Weigensberg M, Morecki S, Weiss L, Fuks Z, Slavin S
J Immunol. 1984 Feb;132(2):971-8.
Total lymphoid irradiation (TLI) was administered to (BALB/c X C57BL/6)F1 mice in eight daily doses of 200 rad (total 1600 rad). Spleen cells isolated from mice after treatment with TLI do not respond to alloantigens in vitro in a one-way mixed lymphocyte reaction (MLR), but normal reactivity recovers after approximately 2 mo. Radioresistant, antigen-nonspecific suppressor cells are documented in the spleens of TLI-treated mice immediately after radiotherapy, but suppressive capacity gradually disappears within 30 days. After TLI, the spleen is repopulated with large cells, the proportion of which is greatest at a time when theta-bearing cells are still depleted. Radioresistant suppression is mediated predominantly by the large cell subset and is thymus independent. Suppressor function can be abolished by lethal physicochemical procedures including formaldehyde fixation, multiple freeze-thawing, and heating to 56 degrees C, and it cannot be conferred by supernatants of TLI-suppressed MLR suspensions. Suppression cannot be overcome by adding various cell factors including T cell growth factor (TCGF) and lymphocyte-activating factor (LAF), nor is it affected by a prostaglandin inhibitor. Equally potent radioresistant suppressive activity is documented by co-culturing cells derived from other sources enriched in large, immature hematopoietic cells, including fetal liver cells and bone marrow cells obtained from normal and congenitally athymic mice. The presence of a large cell population and MLR suppressor function is also documented in the spleens of mice treated with single dose or fractionated doses of lethal whole body irradiation, followed by reconstitution with bone marrow cells obtained from normal mice. The data suggest that MLR suppressor cells, which are large, immature and predominantly radioresistant, can be induced after a short and well-tolerated TLI regimen.
对（BALB/c×C57BL/6）F1小鼠进行全身淋巴照射（TLI），每日剂量为200拉德，共8天（总计1600拉德）。经TLI处理后的小鼠分离出的脾细胞在单向混合淋巴细胞反应（MLR）中对同种异体抗原无体外反应，但大约2个月后正常反应性恢复。放疗后立即在TLI处理的小鼠脾脏中发现了抗辐射、抗原非特异性抑制细胞，但其抑制能力在30天内逐渐消失。TLI后，脾脏中重新填充了大细胞，在含θ细胞仍处于耗竭状态时，大细胞的比例最高。抗辐射抑制主要由大细胞亚群介导，且不依赖胸腺。抑制功能可通过包括甲醛固定、多次冻融和加热至56℃等致死性物理化学程序消除，TLI抑制的MLR悬浮液的上清液不能赋予抑制功能。添加包括T细胞生长因子（TCGF）和淋巴细胞激活因子（LAF）在内的各种细胞因子无法克服抑制作用，前列腺素抑制剂也不会对其产生影响。通过将来自其他富含大的未成熟造血细胞的来源（包括从正常和先天性无胸腺小鼠获得的胎肝细胞和骨髓细胞）的细胞共同培养，也证明了同样强大的抗辐射抑制活性。在用单剂量或分次剂量的致死性全身照射处理小鼠，然后用从正常小鼠获得的骨髓细胞进行重建的小鼠脾脏中，也记录到了大细胞群体的存在和MLR抑制功能。数据表明，在短时间且耐受性良好的TLI方案后，可诱导出大的、未成熟的且主要具有抗辐射能力的MLR抑制细胞。
