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对天然葡聚糖的抑制性二次反应的个体发生发展。

Ontogenic development of the suppressed secondary response to native dextran.

作者信息

Wood C, Fernandez C, Möller G

出版信息

Scand J Immunol. 1982 Oct;16(4):287-92. doi: 10.1111/j.1365-3083.1982.tb00725.x.

Abstract

The ontogenic development of the plaque-forming cell (PFC) response to the thymus-independent (TI) antigen alpha 1-6 native dextran B512 was studied to determine when the first minimal amounts of anti-dextran antibodies are formed. Substantial antibody responses to certain other TI polysaccharide antigens arise during the first month of life, whereas the development of the response to native dextran has been found to be conspicuously delayed in high-responder mice. Results indicated that CBA mice began to produce minimal amounts of anti-dextran antibodies between 15 and 21 days of age, and the development continued progressively until peak levels were reached at 90 days of age. The alpha 1-6 native dextran system is also one of the few murine models in which endogenous anti-idiotypic antibodies are formed subsequent to anti-dextran production. It has been shown that the anti-idiotypic antibodies are responsible for specific inhibition of secondary PFC responses to dextran. Suppression of the secondary response was used here to ascertain whether the initial low level of anti-dextran antibodies elicited in 15-day-old animals was sufficient to lead to inhibition of the secondary response. The approach confirmed the initiation of anti-dextran production at 15-21 days of age and indicated that the small amount of anti-dextran antibodies produced at this age was sufficient to induce the mechanism leading to suppression of the secondary response.

摘要

研究了对胸腺非依赖性(TI)抗原α1-6天然右旋糖酐B512的空斑形成细胞(PFC)反应的个体发生发育,以确定何时形成最初少量的抗右旋糖酐抗体。对某些其他TI多糖抗原的显著抗体反应在生命的第一个月出现,而在高反应性小鼠中,对天然右旋糖酐反应的发育明显延迟。结果表明,CBA小鼠在15至21日龄开始产生少量抗右旋糖酐抗体,并且发育持续进行,直至在90日龄达到峰值水平。α1-6天然右旋糖酐系统也是少数几种小鼠模型之一,其中在产生抗右旋糖酐抗体之后形成内源性抗独特型抗体。已经表明,抗独特型抗体负责特异性抑制对右旋糖酐的二次PFC反应。这里使用二次反应的抑制来确定在15日龄动物中引发的初始低水平抗右旋糖酐抗体是否足以导致二次反应的抑制。该方法证实了在15至21日龄开始产生抗右旋糖酐抗体,并表明在这个年龄产生的少量抗右旋糖酐抗体足以诱导导致二次反应抑制的机制。

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