Okuda K, Nagaoka S, Katoh K, Matsunaga K, Ishigatubo Y, Minami M, Tani K
Immunology. 1984 Nov;53(3):553-61.
The suppressor T cell (Ts) function of old NZW, NZB, C57BL/6 and (NZB X NZW) F1 [B/W)F1), mice to the 2,4-dinitro-1-fluorobenzene (DNFB) hapten was studied. Intravenous administration of dinitrophenyl (DNP) coupled syngeneic lymphoid cells (which normally induce DNP specific suppression) did not result in suppression of DNFB-specific contact hypersensitivity (CS) responses in old NZB or (B/W) F1 mice. Nevertheless, when spleen cells from these old mice were injected into young mice (either (B/W)F1 or A/Sn), strong suppression of the induction phase of CS responses was observed. In addition, effector phase suppressor activity was also observed when splenic cells from tolerized old (B/W) F1 donors were transferred into young (B/W)F1 mice during the effector phase of the CS response. In both cases, the significant cells in the transfer were I-J+ T cells. Thus, the old mice retained functional Ts1 and Ts2 suppressor cells. However, the suppressive activity of the old mice could be reconstituted with spleen cells from primed young mice, suggesting that they have a defect in the Ts3 subset. This was further supported by the finding that the significant cells from the primed young mice were I-J positive and cyclophosphamide-sensitive.
研究了老年新西兰白兔(NZW)、新西兰黑兔(NZB)、C57BL/6 及(NZB×NZW)F1 [B/W)F1]小鼠对 2,4 -二硝基 -1 -氟苯(DNFB)半抗原的抑制性 T 细胞(Ts)功能。静脉注射二硝基苯基(DNP)偶联的同基因淋巴细胞(通常可诱导 DNP 特异性抑制)并未导致老年 NZB 或(B/W)F1 小鼠中 DNFB 特异性接触超敏反应(CS)的抑制。然而,当将这些老年小鼠的脾细胞注射到年轻小鼠((B/W)F1 或 A/Sn)中时,观察到 CS 反应诱导期受到强烈抑制。此外,当在 CS 反应的效应期将来自耐受的老年(B/W)F1 供体的脾细胞转移到年轻(B/W)F1 小鼠中时,也观察到了效应期抑制活性。在这两种情况下,转移中的重要细胞均为 I-J + T 细胞。因此,老年小鼠保留了功能性 Ts1 和 Ts2 抑制细胞。然而,老年小鼠的抑制活性可用来自致敏年轻小鼠的脾细胞重建,这表明它们在 Ts3 亚群中存在缺陷。致敏年轻小鼠的重要细胞为 I-J 阳性且对环磷酰胺敏感这一发现进一步支持了这一点。