Morgan E L, Thoman M L, Hoeprich P D, Hugli T E
Immunol Lett. 1985;9(4):207-13. doi: 10.1016/0165-2478(85)90034-3.
Several fragments derived from complement components have been identified as potent effector substances in in vitro assays that measure cell proliferation and antibody synthesis. The anaphylatoxin C3a suppresses the immune response but fails to influence T- or B-cell proliferation. The factor C5a augments both antibody production and antigen-induced, but not mitogen-induced, T-cell proliferation. C3a-mediated suppression occurs through the activation of a suppressor T-cell cascade with macrophage collaboration. C5a-mediated enhancement, depending upon the in vitro system studied, acts at the level of the helper T cell and/or macrophage. A fragment generated from treating iC3b with kallikrein (c3d-K) has aided in defining a structural region of the C3b molecule that can influence the level of circulating leukocytes. The factor C3d-K is also capable of suppressing both specific and non-specific T-cell proliferative responses and mitogen-induced B cell growth. The mechanism of C3d-K action is defined as a direct effect on "activated" T cells, even though IL-2 synthesis of treated cells is diminished. The effect of C3d-K is long lasting, non-reversible and requires only a short exposure to the target cell.
在测量细胞增殖和抗体合成的体外试验中，已鉴定出几种源自补体成分的片段是有效的效应物质。过敏毒素C3a可抑制免疫反应，但不影响T细胞或B细胞增殖。因子C5a可增强抗体产生以及抗原诱导的（而非丝裂原诱导的）T细胞增殖。C3a介导的抑制作用是通过激活具有巨噬细胞协作的抑制性T细胞级联反应来实现的。取决于所研究的体外系统，C5a介导的增强作用作用于辅助性T细胞和/或巨噬细胞水平。用激肽释放酶处理iC3b产生的一个片段（C3d-K）有助于确定C3b分子中可影响循环白细胞水平的一个结构区域。因子C3d-K也能够抑制特异性和非特异性T细胞增殖反应以及丝裂原诱导的B细胞生长。C3d-K作用的机制被定义为对“活化”T细胞的直接作用，尽管处理过的细胞的白细胞介素-2合成减少。C3d-K的作用持久、不可逆，并且只需要与靶细胞短暂接触。
