Shinomiya Y, Harada M, Kurosawa S, Okamoto T, Terao H, Matsuzaki G, Shirakusa T, Nomoto K
Department of Immunology, Kyushu University, Japan.
Immunobiology. 1995 Aug;193(5):439-55. doi: 10.1016/s0171-2985(11)80429-8.
The Th1 type Cd4+ T cell clone (MH2), which is capable of recognizing purified protein derivative from Mycobacterium tuberculosis (PPD), was examined for its anti-metastatic activity against melanoma. In using an in vitro proliferative assay, MH2 was able to recognize PPD-derived antigen in a major histocompatibility complex class II-restricted manner. MH2 showed neither any natural killer (NK) activity nor cytolytic activity against syngeneic B16 melanoma. This clone produced interferon-gamma, tumor necrosis factor and interleukin-2, but not interleukin-4, when co-cultured with PPD and irradiated syngeneic C57BL/6 spleen cells, suggesting that this clone could thus be assigned to the Th1 subset. An intraperitoneal (i.p.) co-injection of 2 x 10(6) MH2 and 50 micrograms PPD increased the NK activity of the peritoneal exudate cells (PEC) and the percentage of NK1.1+ cells in the PEC. These activated NK cells showed a low but significantly cytolytic activity against B16 melanoma. The augmented NK activity induced by the co-injection of MH2 and PPD was maintained by the weekly additional i.p. injections of PPD alone. Using a murine metastatic model, and i.p. co-injection of MH2 and PPD-induced anti-metastatic activity against B16 melanoma. This anti-metastatic activity was then abrogated by the in vivo administration of anti-asialo GM1 serum. In addition, the NK activity in both peripheral blood and metastatic lungs was significantly augmented in the mice which were co-injected with MH2 and PPD. Taken together, these findings indicate that the in vivo activation of Th1 type CD4+ T cells augmented the NK activity in vivo and thus could potentially be an efficient immunotherapeutic weapon against metastasis of melanoma. These results also imply that adoptive immunotherapy could induce anti-metastatic activity through cytokine production but not through any direct cytolytic activity.
对能够识别结核分枝杆菌纯蛋白衍生物(PPD)的Th1型Cd4+ T细胞克隆(MH2)进行了其对黑色素瘤的抗转移活性检测。在体外增殖试验中,MH2能够以主要组织相容性复合体II类限制的方式识别PPD衍生抗原。MH2对同基因B16黑色素瘤既无天然杀伤(NK)活性也无细胞溶解活性。当与PPD和经照射的同基因C57BL/6脾细胞共培养时,该克隆产生γ干扰素、肿瘤坏死因子和白细胞介素-2,但不产生白细胞介素-4,提示该克隆可归为Th1亚群。腹腔内(i.p.)共注射2×10(6)个MH2和50微克PPD可增加腹腔渗出细胞(PEC)的NK活性以及PEC中NK1.1+细胞的百分比。这些活化的NK细胞对B16黑色素瘤表现出低但显著的细胞溶解活性。单独每周腹腔内额外注射PPD可维持由MH2和PPD共注射诱导的增强的NK活性。使用小鼠转移模型,腹腔内共注射MH2和PPD可诱导对B16黑色素瘤的抗转移活性。然后,体内给予抗去唾液酸GM1血清可消除这种抗转移活性。此外,在共注射MH2和PPD的小鼠中,外周血和转移肺中的NK活性均显著增强。综上所述,这些发现表明Th1型CD4+ T细胞的体内活化增强了体内NK活性,因此可能是对抗黑色素瘤转移的有效免疫治疗武器。这些结果还意味着过继性免疫疗法可通过细胞因子产生而非任何直接细胞溶解活性诱导抗转移活性。