Finkelman F D, Mond J J, Metcalf E S
J Immunol. 1983 Aug;131(2):593-600.
Lymphocytes that bear surface (s) IgD make up the majority of B cells in mature mice and are the precursors of most antibody secreting cells in primary immune responses made by these mice. In order to study the functional capabilities of the minority sIgD- B lymphocyte population and to gain insight into the possible roles of sIgD, we attempted to abort the development of sigD+ B cells and to expand the sigM+IgD- B cell population by treating mice from birth with affinity-purified rabbit antibodies specific for mouse IgD (RaM delta). RaM delta-suppressed mice had no detectable sIgD+ spleen, lymph node, or bone marrow cells and, on average, only 20% as many sIgM+Ia+ splenic B cells as control mice but had normal numbers of splenic T cells. Lymph nodes from anti-delta suppressed mice were even more depleted of B cells than were spleens from these mice, whereas the percentage of bone marrow B cells in these mice was relatively normal. Germinal centers of anti-delta suppressed mice were fairly normal in appearance, whereas follicular mantle layers, the locus of most sIgD+ B cells in normal mice, were greatly depleted. In addition to their lack of sIgD, splenic B cells of anti-delta suppressed mice differed from those found in control mice in that they bore, on average, twice as much sIgM as control cells, and in that they included an increased percentage of large, DNA synthesizing cells as compared with spleen cells from control mice. However, most sIgM+IgD- splenic B cells from anti-delta suppressed mice were small, nonproliferating cells. B cells from anti-delta suppressed mice insert little or no sIgD into their cell membranes since they continued to bear no detectable sIgD 2 days after in vivo neutralization of RaM delta and since, unlike B cells from control mice, they failed to be activated by a single in vitro injection of a goat anti-mouse delta antibody. Despite their lack of sIgD+ B cells, anti-delta suppressed mice had relatively normal levels of serum IgG as well as normal to increased levels of serum IgM. Thus, sIgM+IgD- B cells appear to have the potential of differentiating into Ig secreting cells in vivo without acquiring sIgD.
带有表面（s）IgD的淋巴细胞构成了成熟小鼠中B细胞的大部分，并且是这些小鼠在初次免疫反应中大多数抗体分泌细胞的前体。为了研究少数sIgD - B淋巴细胞群体的功能能力，并深入了解sIgD的可能作用，我们试图通过用对小鼠IgD特异的亲和纯化兔抗体（RaMδ）从出生起就处理小鼠，来阻断sIgD + B细胞的发育并扩大sIgM + IgD - B细胞群体。经RaMδ抑制的小鼠没有可检测到的sIgD + 脾细胞、淋巴结细胞或骨髓细胞，并且平均而言，其脾脏中sIgM + Ia + B细胞数量仅为对照小鼠的20%，但其脾脏T细胞数量正常。抗δ抑制小鼠的淋巴结中B细胞比其脾脏中的B细胞耗竭得更严重，而这些小鼠骨髓B细胞的百分比相对正常。抗δ抑制小鼠的生发中心外观相当正常，而滤泡套层（正常小鼠中大多数sIgD + B细胞的所在部位）则大量耗竭。除了缺乏sIgD外，抗δ抑制小鼠的脾脏B细胞与对照小鼠的脾脏B细胞不同之处在于，它们平均携带的sIgM是对照细胞的两倍，并且与对照小鼠的脾细胞相比，它们中进行DNA合成的大细胞百分比增加。然而，来自抗δ抑制小鼠的大多数sIgM + IgD - 脾脏B细胞是小的、不增殖的细胞。来自抗δ抑制小鼠的B细胞在其细胞膜上几乎不插入或不插入sIgD，因为在体内中和RaMδ后2天它们仍然没有可检测到的sIgD，并且与对照小鼠的B细胞不同，它们不能被单次体外注射山羊抗小鼠δ抗体激活。尽管缺乏sIgD + B细胞，抗δ抑制小鼠的血清IgG水平相对正常，血清IgM水平正常或升高。因此，sIgM + IgD - B细胞似乎有在体内分化为Ig分泌细胞而无需获得sIgD的潜力。
