Ponzio N M, Speirs R S
Immunology. 1975 Feb;28(2):243-51.
Spleens from mice primed with tetanus toxoid 30 days earlier contain memory cells capable of adoptively transferring secondary type cell-mediated (eosinophil) and humoral (antitoxin) responses to irradiated, reconstituted recipients. Spleen cells derived from 10-day-primed donors, on the other hand, possess the capacity after transfer to elicit secondary type eosinophil responses, but not anamnestic antitoxin responses. Treatment of 30-day-primed cells with anti-theta serum and C' prevented transfer of memory for both responses, whereas similar treatment with rabbit anti-mouse IgG (RAM-IgG) serum and C' only inhibited transfer of memory for the antitoxin response. Addition of non-primed spleen cells to antisera-treated primed cells failed to restore secondary type responses. Recombination of 30-day-primed anti-theta and RAM-IgG-treated cells re-established the capacity to transfer these responses. To determine whether the same T cells which mediate the eosiniphil response also act as helper cells in antitoxin production, antisera treated 10- and 30-day-primed cells were combined prior to transfer. Ten-day-primed T cells induced eisoniphil responses and also co-operated with 30-day-primed B cells to produce antitoxin. In contrast, 30-day-primed T cells elicited eisinophil responses, but were unable to induce antitoxin production when combined with anti-theta-treated 10-day-primed cells. These results indicate that B memory cells are not present in the spleens of the donor mice 10 days after priming, but T memory cells are present. It is concluded that primed T cells mediated both eosinophil and antitoxin responses, while B memory cells are involved only with antitoxin production. Following subcutaneous priming T memory cells are present in the spleen prior to B memory cells, and T memory cells which mediate the eosinophil response at 10 days after priming also augment the production of antitoxin by B memory cells.
30天前用破伤风类毒素致敏的小鼠脾脏中含有记忆细胞，这些记忆细胞能够将二次细胞介导（嗜酸性粒细胞）和体液（抗毒素）反应过继性转移给经辐射、重建的受体。另一方面，来自10天前致敏供体的脾细胞在转移后具有引发二次嗜酸性粒细胞反应的能力，但没有回忆性抗毒素反应。用抗θ血清和补体处理30天前致敏的细胞可阻止两种反应的记忆转移，而用兔抗小鼠IgG（RAM-IgG）血清和补体进行类似处理仅抑制抗毒素反应的记忆转移。将未致敏的脾细胞添加到经抗血清处理的致敏细胞中不能恢复二次反应。将30天前致敏的抗θ和RAM-IgG处理的细胞重组可重新建立转移这些反应的能力。为了确定介导嗜酸性粒细胞反应的相同T细胞是否也作为抗毒素产生中的辅助细胞，在转移前将经抗血清处理的10天和30天前致敏的细胞合并。10天前致敏的T细胞诱导嗜酸性粒细胞反应，并与30天前致敏的B细胞合作产生抗毒素。相反，30天前致敏的T细胞引发嗜酸性粒细胞反应，但与经抗θ处理的10天前致敏的细胞合并时无法诱导抗毒素产生。这些结果表明，在致敏10天后供体小鼠的脾脏中不存在B记忆细胞，但存在T记忆细胞。得出的结论是，致敏的T细胞介导嗜酸性粒细胞和抗毒素反应，而B记忆细胞仅参与抗毒素产生。皮下致敏后，T记忆细胞在B记忆细胞之前出现在脾脏中，并且在致敏10天后介导嗜酸性粒细胞反应的T记忆细胞也增强了B记忆细胞的抗毒素产生。
