The authors investigated mechanisms of suppression of contact sensitivity to 1-fluoro-2,4-dinitrobenzene (DNFB) in mice. In particular, they studied the suppression produced by suppressor T cells which had been induced by injection of syngeneic DNP-modified lymphoid cells (syninduced Ts). Syninduced Ts were found by several criteria to inhibit the efferent limb of sensitivity by inhibiting the expression of lymph node (LN) cells from DNFB-sensitized animals. First, syninduced Ts can suppress previously sensitized recipients in an antigen-specific manner. Second, co-transferred syninduced Ts could block the passive transfer of contact sensitivity by DNFB-immune LN cells given to normal recipients. This inhibition was shown to be dose dependent, antigen specific, and non-MHC restricted. Third, in reverse transfers of sensitized cells into tolerant recipients, only those recipients containing active syninduced Ts could inhibit the expression of sensitivity by the passively transferred immune T cells. In contrast, syninduced Ts were capable of inhibiting the afferent limb of the response as assessed by the normal, post-sensitization DNA synthetic response of draining LN cells in Ts recipient mice. Syninduced Ts were not inhibitable by prior treatment with anti-TNP antiserum, indicating a lack of surface-associated tolerogen. The locus of suppression was most clearly shown in experiments where mice received syninduced Ts at the same time they were sensitized. These mice were themselves unresponsive, but did contain immune lymphoid cells able to express contact sensitivity after transfer to normal recipients followed by DNFB challenge. The data suggest that the suppressive environment allows the development of a normal complement of DNFB-specific immune T cells, but inhibits the expression of this sensitivity. The data are discussed in terms of current models of suppression, and are compared with mechanisms of suppression in other contact sensitivity models.
|Original language||English (US)|
|Number of pages||9|
|Journal||Journal of Immunology|
|State||Published - Dec 1 1978|
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