Abstract
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.
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Selected References
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