在T细胞缺失的A/J小鼠抗偶氮苯砷酸盐反应中诱导独特型抑制。
Induction of idiotope suppression in the anti-azophenylarsonate response of T-depleted A/J mice.
作者信息
Rothstein T L, Miller R A, Parker D J, Kelly E, Vastola A P, Marshak-Rothstein A
出版信息
J Exp Med. 1984 Apr 1;159(4):1283-8. doi: 10.1084/jem.159.4.1283.
Abstract
The homologous, monoclonal antiidiotope, MB, induced idiotope suppression that was remarkably stable and could be transferred by B lymphocytes. Marked depletion of T cell function, confirmed by limiting diluting analysis, did not affect the ability of MB to suppress the corresponding idiotope. Suppression induced by MB appears to result from direct interaction with idiotope-positive B cells, without the intervention of idiotope-specific T suppressor cells.
摘要
同源单克隆抗独特型抗体MB可诱导独特型抑制，这种抑制作用非常稳定，且能由B淋巴细胞传递。通过有限稀释分析证实的T细胞功能显著耗竭，并不影响MB抑制相应独特型的能力。MB诱导的抑制作用似乎是由于与独特型阳性B细胞直接相互作用，而无需独特型特异性T抑制细胞的干预。
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Control idiotope expression by monoclonal anti-idiotope antibodies.通过单克隆抗独特型抗体控制独特型表位表达。
Immunol Rev. 1980;52:75-88. doi: 10.1111/j.1600-065x.1980.tb00331.x.
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