆转录聚合酶链反应（RT-PCR）检测这些分子的信使核糖核酸（mRNA）。
Gl-PS 可增强 B16F10 细胞上的 H-2K(b)和 H-2D(b)、B7-1 和 B7-2 以及这些分子的 mRNA，并用 Gl-PS 处理过的细胞诱导出更有效的抗肿瘤细胞毒性。
Gl-PS 可增强 MHC Ⅰ类分子和共刺激分子，诱导针对这些 B16F10 细胞的更有效的免疫细胞介导的细胞毒性，从而有利于癌症治疗。
