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  • Title: Mechanism by which pertussis toxin breaks unresponsiveness of delayed-type hypersensitivity to sheep red blood cells in mice.
    Author: Tamura S, Tanaka H, Kikuta K, Kobayashi T, Sato H, Sato Y.
    Journal: Cell Immunol; 1986 Jul; 100(2):351-63. PubMed ID: 3093086.
    Abstract:
    The mechanism by which pertussis toxin (PT) breaks the unresponsiveness of delayed-type hypersensitivity (DTH) to sheep red blood cells (SRBC) was examined in B10 mice. The unresponsiveness of DTH was induced in mice by iv injection of 10(9) SRBC and broken antigen-specifically by iv injection of 500 ng of PT into mice 1 or more days after SRBC injection. The restored DTH response in the SRBC-primed and PT-treated mice was accompanied by the appearance of Lyt-1-positive splenic T cells, capable of mediating DTH, fractionated in the low-density layers on a discontinuous bovine serum albumin density gradient. To examine the action of PT on the appearance of the DTH-effector cells, the splenic T cells from 10(9) SRBC-primed mice were treated with 100 ng/ml of PT for 60 min in vitro and then transferred into naive recipient mice. The PT-treated T cells acquired the ability to manifest DTH in the recipient mice several days after transfer. A large proportion of them were Lyt-1-positive small cells fractionated in the high-density layers before transfer and transformed into DTH-effector cells fractionated in the low-density layers in the recipient mice after transfer. Moreover, the ability of the PT-treated cells to manifest DTH on transfer was resistant to treatment with mitomycin C. These results suggest that PT acts on the sensitized, small Lyt-1-positive T cells from the unresponsive mice to differentiate them into large T-cell blasts, capable of mediating DTH, as one of the mechanisms by which PT breaks the unresponsiveness of DTH to SRBC.
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