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中毒性休克综合征毒素-1上一个具有生物学重要性的表位的定位

Localization of a biologically important epitope on toxic-shock-syndrome toxin-1.

作者信息

Murphy B G, Kreiswirth B N, Novick R P, Schlievert P M

机构信息

Department of Microbiology, University of Minnesota Medical School, Minneapolis 55455-0312.

出版信息

J Infect Dis. 1988 Sep;158(3):549-55. doi: 10.1093/infdis/158.3.549.

Abstract

A monoclonal antibody, designated B-14, inhibits the nonspecific T lymphocyte mitogenicity of toxic-shock-syndrome toxin-1 (TSST-1), and the antibody binds to an internal cyanogen bromide (CNBr) fragment (Mr, 14,000) of the toxin. The epitope recognized by B-14 was further localized to include a decapeptide at the NH2-terminus of the CNBr fragment. The decapeptide inhibited the ELISA and western blot reactivity of B-14 with TSST-1, although it was approximately 10,000-fold less effective than the native toxin. The peptide also inhibited the capacity of B-14 to block TSST-1-induced mitogenicity. A conjugate, consisting of decapeptide4-ovalbumin, was used to hyperimmunize three rabbits. Serum from these rabbits reacted specifically with intact TSST-1 in ELISA and western blots and partially neutralized toxin mitogenicity; however, the serum did not prevent fever and enhancement of susceptibility to endotoxin shock typically seen in rabbits after administration of TSST-1.

摘要

一种名为B - 14的单克隆抗体可抑制中毒性休克综合征毒素-1(TSST - 1)的非特异性T淋巴细胞促有丝分裂活性,且该抗体可与毒素的一个内部溴化氰(CNBr)片段(分子量为14,000)结合。B - 14识别的表位进一步定位至CNBr片段NH2末端的一个十肽。该十肽可抑制B - 14与TSST - 1的ELISA和蛋白质印迹反应性,尽管其效力比天然毒素低约10,000倍。该肽还可抑制B - 14阻断TSST - 1诱导的促有丝分裂活性的能力。由十肽4 - 卵清蛋白组成的偶联物用于对三只兔子进行超免疫。这些兔子的血清在ELISA和蛋白质印迹中与完整的TSST - 1发生特异性反应,并部分中和毒素的促有丝分裂活性;然而,该血清并不能预防TSST - 1给药后兔子中常见的发热和对内毒素休克易感性的增强。

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