Sex hormones (estrogen, progesterone, androgens and prolactin) are apparent candidates for rendering susceptibility to ADs, and many studies have suggested that they affect both the innate and the adaptive immune system [6–8]. In order to modulate immune function, sex hormones should be able to bind to androgen and estrogen receptors (ERs) expressed by the immune cells. Indeed, cells have been shown to express both estrogen and androgen receptors, but not progesterone receptors. Among the T-cell population, only CD8+ T cells express ERs, along with monoctyes, neutrophils and murine natural killer cells. Evidence that sex hormones have an immunomodulatory effect on the immune system also exists; T cells were found to increase Th1 cytokine production (mainly IFN-γ, IL-1 and IL-10) when exposed to estrogen in vitro, while androgens had the opposite effect [9]. Other studies have demonstrated that sex hormones regulate antigen presentation by dendritic cells and macrophages, possibly through the production of TGF-β, which is also regulated by estrogen [10]. Estrogen might also have