Asherson G L, Zembala M, Barnes R M
Clin Exp Immunol. 1971 Jul;9(1):111-21.
Mice were rendered specifically unresponsive to picryl chloride by pretreatment with picryl sulphonic acid. These mice fail to develop contact sensitivity, as judged by increment of ear thickness, when subsequently sensitized on the abdomen and challenged 6 days later with picryl chloride on the ear. These mice were not in a pure state of classical immune tolerance. This was shown in two ways. (1) Cells from unresponsive donors were injected intravenously into normal CBA mice. The mice were then sensitized on the same day and challenged 6 days later. Unresponsive' (but not a variety of control) lymph node cells impaired the development of contact sensitivity to picryl chloride. The impairment was immunologically specific and unresponsive' cells did not impair the development of contact sensitivity to oxazolone'. (2) Unresponsive mice were irradiated and restored with unresponsive' bone marrow cells. They regained immune competence to picryl chloride when injected with normal lymph node cells and sensitized on the same day, and failed to regain competence when injected with unresponsive lymph node cells. The distinctive finding was that the injection of a mixture of normal and unresponsive lymph node cells failed to restore immune competence. Similar results were obtained when irradiated but otherwise normal recipients were used. Unresponsive cells also impaired the passive (adoptive) transfer of contact sensitivity. These results show that lymph node cells from mice which are unresponsive to picryl chloride actively and specifically impair the induction or manifestation of contact sensitivity to picryl chloride. It was concluded that this form of unresponsiveness is not classical tolerance and the hypothesis is put forward that the unresponsiveness is due at least in part to antibody mediated depression of contact sensitivity.
用苦味磺酸预处理使小鼠对苦味酰氯产生特异性无反应性。当随后在腹部致敏并在6天后用苦味酰氯刺激耳部时，这些小鼠未能产生接触敏感性，这可通过耳部厚度增加来判断。这些小鼠并非处于经典免疫耐受的纯态。这通过两种方式得以证明。（1）将来自无反应供体的细胞静脉注射到正常CBA小鼠体内。然后在同一天使小鼠致敏，并在6天后进行刺激。“无反应”（而非多种对照）淋巴结细胞损害了对苦味酰氯接触敏感性的发展。这种损害具有免疫特异性，“无反应”细胞并未损害对“恶唑酮”接触敏感性的发展。（2）对无反应小鼠进行照射并用“无反应”骨髓细胞进行恢复。当注射正常淋巴结细胞并在同一天致敏时，它们恢复了对苦味酰氯的免疫能力，而当注射无反应淋巴结细胞时则未能恢复免疫能力。独特的发现是，注射正常和无反应淋巴结细胞的混合物未能恢复免疫能力。当使用经过照射但其他方面正常的受体时，也获得了类似的结果。无反应细胞还损害了接触敏感性的被动（过继性）转移。这些结果表明，对苦味酰氯无反应的小鼠的淋巴结细胞积极且特异性地损害了对苦味酰氯接触敏感性的诱导或表现。得出的结论是，这种无反应形式并非经典耐受，并提出了这样的假设，即这种无反应至少部分是由于抗体介导的接触敏感性抑制所致。
