Mikecz K, Glant T T, Buzás E, Poole A R
Joint Diseases Laboratory, Shriners Hospital for Crippled Children, Montreal, Quebec, Canada.
Arthritis Rheum. 1990 Jun;33(6):866-76. doi: 10.1002/art.1780330614.
Mononuclear cells from BALB/c mice with progressive polyarthritis and spondylitis induced by injection of fetal human articular cartilage proteoglycan (PG) were used to transfer arthritis by intravenous injection into irradiated, nonimmunized syngeneic mice. Successful transfer of arthritis to BALB/c mice required the injection of lymphocytes from mice with arthritis, along with 50 micrograms of human fetal PG, or lymphocytes stimulated in vitro with either fetal human PG or with mouse cartilage PG. In addition, interleukin-2 or immune sera from animals with arthritis significantly reduced the time to onset of transferred disease. The onset of adoptively transferred arthritis, using cells and antigen, from the time of the first injection (38.2 +/- 18.2 days, mean +/- SD) was shortened if lymphocytes from mice with transferred arthritis were reinjected (retransferred) into other, irradiated syngeneic mice (6.1 +/- 2.6 days). The appearance of autoreactive antibodies to mouse cartilage PG in the sera of mice with adoptively transferred arthritis (secondary or tertiary) preceded the appearance of the first clinical symptoms by a few days. The transfer of arthritis was blocked by pretreatment of donor (arthritic) lymphocytes with either anti-T cell or anti-B cell antibodies and complement. Exposure of mononuclear cells from mice with arthritis to PG, and its removal prior to transfer, also resulted in transfer of the arthritis. PG-induced arthritis was not transferred to nonirradiated mice, nor to irradiated mice injected with lymphocytes from animals with primary arthritis without chondroitinase ABC-digested fetal human PG. Arthritis never developed after injection of immune sera from mice with arthritis (without cells), nor when cells of nonarthritic animals were used with chondroitinase ABC-digested fetal human PG, with or without interleukin-2.
将注射人胎儿关节软骨蛋白聚糖（PG）诱导出进行性多关节炎和脊柱炎的BALB/c小鼠的单核细胞，通过静脉注射转移至经辐射、未免疫的同基因小鼠体内，以诱发关节炎。要成功将关节炎转移至BALB/c小鼠，需要注射患有关节炎小鼠的淋巴细胞，同时注射50微克人胎儿PG，或者注射用胎儿人PG或小鼠软骨PG体外刺激过的淋巴细胞。此外，来自患有关节炎动物的白细胞介素-2或免疫血清可显著缩短转移疾病的发病时间。如果将患有关节炎转移的小鼠的淋巴细胞再次注射（重新转移）到其他经辐射的同基因小鼠体内，那么从首次注射（38.2±18.2天，平均值±标准差）开始，采用细胞和抗原进行过继转移的关节炎的发病时间会缩短（6.1±2.6天）。在过继转移关节炎（继发性或三级性）的小鼠血清中，针对小鼠软骨PG的自身反应性抗体在首次出现临床症状前几天就已出现。用抗T细胞或抗B细胞抗体及补体对供体（患关节炎的）淋巴细胞进行预处理，可阻断关节炎的转移。将患关节炎小鼠的单核细胞暴露于PG，并在转移前去除PG，也会导致关节炎的转移。PG诱导的关节炎不会转移至未受辐射的小鼠，也不会转移至注射了未经软骨素酶ABC消化的胎儿人PG的原发性关节炎动物的淋巴细胞的受辐射小鼠。注射患有关节炎小鼠的免疫血清（无细胞）后，或者使用非关节炎动物的细胞与经软骨素酶ABC消化的胎儿人PG（无论有无白细胞介素-2）后，关节炎都不会发生。
