Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice
Immunoregulatory circuits among T-cell sets. II. Physiologic role of feedback inhibition in vivo: absence in NZB mice
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T 细胞组之间的免疫调节回路。
DOI：
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发表时间：
1978
影响因子：
15.3
通讯作者：
R. Gershon
中科院分区：
文献类型：
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作者：
Harvey Cantor;L. McVAY;J. Hugenberger;K. Naidorf;F. Shen;R. Gershon
我们已经证明：(A)纯化的T辅助细胞诱导表达Ly123+QA1+表面表型的另一种T细胞集的细胞发挥强大的抑制活性，(B)这种T-T相互作用在调节体内免疫反应中发挥重要作用，以及(C)这种相互作用对旨在通过过继(或主动)免疫治疗增强个体免疫状态的方案构成了重要障碍。我们的结果还表明，体内介导反馈抑制的Ly123+T细胞集对小剂量环磷酰胺和成年后胸腺切除都很敏感。这种T-T相互作用对免疫系统正常、生理调节的重要性得到了强调，因为发现NZB小鼠(一种自发发展成自身免疫疾病的近亲交配品系)的主要T细胞缺陷是负责反馈抑制的Ly123+T细胞集的缺失或故障。
We have shown that (a) purified T-helper cells induce cells of another T-cell set-, expressing the Ly123+Qa1+ surface phenotype, to exert potent suppressive activity, (b) this T-T interaction plays an important role in regulating in vivo immune responses, and (c) this interaction represents an important barrier to protocols intended to augment the immune status of individuals by adoptive (or active) immunotherapy. Our results also indicate that the Ly123+ T-cell set mediating feedback suppression in vivo is sensitive to both low doses of cyclophosphamide and removal of the thymus in adult life. The importance of this T-T interaction to normal, physiologic regulation of the immune system is emphasized by the finding that the major T-cell deficit of NZB mice (an inbred strain of mice that spontaneously develops an autoimmune disorder) is the absence or malfunction of an Ly123+ T-cell set responsible for feedback inhibition.