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Impairment of T-cell-dependent B-cell responses and B-1 cell development in CD19-deficient mice.

机译:CD19缺陷小鼠中T细胞依赖性B细胞应答和B-1细胞发育的损害。

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摘要

CD19 is the hallmark differentiation antigen of the B lineage. Its early expression has implicated a role for CD19 during the antigen-independent phases of B-cell development, whereas in mature B cells CD19 can act synergistically with surface immunoglobulin to induce activation. We have generated CD19-deficient mice and found that development of conventional B cells is unperturbed. However, mature CD19-/- B cells show a profound deficiency in responding to protein antigens that require T-cell help. This is accompanied by a lack of germinal centre formation and affinity maturation of serum antibodies. Thus CD19 is crucial for both initial B-cell activation by T-cell-dependent antigens and the maturation and/or selection of the activated cells into the memory compartment. An impairment in ligand-driven selection may also be responsible for the observation of a striking reduction in the B-1 (formerly Ly-1) B-cell subset, thought to develop under the control of self-antigens and bacterial antigens (reviewed in ref. 2).
机译:CD19是B谱系的标志性分化抗原。它的早期表达与CD19在B细胞发育的抗原非依赖性阶段有关,而在成熟的B细胞中,CD19可与表面免疫球蛋白协同作用以诱导活化。我们已经产生了CD19缺陷型小鼠,并发现常规B细胞的发育不受干扰。但是,成熟的CD19-/-B细胞在对需要T细胞帮助的蛋白质抗原的应答中显示出严重的缺陷。这伴随着生发中心形成的缺乏和血清抗体的亲和力成熟。因此,CD19对于通过T细胞依赖性抗原的初始B细胞活化以及活化细胞成熟和/或选择进入记忆区室都是至关重要的。配体驱动选择的损害也可能是观察到B-1(以前为Ly-1)B细胞亚群显着减少的原因,据认为这是在自身抗原和细菌抗原的控制下发展的。参考2)。

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