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小鼠中的抗苯基三甲基氨基免疫。II. L-酪氨酸对偶氮苯基三甲基铵诱导的抑制性T细胞选择性抑制带有交叉反应性独特型的B细胞克隆的表达。

Anti-phenyltrimethylamino immunity in mice. II. L-Tyrosine-p-azophenyltrimethylammonium-induced suppressor T cells selectively inhibit the expression of B-cell clones bearing a cross-reactive idiotype.

作者信息

Alevy Y G, Bellone C J

出版信息

J Exp Med. 1980 Mar 1;151(3):528-41. doi: 10.1084/jem.151.3.528.

Abstract

The anti-phenyltrimethylamino (TMA) response in A/J mice is characterized by a cross-reactive idiotype(s) (CRI) that appears linked to the Ig-Ie allotype. These findings made it attractive to look for a CRI on T cells reactive to the same TMA determinant. Thus a suppressor T-cell (Ts) assay specific for L-tyrosine-p-azophenyltrimethylammonium [tyr(TMA)] was developed. A/J mice were primed with either tyr(TMA) in complete Freund's adjuvant (CFA), L-tyrosine-azobenzenearsonate [tyr(ABA)] in CFA, or with CFA alone. 6 wk later all mice were inoculated with TMA-bovine serum albumin (BSA) in CFA, boosted with soluble TMA-BSA 3 wk later, and plaqued 7 d after the soluble boost. Priming with tyr(TMA) in CFA resulted in 66% suppression of anti-TMA plaque-forming cells (PFC) as compared with control groups primed with tyr(ABA) in CFA or CFA alone. The suppression was shown to be mediated by Ts, as only T cells but not B cells from suppressed animals transfer the suppression in adoptive cell transfer experiments into lethally irradiated recipients. The profile of the anti-TMA PFC in the suppressed and nonsuppressed animals was examined via incorporation of anti-idiotypic sera (specific for CRI-TMA) into the plaquing medium. The results of these experiments indicate that the suppression of the major CRI+-TMA PFC was virtually complete, whereas the CRI--TMA PFC are left intact. When A/J mice were primed with idiotypic antisera (anti-Id) or normal rabbit serum (NRS) rather than with the antigen on CFA alone, and the same protocol was followed thereafter, the anti-Id-inoculated mice were suppressed by 63% when compared with the NRS-primed controls. Again the suppression could be accounted for by the exclusive elimination of CRI+ anti-TMA PFC. The possibility that the antigen-induced idiotype suppression may result from idiotypic restrictions between interacting CRI+-Ts and CRT+-B cells will be discussed.

摘要

A/J小鼠中的抗苯基三甲基氨基(TMA)反应的特征是存在一种与Ig-Ie同种异型相关的交叉反应独特型(CRI)。这些发现使得寻找对相同TMA决定簇有反应的T细胞上的CRI变得很有吸引力。因此,开发了一种针对L-酪氨酸对氨基苯三甲基铵[tyr(TMA)]的抑制性T细胞(Ts)检测方法。用完全弗氏佐剂(CFA)中的tyr(TMA)、CFA中的L-酪氨酸偶氮苯砷酸盐[tyr(ABA)]或仅用CFA对A/J小鼠进行免疫。6周后,所有小鼠在CFA中接种TMA-牛血清白蛋白(BSA),3周后用可溶性TMA-BSA加强免疫,并在可溶性加强免疫7天后进行空斑形成检测。与在CFA中用tyr(ABA)或仅用CFA免疫的对照组相比,在CFA中用tyr(TMA)免疫导致抗TMA空斑形成细胞(PFC)的抑制率为66%。这种抑制作用被证明是由Ts介导的,因为在过继性细胞转移实验中,只有来自受抑制动物的T细胞而不是B细胞能将抑制作用转移到经致死性照射的受体中。通过将抗独特型血清(针对CRI-TMA)加入空斑形成培养基中,检测了受抑制和未受抑制动物中抗TMA PFC的情况。这些实验结果表明,主要的CRI+ -TMA PFC的抑制作用几乎是完全的,而CRI- -TMA PFC则未受影响。当A/J小鼠仅用独特型抗血清(抗-Id)或正常兔血清(NRS)而不是用CFA中的抗原进行免疫,然后遵循相同的方案时,与用NRS免疫的对照组相比,接种抗-Id的小鼠的抑制率为63%。同样,这种抑制作用可以通过CRI+抗TMA PFC的排他性消除来解释。将讨论抗原诱导的独特型抑制可能是由于相互作用的CRI+ -Ts和CRT+ -B细胞之间的独特型限制所导致的可能性。

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