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对迟发型超敏反应中B淋巴细胞抑制作用的进一步研究,揭示了琼斯-莫特超敏反应的一种可能机制。

Further studies on B-lymphocyte suppression in delayed hypersensitivity, indicating a possible mechanism for Jones-Mote hypersensitivity.

作者信息

Turk J L, Parker D

出版信息

Immunology. 1973 Apr;24(4):751-8.

Abstract

A previous report of increased intensity and prolongation of contact hypersensitivity in animals pre-treated with cyclophosphamide (CY) has been confirmed using other immunosuppressive agents. Melphalan, ICRF 159 and azathioprine caused a similar increase in contact sensitivity reactions, whereas busulphan, procarbazine and chlorambucil were inactive in this respect. The increased contact hypersensitivity was not associated with increased lymph node activity. Pre-treatment with CY, ICRF 159 and melphalan also caused increased intensity and prolonged Jones—Mote type reactions so that they resembled tuberculin-type reactions. This was associated with a marked reduction in γ antibody production. It is therefore suggested that Jones—Mote hypersensitivity is a further example of a T-lymphocyte reaction modulated by a B-lymphocyte response.

摘要

先前有报告称,用环磷酰胺(CY)预处理的动物接触性超敏反应的强度增加且持续时间延长,使用其他免疫抑制剂已证实了这一点。美法仑、ICRF 159和硫唑嘌呤引起接触敏感性反应类似增加,而白消安、丙卡巴肼和苯丁酸氮芥在这方面无活性。接触性超敏反应增加与淋巴结活性增加无关。用CY、ICRF 159和美法仑预处理也导致琼斯-莫特型反应强度增加且持续时间延长,使其类似于结核菌素型反应。这与γ抗体产生显著减少有关。因此有人提出,琼斯-莫特超敏反应是由B淋巴细胞反应调节的T淋巴细胞反应的又一实例。

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Effect of ICRF 159 on immune responses.ICRF 159对免疫反应的影响。
Proc R Soc Med. 1972 Mar;65(3):264-5. doi: 10.1177/003591577206500317.

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