Oestrogens are key regulators of immune function, with effects that depend on hormonal concentration, biological context, and the pattern of receptor engagement. At low or intermediate levels, as typically observed during reproductive life and at defined stages of the menstrual cycle, oestrogens tend to strengthen innate and adaptive immune reactivity. In this setting, they can increase the release of pro-inflammatory mediators, including IL-1β, IL-6, TNF-α, and type I interferon (IFN-I). These actions are partly mediated through enhanced expression of Toll-like receptor (TLR) 7 and TLR9, increased responsiveness of plasmacytoid dendritic cells (DCs), and promotion of B-cell persistence, maturation and differentiation, together with support of Th17 polarisation [15]. In contrast, the high oestrogen concentrations reached during pregnancy are associated with a more tolerogenic immune environment. Under these conditions, immune responses are redirected towards Th2- and Treg profiles, FOXP3 expression is increased, and anti-inflammatory mediators such as IL-10 and transforming growth factor-β (TGF-β) are favoured. These changes contribute to the establishment and maintenance of immune tolerance at the maternal-foetal interface [16]. In addition, the biological effects of oestrogens are complicated by the distinct signalling properties of oestrogen receptors (ERs). ERα activation is generally linked to inflammatory immune pathways, whereas ERβ signalling is more often associated with regulatory or anti-inflammatory responses. Since the relative expression of ERα and ERβ differs among immune cell populations, tissues, and stages of life, the ERα/ERβ balance may influence both the intensity and the functional orientation of immune responses [17]. Overall, these observations indicate that oestrogens may initially amplify immune activation, thereby supporting effective pathogen control, while later favour regulatory mechanisms that limit prolonged or excessive inflammation. Alterations in this dynamic equilibrium may help explain the greater predisposition of females to several inflammatory and immune-mediated disorders. Adapted from [8] under a Creative Commons CC-BY license.