Pierce S K, Klinman N R
J Exp Med. 1975 Nov 1;142(5):1165-79. doi: 10.1084/jem.142.5.1165.
The ability of T cells to enhance the response of syngeneic and allogeneic B cells to thymus-dependent hapten-carrier conjugates was analyzed. This analysis was carried out on individual primary B cells in splenic fragment cultures derived from irradiated reconstituted mice. This system has several advantages: (a) the response of the B cells is entirely dependent on carrier priming of the irradiated recipient; (b) this B-cell response can be quantitated in terms of the number of responding cells; and (c) very small B-cell responses can be readily detected and analyzed. The results indicate that the majority of hapten-specific B cells were stimulated in allogeneic and syngeneic recipients only if these recipients were previously carrier primed. The number of B cells responding in carrier-primed allogeneic recipients was 60-70% of that in syngeneic carrier-primed recipients. The antibody-forming cell clones resulting from B cells stimulated in the allogeneic environment produced small amounts of antibody and antibody solely of the IgM immunoglobulin class, while the larger responses in syngeneic recipients were predominantly IgG1 or IgM plus IgG1. The capacity of collaborative interactions between carrier-primed T cells and primary B cells to yield IgG1 antibody-producing clones was shown to be dependent on syngeny between these cells in the H-2 gene complex. It is concluded that: (a) B cells can be triggered by T-dependent antigens to clone formation through collaboration with T cells which differ at the H-2 complex as long as these T cells recognize the antigen; (b) the immunoglobulin class produced by the progeny of stimulated B cells generally depends on the nature of the stimulatory event rather than the nature of the B cell itself; and (c) stimulation to IgG1 production is dependent on syngeny between the collaborating T and B cells probably within the Ir-1A region. The role of the Ia antigens in the formation of IgG1-producing clones is not yet clear; Ia identity could permit IgG1 production or, conversely, nonidentity of Ia could induce all allogeneic interactions which prohibit IgG1 production.
分析了T细胞增强同基因和异基因B细胞对胸腺依赖性半抗原-载体偶联物反应的能力。该分析是在来自经辐照后重建小鼠的脾片段培养物中的单个原代B细胞上进行的。该系统有几个优点：(a) B细胞的反应完全依赖于经辐照受体的载体致敏；(b) 这种B细胞反应可以根据反应细胞的数量进行定量；(c) 非常小的B细胞反应可以很容易地检测和分析。结果表明，只有在这些受体预先接受载体致敏的情况下，大多数半抗原特异性B细胞才会在异基因和同基因受体中受到刺激。在载体致敏的异基因受体中反应的B细胞数量是同基因载体致敏受体中的60%-70%。在异基因环境中受刺激的B细胞产生的抗体形成细胞克隆产生少量抗体，且仅产生IgM免疫球蛋白类的抗体，而同基因受体中较大的反应主要是IgG1或IgM加IgG1。结果表明，载体致敏的T细胞与原代B细胞之间协同相互作用产生IgG1抗体产生克隆的能力取决于H-2基因复合体中这些细胞之间的同基因性。得出以下结论：(a) B细胞可以被T依赖性抗原触发，通过与在H-2复合体上不同的T细胞协作形成克隆，只要这些T细胞识别该抗原；(b) 受刺激B细胞后代产生的免疫球蛋白类别通常取决于刺激事件的性质，而不是B细胞本身的性质；(c) 对IgG1产生的刺激取决于协作的T细胞和B细胞之间可能在Ir-1A区域内的同基因性。Ia抗原在产生IgG1的克隆形成中的作用尚不清楚；Ia的一致性可能允许产生IgG1，或者相反，Ia的不一致可能引发所有禁止产生IgG1的异基因相互作用。
