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链球菌M蛋白的合成肽片段

Synthetic peptide fragments of streptococcal M proteins.

作者信息

Seyer J M, Dale J B, Beachey E H

出版信息

Dev Biol Stand. 1986;63:101-8.

PMID:2427375
Abstract

The surface M proteins of group A streptococci prevent phagocytosis by the non-immune host but antibodies subsequently developed against these M proteins opsonize the organism to allow phagocytosis and killing. In some cases, antibodies developed against M proteins are cross-reactive with host tissue and have been implicated in rheumatic fever. Peptide fragments of several serotypes, namely type 24, 5 and 6 M proteins were chemically synthesized and tested for their ability to induce protective and tissue cross-reactive antibodies in rabbits. Two synthetic 35 residue peptides of type 24 M protein, S-CB3 and S-CB7 had previously been shown to evoke high ELISA titers as well as opsonic antibody titers in each of three rabbits. Neither contained host tissue cross-reactive antibodies when examined with human heart tissue. Subpeptides of CB7 were synthesized to identify the smallest protective epitope. Three synthetic subpeptides (S-CB7-(13-35), - (18-35) and - (23-35) C were covalently linked to tetanus toxoid and evoked opsonic antibodies in rabbits and thus protective immunity with no tissue cross-reactive epitopes. Synthetic peptides of the NH2-terminal region of peptide M 5, which is known to contain cardiac tissue cross-reactive epitopes, were also tested. When covalently linked to tetanus toxoid, the synthetic peptide S-M 5 (1-20), but not S-M5 (20-40), evoked antibodies which were protective against type 5 streptococci; no heart cross-reactive antibodies were evoked even when large excesses of the synthetic peptides were injected.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

A组链球菌的表面M蛋白可阻止非免疫宿主的吞噬作用,但随后针对这些M蛋白产生的抗体可调理该微生物,使其易于被吞噬和杀灭。在某些情况下,针对M蛋白产生的抗体与宿主组织发生交叉反应,并与风湿热有关。化学合成了几种血清型(即24型、5型和6型M蛋白)的肽片段,并检测了它们在兔体内诱导保护性和组织交叉反应性抗体的能力。先前已证明,24型M蛋白的两种合成的35个氨基酸残基的肽S-CB3和S-CB7,在三只兔中的每只中都能引起高ELISA滴度以及调理抗体滴度。用人心脏组织检测时,两者均不含有宿主组织交叉反应性抗体。合成了CB7的亚肽以鉴定最小的保护性表位。三种合成亚肽(S-CB7-(13-35)、-(18-35)和-(23-35)C)与破伤风类毒素共价连接,并在兔体内诱导体液抗体,从而产生无组织交叉反应性表位的保护性免疫。还检测了已知含有心脏组织交叉反应性表位的肽M 5氨基末端区域的合成肽。当与破伤风类毒素共价连接时,合成肽S-M 5(1-20)可诱导体液抗体,对5型链球菌具有保护作用;即使注射大量过量的合成肽,也不会诱导体液抗体。(摘要截短为250字)

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