Resistance of infectious canine hepatitis virus-immunized hamsters against transplantation of established ICH virus-induced tumors (Department of Animal Husbandry)

イヌ伝染性肝炎ウイルス誘発腫瘍において抗移植性免疫が成立するか否かを検討する目的で, ハムスターをあらかじめウイルスで3日おき3回免疫しておき, 初回接種後3週目に, 同ウイルス誘発ハムスター腫瘍よりin vitroで株化したHT-7細胞を移植し, 腫瘍移植に対する抑制効果の有無を観察した。得られた成績は次の通りである。1.ICHウイルス(10)^7あるいは(10)^5TCID_50を腹腔内接種し免疫した場合, 50%腫瘍発現に要するHT-7腫瘍細胞数(TPD_50)は対照の非免疫ハムスター群のそれに比して, (10)^7免疫群で約60倍, (10)^5免疫群で約10倍多く要し, ウイルス接種によって抗移植免疫が成立した。2.ウイルス免疫ルートを皮下接種に代えると, 抗移植性免疫の程度が腹腔内接種のそれに比しやゝ低下する。3.免疫原としてウイルスの代りに, ウイルス接種ハムスター胎児細胞を用いた場合, ウイルス単独接種の場合に比し, ウイルス中和抗体の産生は低いに拘わらず, 抗移植性免疫効果は同程度に高い。4.以上の成績より著者の確立したICHウイルス腫瘍の系でもウイルスに特異的な抗移植性免疫が成立し, しかもそれはウイルス粒子に対する液性抗体とは必ずしも同一のものでないことが示唆された。To determine whether a transplantation immunity could be demonstrated in infectious canine hepatitis (ICH) virus-induced tumor system, hamsters were immunized by 3 intraperitoneal or subcutaneous injections of ICH virus at intervals of 3 days and at 3 weeks after the 1st injection were challenged with graded doses of HT-7 cells, established from ICH virus-induced hamster tumors. The existence of transplantation immunity was conjectured by difference in 50% tumor producing doses ((TPD)_) of test and control animals. In the hamsters immunized intraperitoneally with the virus of (10)^7 or (10)^5 (TCID)_, (TPD)_ were usually about 60 or 10 times higher than in controls, respectively. In the subcutaneous immunization groups, an effect of transplantation immunity was somewhat lower than that of the intraperitoneal groups. When the hamsters were preimmunized with ICH virus-infected hamster embryo cells instead of free virus, the same degree of transplantation immunity was demonstrated. In these cases, however, no correlation was existed between degree of transplantation immunity and neutralization antibody titer. From the presented data, it was found that preimmunized hamsters with ICH virus or the virus infected hamster cells induce a state of relative resistance against the transplantation of established HT-7 cells, originally induced by ICH virus. Evidence was also suggested that the resistance was not due to humoral antibody to virion atigen