Takahashi K, Ono K, Hirabayashi Y, Taniguchi M
Department of Immunology, School of Medicine, Chiba University, Japan.
J Immunol. 1988 May 1;140(9):3244-8.
We demonstrate in the B16 melanoma (C57BL/6 derived) system that the soluble form of tumor Ag preferentially suppresses immune responses 1) by inhibiting CTL activity in the effector phase and 2) by induction of specific Ts that block CTL generation in the induction phase. Soluble melanoma antigen Ag injected i.p. into the tumor-bearing host can effectively augment melanoma growth in vivo. Two T cell types with the L3T4+ or double-negative/I-J+ phenotype are involved in the suppression of anti-melanoma CTL responses and can easily be generated in the in vitro primary 12 h-culture. Anti-melanoma Ts recognizes the GM3(NeuAc) structure and distinguishes GM3 molecular species. This is because liposomes constructed with GM3(NeuAc) but not with GM3(NeuGc) gangliosides alone can effectively induce the melanoma-specific Ts. It is thus likely that tumor cells can escape from the immunologic surveillance system by stimulating the repertoire of Ts for self-Ag, GM3, which has existed even in the unprimed conditions in order to maintain self-tolerance. These would appear to be the major escape mechanisms.
我们在B16黑色素瘤（源自C57BL/6）系统中证明，肿瘤抗原的可溶性形式优先抑制免疫反应：1）在效应阶段通过抑制CTL活性；2）在诱导阶段通过诱导特异性Ts细胞来阻断CTL的产生。经腹腔注射到荷瘤宿主中的可溶性黑色素瘤抗原Ag可在体内有效促进黑色素瘤生长。两种具有L3T4+或双阴性/I-J+表型的T细胞类型参与了抗黑色素瘤CTL反应的抑制，并且可以在体外原代12小时培养中轻松产生。抗黑色素瘤Ts细胞识别GM3（NeuAc）结构并区分GM3分子种类。这是因为仅用GM3（NeuAc）而非GM3（NeuGc）神经节苷脂构建的脂质体可有效诱导黑色素瘤特异性Ts细胞。因此，肿瘤细胞可能通过刺激针对自身抗原GM3的Ts细胞库来逃避免疫监视系统，GM3即使在未致敏的条件下也存在，以维持自身耐受性。这些似乎是主要的逃逸机制。
