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Testosterone suppresses immunity against malaria caused by Plasmodium chabaudi in B10 mice. Since this effect is probably not mediated through the classical androgen-receptor response, we investigated whether testosterone might act, after aromatization to oestradiol (OE₂), through the oestrogen receptor (ER). Indeed, OE₂ was found to act immunosuppressively when used at only about 1% of the immunosuppressive dose of testosterone. This becomes evident as an OE₂-induced suppression of self-healing of P. chabaudi infections in female and castrated male B10 mice. The immunosuppressive OE₂ effect is associated with a 16-fold increase in the circulating level of OE₂ and can be prevented by ER blockers such as tamoxifen and clomifene. In contrast, the immunosuppressive effect of testosterone, which is not associated with any changes in the level of OE₂, cannot be abolished by ER blockers or by aromatase inhibitors, such as atamestane and drofazar hydrochloride. Moreover, OE₂ and testosterone act differently on spleen cells; OE₂ induces a decrease in CD4⁺-T-cells, whereas testosterone causes an increase in CD8⁺-T-cells and a decrease in total nucleated spleen cells. The immunosuppressive effect of testosterone, but not that of OE₂, can be adoptively transferred to syngeneic mice by nucleated spleen cells, predominantly T-cells. Our data show that the immunosuppressive activity of testosterone, in contrast to OE₂, is not mediated through the ER. The immunosuppressive action of testosterone is therefore thought to be primarily mediated through a non-genomic mechanism.

Journal of Endocrinology (1993) 139, 487–494

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