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通过抑制IgE合成延长新生小鼠对同基因IgE的反应性。

Prolongation of the responsiveness of newborn mice to syngeneic IgE by inhibition of IgE synthesis.

作者信息

Haba S, Nisonoff A

机构信息

Rosenstiel Research Center and Department of Biology, Brandeis University, Waltham, MA 02254, USA.

出版信息

Immunol Lett. 1995 Sep;47(3):205-8. doi: 10.1016/0165-2478(95)00087-3.

Abstract

Between the ages of 2 to approximately 11 days mice respond to a challenge with syngeneic IgE by producing anti-IgE antibodies; by the age of 2 weeks they are unresponsive. Even adult mice, however, produce high titers of anti-IgE antibodies when immunized with a conjugate of syngeneic IgE and a foreign antigen such as keyhole limpet hemocyanin (KLH), indicating that adult tolerance to unconjugated IgE resides in the T-cell compartment. The loss of responsiveness in 2-week-old mice follows closely after the first appearance of IgE-secreting cells and detectable serum IgE. This suggests that the delayed onset of tolerance is attributable to the delay in synthesis of IgE. Data presented here provide support for this hypothesis. A further delay in the initial synthesis of IgE, induced by neonatal administration of anti-IgM antibodies, caused a corresponding extension of the period after birth during which mice remain responsive to unconjugated IgE.

摘要

在2至大约11日龄之间,小鼠对同基因IgE的刺激会产生抗IgE抗体;到2周龄时,它们就不再有反应。然而,即使是成年小鼠,在用同基因IgE与钥孔戚血蓝蛋白(KLH)等外来抗原的偶联物免疫时,也会产生高滴度的抗IgE抗体,这表明成年小鼠对未偶联IgE的耐受性存在于T细胞区室。2周龄小鼠反应性的丧失紧跟在分泌IgE的细胞首次出现和可检测到血清IgE之后。这表明耐受性延迟出现是由于IgE合成延迟所致。本文提供的数据支持这一假说。新生小鼠注射抗IgM抗体导致IgE初始合成进一步延迟,相应地延长了出生后小鼠对未偶联IgE仍有反应的时期。

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