Le Gros G S, Herbert A G, Watson J D
Immunology. 1984 Jan;51(1):103-13.
Treatment of mice with ascitic fluid containing high titres of T24-31.7 monoclonal antibody (rat anti-mouse Thy-1) lead to a rapid loss of T cells from peripheral lymphoid organs. Spleen and lymph node tissue lost all detectable Thy-1+ and mitogen-responsive T cells within 72 hr. These tissues were completely T cell-depleted for more than a week before repopulation with T cells began. Lectin-induced splenic T cell cytoxicity in culture was lost within 72 hr after treatment of mice in vivo. In contrast, treatment of mice with T24-31.7 ascitic fluid was followed by an immediate increase in natural killer (NK) cell-mediated cytolytic activity. After 96 hr, NK activity began to decrease and did not reappear in the T cell-depleted spleens. While purified T24-31.7 antibody was responsible for T cell depletion in vivo, a non-immunoglobulin component of the ascitic fluid stimulated splenic NK cell activity. The presence of phytohaemagglutinin (PHA) on target cells in the lytic assay was shown to inhibit NK activity but enhance T cell-mediated cytotoxicity. The relationship of NK cells and cytotoxic T lymphocytes (CTL) to the T cell lineage is discussed.
用含有高滴度T24 - 31.7单克隆抗体(大鼠抗小鼠Thy - 1)的腹水液处理小鼠,会导致外周淋巴器官中的T细胞迅速减少。脾脏和淋巴结组织在72小时内失去了所有可检测到的Thy - 1⁺和对有丝分裂原反应的T细胞。在开始重新填充T细胞之前,这些组织完全缺乏T细胞超过一周。体内处理小鼠后72小时内,培养中凝集素诱导的脾脏T细胞细胞毒性丧失。相比之下,用T24 - 31.7腹水液处理小鼠后,自然杀伤(NK)细胞介导的细胞溶解活性立即增加。96小时后,NK活性开始下降,并且在T细胞耗竭的脾脏中未再次出现。虽然纯化的T24 - 31.7抗体在体内导致T细胞耗竭,但腹水液中的一种非免疫球蛋白成分刺激了脾脏NK细胞活性。在裂解试验中,靶细胞上植物血凝素(PHA)的存在被证明会抑制NK活性,但增强T细胞介导的细胞毒性。本文讨论了NK细胞和细胞毒性T淋巴细胞(CTL)与T细胞谱系的关系。