Hinchman S M, Battisto J R
J Immunol. 1979 Aug;123(2):688-91.
The B cell-derived soluble factor that has been described as an IgG-recruiting component (GRC) was investigated to: a) ascertain whether it is governed by genetic constraints, b) determine what triggers its synthesis, and c) identify its cellular target. GRC has been shown to be unrestricted by histocompatibility barriers since it enhanced IgG antibody production in mice of diverse genetic backgrounds. Further, we report that eliminating IgG-bearing cells from B cells to be immunized in vitro allows T cells-replacing factor (TRF) to increase the number of IgM but not IgG PFC. Thus, TRF appears to act on IgM-bearing cells by expanding the IgM PFC number. Adding GRC 48 hr after the addition of TRF to such IgG-depleted cells caused expression of IgG PFC. Hence, B cells lacking IgG but possessing IgM surface immunoglobulins appear to be those that are acted upon by GRC. These data indicate that in whole splenic cell populations, GRC is derived from IgG-bearing B cells that are stimulated by antigen and a component in TRF.
一种被描述为IgG募集成分（GRC）的B细胞衍生可溶性因子，被研究用于：a）确定它是否受遗传限制，b）确定触发其合成的因素，以及c）识别其细胞靶点。由于GRC能增强不同遗传背景小鼠的IgG抗体产生，因此已证明它不受组织相容性屏障的限制。此外，我们报告称，在体外对用于免疫的B细胞中去除携带IgG的细胞，会使T细胞替代因子（TRF）增加IgM而非IgG空斑形成细胞（PFC）的数量。因此，TRF似乎通过增加IgM PFC数量作用于携带IgM的细胞。在向此类IgG缺失细胞中添加TRF 48小时后添加GRC，会导致IgG PFC的表达。因此，缺乏IgG但拥有IgM表面免疫球蛋白的B细胞似乎是受GRC作用的细胞。这些数据表明，在整个脾细胞群体中，GRC源自被抗原和TRF中的一种成分刺激的携带IgG的B细胞。
