Bos J D, Hamerlinck F, Cormane R H
Br J Vener Dis. 1980 Apr;56(2):69-73. doi: 10.1136/sti.56.2.69.
The delay in antibody production in response to infection with Treponema pallidum may be caused by a block in the differentiation of antigen-stimulated B (Bursa-dependent) lymphoid cells towards plasma cells. This hypothesis was tested by a study to detect clonal expansion of immunoglobulin-bearing B lymphoid cells by in-vitro immunofluorescence tests in patients with primary syphilis. In addition, antibodies eluted from circulating lymphoid cells were investigated for treponemal binding by the enzyme-linked immunosorbent assay, the T pallidum immobilisation test, and the immunoglobulin class-specific FTA-ABS test. Results indicated that the number of IgG-bearing lymphoid cells were increased in patients with primary syphilis. However, in only a few cases could antitreponemal antibodies be eluted from isolated lymphoid cells. For this reason, the original hypothesis was rejected.
针对梅毒螺旋体感染产生抗体的延迟可能是由于抗原刺激的B（依赖于法氏囊的）淋巴细胞向浆细胞分化受阻所致。通过一项研究对这一假说进行了验证，该研究通过体外免疫荧光试验检测一期梅毒患者中携带免疫球蛋白的B淋巴细胞的克隆扩增。此外，还通过酶联免疫吸附测定、梅毒螺旋体制动试验和免疫球蛋白类别特异性荧光密螺旋体抗体吸收试验，对从循环淋巴细胞中洗脱的抗体进行梅毒螺旋体结合研究。结果表明，一期梅毒患者中携带IgG的淋巴细胞数量增加。然而，仅在少数病例中能从分离的淋巴细胞中洗脱抗梅毒螺旋体抗体。因此，最初的假说被否定。
