Bell E B, Shand F L
Eur J Immunol. 1975 Jan;5(1):1-7. doi: 10.1002/eji.1830050102.
Thoracic duct lymphocytes from previously immunized (AS2 x AS)F1 rats ('TDL) were adoptively transferred to syngeneic recipients and triggered by soluble HSA (s-HSA) the following day. The response of 'TDL in an irradiated recipient was almost two orders of magnitude greater than the response in a nonirradiated adult host. The affinity of the antibody in the adult recipients was significantly reduced but increased with time. Nonirradiated young recipients (3 weeks old) also supported an adoptive memory response which was comparable in quantity and quality to that found in irradiated hosts. The response of 'TDL declined progressively when transferred into 2-week-old or 4-week-old radiation chimeras, or was reduced in irradiated hosts when the memory cells were mixed together with nonimmune TDL. The experiments indicate that the differential response between the adult and irradiated recipient is the result of a restrictive control in the former host rather than an enhancing factor in the latter. Lymphocytes in the nonimmune population regulate both the expansion and maturation of the adoptive memory response, the high energy-binding B cells being at a selective disadvantage. Host irradiation effectively liberates the adoptive response from this cellular control mechanism. A comparative study of transferred, [14C]leucine-labeled TDL showed that distribution and homing of lymphocytes to lymph nodes and spleen was not altered by irradiating the recipients. However, adoptively transferred cells almost completely failed to recirculate in irradiated rats, in contrast to normal recipients. But, the injection of large numbers of unlabeled TDL following irradiation forced more labeled cells into the recirculating pool, suggesting that saturation of depleted lymphoid tissue with lymphocytes is an important factor regulating lymphocyte traffic. The relevance of this "saturation effect" in regulating the adoptive memory response is discussed.
将先前免疫过的（AS2×AS）F1大鼠的胸导管淋巴细胞（“TDL”）过继转移至同基因受体，并于次日用可溶性人血清白蛋白（s - HSA）激发。照射受体中“TDL”的反应比未照射的成年宿主中的反应几乎高两个数量级。成年受体中抗体的亲和力显著降低，但随时间增加。未照射的年轻受体（3周龄）也支持过继记忆反应，其数量和质量与照射宿主中的相当。当将“TDL”转移至2周龄或4周龄的辐射嵌合体中时，其反应逐渐下降，或者当记忆细胞与非免疫TDL混合时，照射宿主中的反应降低。实验表明，成年宿主与照射受体之间的差异反应是前者宿主中限制性控制的结果，而非后者中的增强因子。非免疫群体中的淋巴细胞调节过继记忆反应的扩增和成熟，高能结合B细胞处于选择性劣势。宿主照射有效地使过继反应从这种细胞控制机制中解放出来。对转移的、[14C]亮氨酸标记的TDL的比较研究表明，照射受体不会改变淋巴细胞向淋巴结和脾脏的分布及归巢。然而，与正常受体相比，过继转移的细胞在照射大鼠中几乎完全无法再循环。但是，照射后注射大量未标记的TDL迫使更多标记细胞进入再循环池，这表明淋巴细胞使耗尽的淋巴组织饱和是调节淋巴细胞运输的一个重要因素。讨论了这种“饱和效应”在调节过继记忆反应中的相关性。
