抗人过敏毒素C5a的拮抗肽
Antagonistic peptides against human anaphylatoxin C5a.
作者信息
Kaneko Y, Okada N, Baranyi L, Azuma T, Okada H
机构信息
Department of Molecular Biology, Nagoya City University School of Medicine, Japan.
出版信息
Immunology. 1995 Sep;86(1):149-54.
Multivalent synthetic peptides derived from C5a were prepared in order to examine their effects on the C5a receptor (C5aR). Multiple antigen peptide (MAP) of the C5a C-terminal region (MAP61-74) bound to cells expressing C5aR with high affinity. On the other hand, N-terminal peptides (MAP3-16 and MAP12-26) and one with a sequence from the mid-portion of C5a (MAP37-53) did not bind to the cells. In addition, MAP61-74 inhibited Ca2+ mobilization and release of beta-hexosaminidase by C5a from dibutyryl cAMP-activated U937 cells. This Ca2+ mobilization was also inhibited by MAP12-26 and Mono61-74, the monomeric C-terminal peptide. Taken together, these data indicate that C5a binds to the C5aR via its C-terminal region. Furthermore, MAP61-74, a 14mer peptide that has additional amino acids at the N-terminal compared with the C-terminal octapaptide, can bind to C5aR and can be considered an antagonist of C5a which may prove useful as an agent for controlling the allergic response caused by complement activation.
为了研究源自C5a的多价合成肽对C5a受体（C5aR）的作用，制备了这些肽。C5a C末端区域的多抗原肽（MAP）（MAP61 - 74）以高亲和力与表达C5aR的细胞结合。另一方面，N末端肽（MAP3 - 16和MAP12 - 26）以及一个具有C5a中部序列的肽（MAP37 - 53）不与细胞结合。此外，MAP61 - 74抑制了C5a从二丁酰环磷腺苷激活的U937细胞中引起的Ca2+动员和β - 己糖胺酶释放。这种Ca2+动员也被MAP12 - 26和单体C末端肽Mono61 - 74抑制。综上所述，这些数据表明C5a通过其C末端区域与C5aR结合。此外，与C末端八肽相比，在N末端具有额外氨基酸的14聚体肽MAP61 - 74可以与C5aR结合，并且可以被认为是C5a的拮抗剂，这可能被证明是一种用于控制补体激活引起的过敏反应的有用药物。
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