Dukor P, Schumann G, Gisler R H, Dierich M, König W, Hadding U, Bitter-Suermann D
J Exp Med. 1974 Feb 1;139(2):337-54. doi: 10.1084/jem.139.2.337.
It has been proposed that two distinct signals are required for the triggering of the precursors of antibody-forming bone marrow-derived cells (B cells): (a) the binding of antigen or of a mitogen to the corresponding receptor sites on B-cell membranes and (b) the interaction of activated C3 with the C3 receptor of B lymphocytes. There is growing evidence that B-cell mitogens and T (thymus-derived cell)-independent antigens are capable of activating the alternate pathway of the complement system (bypass). Therefore, the effect of another potent bypass inducer was investigated with regard to B-cell activation and the role of C3. Purified, pyrogen-free cobra venom factor was mitogenic for both T and B lymphocytes (cortisone-resistant mouse thymus cells and lymph node lymphocytes from congenitally athymic mice). Venom factor could substitute for T cells by restoring the potential of antibody formation to sheep red blood cells in mouse B-cell cultures supplemented with macrophages or 2-mercaptoethanol. Venom factor may be capable of conferring activated C3 to the C3 receptor of B lymphocytes: preincubation of lymphoid cells with homologous serum or plasma, 10 mM EDTA, and sepharose-coupled venom factor converted with serum to an enzyme active against C3, inhibited their capacity to subsequently form rosettes with sheep erythrocytes sensitized with amboceptor and C5-deficient mouse complement. In the absence of EDTA, preincubation of freshly prepared B-cell suspensions with C3-sufficient homologous serum also blocked their subsequent interaction with complement-sensitized erythrocytes and at the same time rendered them reactive to an otherwise T-cell-specific mitogen. Moreover, mitogen induced B-cell proliferation in lymph node (but not in spleen) cell cultures, appeared to depend on the availability of exogenous C3: zymosan-absorbed fetal bovine serum (only 8.3% site-forming units remaining) supported T-cell activation by phytohemagglutinin, concanavalin A, and venom factor, but failed to sustain B-cell stimulation by pokeweed mitogen, lipopolysaccharide, and venom factor. T-cell-dependent antibody formation in composite cultures containing T cells or T-cell-substituting B-cell mitogens, B cells, and macrophages, always required the presence of C3-sufficient serum.
有人提出,触发抗体形成的骨髓来源细胞(B细胞)前体需要两种不同的信号:(a)抗原或有丝分裂原与B细胞膜上相应受体位点的结合,以及(b)活化的C3与B淋巴细胞的C3受体的相互作用。越来越多的证据表明,B细胞有丝分裂原和T(胸腺来源细胞)非依赖性抗原能够激活补体系统的替代途径(旁路)。因此,研究了另一种有效的旁路诱导剂对B细胞活化和C3作用的影响。纯化的、无热原的眼镜蛇毒因子对T和B淋巴细胞(耐可的松的小鼠胸腺细胞和先天性无胸腺小鼠的淋巴结淋巴细胞)都有促有丝分裂作用。在补充有巨噬细胞或2-巯基乙醇的小鼠B细胞培养物中,毒液因子可以通过恢复对绵羊红细胞的抗体形成潜力来替代T细胞。毒液因子可能能够将活化的C3赋予B淋巴细胞的C3受体:用同源血清或血浆、10 mM EDTA和用血清转化为对C3有活性的酶的琼脂糖偶联毒液因子对淋巴细胞进行预孵育,抑制了它们随后与用双价抗体和C5缺陷小鼠补体致敏的绵羊红细胞形成玫瑰花结的能力。在没有EDTA的情况下,用C3充足的同源血清对新鲜制备的B细胞悬液进行预孵育,也阻断了它们随后与补体致敏红细胞的相互作用,同时使它们对另一种原本是T细胞特异性的有丝分裂原产生反应。此外,有丝分裂原诱导的淋巴结(但不是脾脏)细胞培养物中的B细胞增殖似乎取决于外源性C3的可用性:酵母聚糖吸收的胎牛血清(仅剩余8.3%的位点形成单位)支持植物血凝素、刀豆球蛋白A和毒液因子对T细胞的激活,但不能维持商陆有丝分裂原、脂多糖和毒液因子对B细胞的刺激。在含有T细胞或替代T细胞的B细胞有丝分裂原、B细胞和巨噬细胞的复合培养物中,T细胞依赖性抗体形成始终需要C3充足的血清存在。