McCartney-Francis N, Mandy W J
J Immunol. 1981 Jul;127(1):352-7.
Serologic and chemical studies have suggested that immunoglobulin structural genes are under nonallelic genetic control. The transient appearance of unexpected (i.e., latent) allotypes in serum further suggests that cellular control mechanisms may be operative. We report here the results of our efforts to induce the expression of latent allotypes by cultured rabbit splenocytes. The protein A plaque assay facilitated with various anti-allotypic antisera was used to enumerate allotype-specific plaque-forming cells. When splenocytes from a b4 b4 rabbit are cultured in the presence of anti-b4 alloantisera, the number of b4 PFC (i.e., nominal) is suppressed and the number of PFC expressing the latent allotype is increased. The specificity of the induced latent PFC is dependent upon the source and allotypic mosaic of the antiserum added to the cultures. Our results suggest that lymphocytes committed to latent allotypes are normally suppressed. Activation by the appropriate alloantiserum directed against the nominal allotype may relieve a cell-mediated suppressive mechanism.
血清学和化学研究表明,免疫球蛋白结构基因受非等位基因的遗传控制。血清中意外(即潜在)同种异型的短暂出现进一步表明细胞控制机制可能起作用。我们在此报告通过培养兔脾细胞诱导潜在同种异型表达的研究结果。用各种抗同种异型抗血清辅助的蛋白A空斑试验来计数同种异型特异性空斑形成细胞。当b4b4兔的脾细胞在抗b4同种异型抗血清存在下培养时,b4空斑形成细胞(即标称的)数量受到抑制,而表达潜在同种异型的空斑形成细胞数量增加。诱导的潜在空斑形成细胞的特异性取决于添加到培养物中的抗血清的来源和同种异型镶嵌情况。我们的结果表明,携带潜在同种异型的淋巴细胞通常受到抑制。针对标称同种异型的适当同种异型抗血清的激活可能会解除细胞介导的抑制机制。