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Published on: August 19, 2014
Suppression of lymphoproliferation by hapten-specific suppressor T lymphocytes from mice exposed to ultraviolet
Application of a contact-sensitizing agent to the skin of mice previously exposed to UV radiation at a different site results in the induction of hapten-specific suppressor T lymphocytes. When splenic lymphocytes from such mice were cultured with normal lymphocytes and hapten-conjugated splenic adherent cells, the primary proliferative response was suppressed. The cell responsible for the suppression in vitro was a T lymphocyte, and two signals were required for its induction, ultraviolet radiation and hapten sensitization. The T cell suppressing lymphoproliferation was specific for the hapten applied after UV radiation. The UV-induced T suppressor cell inhibited only primary lymphoproliferation; the response of lymphocytes from immunized mice was unaffected. The activity of the UV-induced suppressor cell was not affected by mitomycin C treatment. Thus, suppression of the primary proliferative response of lymphocytes to hapten-modified syngeneic cells in vitro correlates with in vivo suppression of contact hypersensitivity by these UV-induced suppressor cells. This suggests that the suppressor cells act by preventing the proliferation of hapten-specific responder clones. Use of this in vitro assay system should facilitate investigation of the characteristics of these cells and the mechanism by which these regulatory T lymphocytes inhibit contact sensitization.
Application of a contact-sensitizing agent to the skin of mice previously exposed to UV radiation at a different site results in the induction of hapten-specific suppressor T lymphocytes. When splenic lymphocytes from such mice were cultured with normal lymphocytes and hapten-conjugated splenic adherent cells, the primary proliferative response was suppressed. The cell responsible for the suppression in vitro was a T lymphocyte, and two signals were required for its induction, ultraviolet radiation and hapten sensitization. The T cell suppressing lymphoproliferation was specific for the hapten applied after UV radiation. The UV-induced T suppressor cell inhibited only primary lymphoproliferation; the response of lymphocytes from immunized mice was unaffected. The activity of the UV-induced suppressor cell was not affected by mitomycin C treatment. Thus, suppression of the primary proliferative response of lymphocytes to hapten-modified syngeneic cells in vitro correlates with in vivo suppression of contact hypersensitivity by these UV-induced suppressor cells. This suggests that the suppressor cells act by preventing the proliferation of hapten-specific responder clones. Use of this in vitro assay system should facilitate investigation of the characteristics of these cells and the mechanism by which these regulatory T lymphocytes inhibit contact sensitization.
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