Fultz M J, Finkelman F D, Metcalf E S
Eur J Immunol. 1987 Aug;17(8):1137-43. doi: 10.1002/eji.1830170810.
To determine whether the expression of surface IgD (sIgD) influences the extent of the expressed B cell repertoire, the clonal diversity of the B cell population in mice treated chronically with anti-IgD (delta) antibodies has been compared with the B cell repertoire observed in control animals, using the splenic focus limiting dilution B cell assay. The results show that the phosphorylcholine (PC)-specific B cell precursor frequency in anti-delta antibody-treated mice is increased when compared with that of control mice. Isotype and idiotype (T15) analyses of PC clonal products from anti-delta antibody-treated and control mice revealed no distributional differences. Analyses of the 2,4-dinitrophenyl (DNP)- and fluoresein isothiocyanate-specific B cell repertoires confirmed that the equal or increased precursor frequencies observed in anti-delta antibody-treated mice are not specific for the PC antigen. The increased precursor frequency of B cells from anti-delta antibody-treated mice was not the result of increased homing of B cells from anti-delta antibody-treated mice to recipient spleens, since B cells from control mice homed twice as well to recipient spleens as did B cells from anti-delta antibody-treated mice. Other studies demonstrated that (a) on average, antibody-secreting clones were generated more slowly when B cells from anti-delta antibody-treated mice were used as a source of precursors than B cells of control mice and (b) both sIg- spleen cells and sIg+ spleen cells from anti-delta antibody-treated mice generated a higher frequency of specific antibody-secreting clones than did the corresponding populations from control mice. These observations suggest that a population of sIgM+sIgD- B cells exists that resembles sIgD+ B cells rather than neonatal or xid B cells in its ability to generate responses to PC and suggests that the sIgM+sIgD- B cells from anti-delta antibody-treated mice are more responsive than are sIgM+IgD+ B cells, regardless of antigenic specificity, to the stimuli provided in the splenic focus system. Finally, this study suggests that the expression of sIgD does not influence the extent of the expressed B cell repertoire.
为了确定表面IgD（sIgD）的表达是否会影响所表达的B细胞库的范围，利用脾集落极限稀释B细胞检测法，将长期用抗IgD（δ）抗体处理的小鼠B细胞群体的克隆多样性与对照动物中观察到的B细胞库进行了比较。结果显示，与对照小鼠相比，抗δ抗体处理的小鼠中磷酸胆碱（PC）特异性B细胞前体频率增加。对抗δ抗体处理和对照小鼠的PC克隆产物进行的同种型和独特型（T15）分析未发现分布差异。对2,4-二硝基苯基（DNP）和异硫氰酸荧光素特异性B细胞库的分析证实，在抗δ抗体处理的小鼠中观察到的相等或增加的前体频率并非PC抗原所特有。抗δ抗体处理的小鼠B细胞前体频率增加并非抗δ抗体处理的小鼠B细胞归巢至受体脾脏增加的结果，因为对照小鼠的B细胞归巢至受体脾脏的能力是抗δ抗体处理的小鼠B细胞的两倍。其他研究表明：（a）平均而言，当使用抗δ抗体处理的小鼠B细胞作为前体来源时，分泌抗体的克隆产生速度比对照小鼠的B细胞慢；（b）抗δ抗体处理的小鼠的sIg-脾细胞和sIg+脾细胞产生特异性抗体分泌克隆的频率均高于对照小鼠的相应群体。这些观察结果表明，存在一群sIgM+sIgD- B细胞，其在产生对PC的反应能力方面类似于sIgD+ B细胞，而不是新生或xid B细胞，并且表明抗δ抗体处理的小鼠的sIgM+sIgD- B细胞比sIgM+IgD+ B细胞对脾集落系统中提供的刺激更具反应性，无论抗原特异性如何。最后，本研究表明sIgD的表达不影响所表达的B细胞库的范围。
