McCoy K L, Baker P J, Stashak P W, Chused T M
J Immunol. 1985 Oct;135(4):2438-42.
Treatment of normal mice with a subimmunogenic dose of type III pneumococcal polysaccharide (SSS-III) results in the development of an antigen-specific state of unresponsiveness termed low-dose paralysis. This unresponsiveness is mediated by T suppressor cells and can be transferred by Lyt-2+ T cells, but not by L3T4+ T cells, obtained 18 hr after priming. As autoimmune New Zealand Black (NZB) mice age, there is a progressive decrease in low-dose paralysis to SSS-III. The defect in older NZB mice resulting in decreased suppressive activity was investigated by transferring primed Lyt-2+ T cells from young into old mice, and vice versa. Enlarged Lyt-2+ T cells from old NZB mice could not suppress the SSS-III response of young recipients. However, Lyt-2+ T cells of normal cell size were efficient in inhibiting the antibody response upon transfer. Primed Lyt-2+ T cells from young NZB mice did not affect the response of old recipients, but effectively suppressed the response of young mice. These results suggest that there are two defects involved in the decline of low-dose paralysis to SSS-III in aging NZB mice: Enlarged Lyt-2+ T cells may lose their ability to function as mediators of suppression; and B cells may become resistant to T cell-mediated suppression.
用亚免疫原剂量的III型肺炎球菌多糖（SSS-III）处理正常小鼠，会导致一种称为低剂量麻痹的抗原特异性无反应状态的发展。这种无反应性由T抑制细胞介导，并且可由致敏18小时后获得的Lyt-2⁺ T细胞传递，但不能由L3T4⁺ T细胞传递。随着自身免疫性新西兰黑（NZB）小鼠年龄增长，对SSS-III的低剂量麻痹会逐渐降低。通过将年轻小鼠致敏的Lyt-2⁺ T细胞转移到老年小鼠中，反之亦然，来研究老年NZB小鼠中导致抑制活性降低的缺陷。来自老年NZB小鼠的肿大Lyt-2⁺ T细胞不能抑制年轻受体对SSS-III的反应。然而，正常细胞大小的Lyt-2⁺ T细胞在转移后能有效抑制抗体反应。来自年轻NZB小鼠的致敏Lyt-2⁺ T细胞不影响老年受体的反应，但能有效抑制年轻小鼠的反应。这些结果表明，衰老的NZB小鼠对SSS-III低剂量麻痹下降涉及两个缺陷：肿大的Lyt-2⁺ T细胞可能失去作为抑制介质发挥功能的能力；并且B细胞可能对T细胞介导的抑制产生抗性。
