Antigen-binding T and B lymphocytes in sensitization and unresponsiveness to dinitrochlorobenzene (DNCB) contact sensitivity.
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Biomedical subjects
Publications and source records attributed to L Polak.
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Normal guinea pigs parabiosed for 10 days with guinea pigs tolerant to DNCB-contact sensitivity became completely and permanently unresponsive when sensitized after parabiosis lasting 10 days and partially tolerant when sensitized after parabiosis lasting 2 days. On the other hand, tolerant parabionts became hypersensitive when parabiosed with normal partners which had been sensitized on the day of the operation or before the parabiosis was effected. From these results it is concluded that tolerance to DNCB-contact sensitivity in guinea pigs is a positive phenomenon affecting the afferent branch of the immune response.
Tolerance to DNCB induced by feeding guinea-pigs with the same hapten has been reversed by a single treatment with cyclophosphamide. This is paralleled by a return of the ability of T cells to proliferate in the draining lymph node following sensitization. Certain quantitative differences between this system and that previously described using intravenous DNBSO3 have been revealed. These may indicate some difference between these two mechanisms of tolerance induction.
Cyclophosphamide (CY) treatment known to enhance the normal cell-mediated immune response by selectively inhibiting the function of suppressor cells abrogates tolerance by pretreatment when tolerant animals are sensitized 3 days after the intraperitoneal injection of CY. The tolerance during the primary response is also reversed by CY treatment, indicating that in both these types of unresponsiveness suppressor cells may be operating. However, CY treatment did not influence the short-lasting unresponsiveness induced in already sensitized guinea-pigs by the intravenous injection of tolerogen. These findings corroborate the idea that the mechanism of desensitization is different from that of tolerance induced by pretreatment of during the primary response.
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