REGULATORY ROLE OF A TRIPEPTIDE (TKP) FROM THE 2ND CONSTANT DOMAIN OF IMMUNOGLOBULIN-G .1. INHIBITION OF RAT AND HUMAN MACROPHAGE ACTIVITIES
REGULATORY ROLE OF A TRIPEPTIDE (TKP) FROM THE 2ND CONSTANT DOMAIN OF IMMUNOGLOBULIN-G .1. INHIBITION OF RAT AND HUMAN MACROPHAGE ACTIVITIES
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DOI：
10.1016/0192-0561(85)90011-6
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发表时间：
1985-01-01
期刊：
影响因子：
--
通讯作者：
CAPRON, A
中科院分区：
文献类型：
--
作者：
AURIAULT, C;JOSEPH, M;CAPRON, A
由寄生虫[血吸虫]蛋白酶切割IgG后释放的肽是巨噬细胞效应子功能对寄生虫幼虫的强抑制剂。一个单一的三肽组，Thr-Lys-Pro（TKP），抑制各种巨噬细胞的功能，可以被认为是一种免疫活性肽。不仅IgE依赖性细胞毒性，而且β-当大鼠巨噬细胞预先与TKP或一些类似物孵育时，葡萄糖醛酸酶释放、化学发光和IL [白细胞介素]产生减少。TKP处理后，大鼠和人巨噬细胞的趋化性和IgE特异性受体表达受到抑制，但不影响细胞活力。Thr的取代或乙酰化减弱或抑制了TKP的抑制作用。
Peptides released after the cleavage of IgG by parasite [Schistosoma] proteinases are strong inhibitors of the macrophage effector functions against schistosome larvae. A single tripeptide set, Thr-Lys-Pro (TKP), inhibits various macrophage functions and can be considered as an immunologically active peptide. Not only IgE-dependent cytotoxicity but also .beta.-glucuronidase release, chemiluminescence and IL [interleukin] production were reduced when rat macrophages were previously incubated with TKP or some analogs. Chemotaxis and IgE-specific receptor expression were inhibited in rat and human macrophages after treatment with TKP, without affecting the cell viability. The substitution or acetylation of Thr diminished or suppressed the inhibitory effect of TKP.