Acute transient lymphopenia in the mouse was induced by whole-body exposure to radiofrequency radiation (RFR) (26 MHz, 2/sup 0/C increase in core temperature over 15 min). Mice experiencing RFR-induced lymphopenia showed a relative increase in splenic T- ad B-lymphocytes; these elevated levels were further pronounced by three RFR exposures delivered at 3-hr intervals. Multiple RFR exposures also led to a significant decrease in thymic weight and thymic and splenic cell density and, moreover, to suppressed cell-mediated immune function as measured in vivo by local delayed-type hypersensitivity. Only splenic B-lymphocyte levels were elevated with no change in delayed hypersensitivity in warm air-exposed mice (2/sup 0/C increase in core temperature over 15 min). Plasma corticoid levels immediately after RFR treatment were severalfold higher than those in mice given warm air or sham exposure. Notably, administration of methyl prednisolone sodium succinate to control animals led to lymphopenia, increased splenic T- and B-lymphocyte frequency, and thymic involution that was oserved in RFR exposed animals. These results indicate that RFR hyperthermia can induce significant alterations in lymphocyte distribution and function and that RFR impact on the immune apparatus appears to be mediated at the cellular level indirectly through steroid-associated actions.
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Robert P. Liburdy (1979) studied this question.
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