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Unresponsiveness was produced in mice by three feeds of high doses of oxazolone or picryl chloride. The mice were then sensitized and contact sensitivity assessed by ear swelling. Adult thymectomy prevented the unresponsiveness caused by feeding. In some but not all experiments adult thymectomy also increased the response to a single skin paint. This effect of thymectomy was apparent at 1 week and reached a plateau at 2-3 weeks. The effect of adult thymectomy, on unresponsiveness caused by feeding and its ability to increase the contact sensitivity skin reaction, was reversed by treatment with crude thymosin fraction V. [ABSTRACT FROM AUTHOR]

Cyclophosphamide was used to assess the role of suppressor cells in the contact sensitivity reaction. A single painting with 300 μg and 30 μg oxazolone produced poor contact sensitivity reactions (ear swelling). Cyclophosphamide (200 mg/kg) 2 days before painting increased the response to the lower doses but had less effect on the response to 3 mg oxazolone. A single feed with 10 mg oxazolone caused strong contact sensitivity while lower doses (10-1000 μg) caused poor responses. Cyclophosphamide increased the response to the lower doses but not to the highest dose of oxazolone. These results suggested that the poor response to painting and feeding lower doses of oxazolone was due to a suppressor system which was sensitive to cyclophosphamide. A different result was obtained when contact sensitivity was measured by arrival of radioactively labelled cells. Cyclophosphamide had the greatest effect on cell arrival when high doses were fed. This indicates that ear swelling and cell arrival measure separate aspects of the contact sensitivity response. The lower doses of oxazolone, which caused little contact sensitivity, reduced the response to a standard immunizing dose. This low dose unresponsiveness occurred after either painting or feeding (Chase-Sulzberger phenomenon). It did not occur in mice treated with cyclophosphamide before the first exposure to oxazolone. This suggested that the low dose unresponsiveness was due to suppressor cells. The response to oxazolone was also assessed by DNA synthesis in the regional lymph nodes. A small dose of oxazolone (30 μg) caused a peak of DNA synthesis on day four while a high dose (3 mg) caused a peak on day three. Pretreatment with cyclophosphamide depressed the response to 30 μg although it increased contact sensitivity. The secondary response was smaller than the primary on days 3, 4 and 5 after immunization but larger on day two. The depression but not the increase was prevented by cyclophosphamide and was probably due to a suppressor system. [ABSTRACT FROM AUTHOR]

Donor mice were painted on the skin of the abdomen with the contact sensitizing agent, oxazolone. One day later 2-5 × 106 cells from the regional lymph nodes were injected into the footpads of recipient mice. Contact sensitivity was detected 6 days later by challenging the ears of the recipients and measuring the increase of thickness at 24 h. Good contact sensitivity was obtained when CBA cells were injected into CBA mice and BALB/c cells injected into BALB/c mice; the injection of BALB/c (H-2d) cells into CBA (H-2k) mice and vice versa failed to give rise to contact sensitivity. Hybrid F1 cells gave intermediate responses. The contact sensitivity caused by the injection of small numbers of lymph node cells into the footpad is interpreted as a mode of active immunization and the present results show that this only occurs when there is genetic matching at the major histocompatibility complex between the donor and the recipient mouse. [ABSTRACT FROM AUTHOR]

Cells taken from the draining lymph nodes of mice 1 day after painting with picryl chloride can induce contact hypersensitivity when injected into the footpads of normal recipients. Previous studies have presented evidence to show that this is an immunizing process rather than a transfer of sensitized cells. This study shows that footpad injection of 5 × 106 1-day draining lymph node cells induces a similar degree of hypersensitivity to the original skin painting with picryl chloride but no antibody, as judged by anti-TNP splenic PFC and serum antibody, in contrast to the moderate antibody response found after skin painting. The apparent inability to induce a response did, however, correlate with the finding that the draining lymph nodes of mice painted with picryl chloride had few PFC. Some effect of the cells on antibody was noted in that after mice were challenged on the ear to produce contact sensitivity reactions they produced an antibody response larger than that of mice not injected with cells. This was not a large phenomenon but was unusual because 25 × 106 cells was more effective than either 106 or 5 × 106 cells, even though 5 × 106 cells produced the largest contact sensitivity reactions. The augmentation was antigen specific and the same dose-response effect could be obtained with irradiated cells (2000 rad). It is suggested that the ability of these cells to induce large contact sensitivity reactions without antibody indicates that they may have an important role in the immunogenicity of contact sensitizing agents, which can induce large delayed-type hypersensitivity reactions accompanied only by moderate antibody responses. [ABSTRACT FROM AUTHOR]