The initiation and perpetuation of innate and adaptive immunity is dependent on the ability of professional antigen-presenting cells (APCs) to sense inflammatory stimuli; produce cytokines; and internalize, degrade, and present antigens via surface major histocompatibility complex (MHC) molecules. Dendritic cells (DCs), macrophages, and B lymphocytes express estrogen receptors, indicating that the steroid sex hormone estrogen might directly modulate the function of these cells during immune responses. Sex-specific parameters of immune function have been identified during autoimmunity and the pathogenesis of infectious disease, which show sex biases in their incidence and manifestation; female immunity also varies as estrogen levels change. In this article, we summarize studies that demonstrate effects of estrogen on the differentiation or function of APCs in model in vitro systems, or under circumstances of natural or imposed variation in estrogen levels in vivo.