Induction of immune response against MHC class I-binding peptides

诱导针对 MHC I 类结合肽的免疫应答

• 批准号: 07670372
• 负责人: NAKAYAMA Eiichi
• 金额: $ 1.41万
• 依托单位: Okayama University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 1995
• 资助国家: 日本
• 起止时间: 1995 至 1996
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-07670372/
• 关键词: MHC clas I; peptide; CTL; CD4; APC; MAP (multiple antigen peptide); 細胞傷害性T細胞(CTL); 多価抗原; MHC; 細胞傷害性T細胞

1. Requirement of CD4 T cells for generation of specific CTL on stimulation with MHC class I-binding peptide.We investigated generation of CTL in spleen cells from BALB/C mice on stimulation with p2Ca and pRL1 peptides. We found that CD4 T cells are necessary for generation of CTL in spleen cells against those peptides even though they are H-2L^d-binding peptides. Antigen presenting cells (APC) has also been shown to be necessary.2. Induction of efficient CTL generation by pRL1peptide bound to MAP.We investigated the effect of in vivo and in vitro stimulation with pRL1 peptide bound to MAP on induction of CTL generation. Stimulation with pRL1 peptide alone did not induce CTL generation, but stimulation with pRL1 peptide bound to MAP induced CTL generation. Cellular mechanisms of induction of CTL generaiton by the peptide bound to MAP should be further investigated.

1. CD4 T 细胞在 MHC I 类结合肽刺激下生成特异性 CTL 的需要。我们研究了在 p2Ca 和 pRL1 肽刺激下 BALB/C 小鼠脾细胞中 CTL 的生成。我们发现 CD4 T 细胞对于在脾细胞中生成针对这些肽的 CTL 是必需的，即使它们是 H-2L^d 结合肽。抗原呈递细胞（APC）也被证明是必要的。2．通过与 MAP 结合的 pRL1 肽诱导有效的 CTL 生成。我们研究了与 MAP 结合的 pRL1 肽的体内和体外刺激对诱导 CTL 生成的影响。单独用pRL1肽刺激不诱导CTL产生，但用与MAP结合的pRL1肽刺激诱导CTL产生。应进一步研究与 MAP 结合的肽诱导 CTL 生成的细胞机制。

项目成果

Ono,T.,et al.: "Production of murine leukemia RL ♂ 1 rejection antigen peptide pRL1a by proteolysis of natural precursor pRL1b." Jpn.J.Cancer Res.87. 1165-1170 (1996)

Ono, T., et al.：“通过天然前体 pRL1b 的蛋白水解生产鼠白血病 RL♂ 1 排斥抗原肽 pRL1a”Jpn.J.Cancer Res.87 (1996)。

Okumura, C., et al.: "Induction of murine gammadelta T cells cytotoxic for xenogeneic rat cells." J.Immunol.154. 1114-1123 (1995)

Okumura, C. 等人：“诱导鼠 γδ T 细胞对异种大鼠细胞具有细胞毒性。”

Wada,H.,et al.: "Rejection antigen peptides on BALB/c RL ♂ 1 leukemia recognized by cytotoxic T lymphocytes : derivation from the normally untranslated 5′-region of the c-akt proto-oncogene activated by LTR." Cancer Research. 7. 233-238 (1995)

Wada, H. 等人：“细胞毒性 T 淋巴细胞识别的 BALB/c RL ♂ 1 白血病上的排斥抗原肽：源自 LTR 激活的 c-akt 原癌基因的正常非翻译 5 区。”研究。7。233-238（1995）

Baba,H.,et al.: "Two isotypes of murine nm23/nucleoside diphosphate kinase,nm23-M11 and nm23-M2 are involved in metastatic suppression of a murine melanoma line." Cancer Research. 55. 1977-1981 (1995)

Baba, H. 等人：“鼠 nm23/核苷二磷酸激酶的两种同种型 nm23-M11 和 nm23-M2 参与鼠黑色素瘤系的转移抑制。”

Harutsumi,M.,et al.: "Rejection of parental Meth A tumor on concomitant inoculation of Meth A cells infecte retrovivally with the interferon-γ gene into (BALB/c x C57BL/6) F_1 mice." Int.J.Oncol.55. 4780-4783 (1995)

Harutsumi,M.,et al.：“将干扰素-γ 基因逆转录感染的 Meth A 细胞同时接种到 (BALB/c x C57BL/6) Int.J.Oncol 小鼠中，可抑制亲本 Meth A 肿瘤。” 55. 4780-4783 (1995)