McIntosh K R, Segre M, Segre D
Immunopharmacology. 1979 Mar;1(2):165-73. doi: 10.1016/0162-3109(79)90052-3.
Spleen cells obtained from mice injected with cyclophosphamide (200 mg/kg body weight) suppressed the secondary IgG antibody response of memory cells to a T-dependent antigen, DNP-HGG, in Millipore diffusion chambers. Significant suppression (greater than 50%) was found from 5 to 14 days following cyclophosphamide treatment, with peak suppression (86%) on day 7. The primary IgM antibody response to DNP-Ficoll, a T-independent antigen, was not suppressed by these cells. In contrast, suppression was observed in the primary IgM response to sheep red blood cells, a T-dependent antigen. In addition, treatment of the suppressor cell population with anti-Thy-1 serum and complement did not inhibit suppressor activity. We concluded that the suppressor activity was not attributable to a typical T cell, and that the target of suppression was not a B cell. Preliminary evidence suggests that the suppressor activity is regulated, directly or indirectly, by a T cell.
从注射环磷酰胺（200毫克/千克体重）的小鼠中获取的脾细胞，在微孔扩散小室中抑制了记忆细胞对T细胞依赖性抗原DNP-HGG的二次IgG抗体应答。在环磷酰胺处理后的第5至14天发现显著抑制（大于50%），第7天抑制达到峰值（86%）。对T细胞非依赖性抗原DNP-Ficoll的初次IgM抗体应答未被这些细胞抑制。相反，对T细胞依赖性抗原绵羊红细胞的初次IgM应答出现了抑制。此外，用抗Thy-1血清和补体处理抑制性细胞群体并未抑制抑制活性。我们得出结论，抑制活性并非归因于典型的T细胞，且抑制靶点不是B细胞。初步证据表明，抑制活性直接或间接受T细胞调节。
