Interleukin (IL)-23 plays a predominant role in the development of autoimmune diseases by inducing IL-17-producing helper T (Th17) cells. The receptor for IL-23 consists of a heterodimer composed of the IL-12 receptor beta1 (IL-12Rbeta1) and the IL-23 receptor (IL-23R), which is mainly expressed on Th17 cells. A recent study showed that macrophages express IL-23R mRNA and can be distinguished from microglia by IL-23R expression. However, in this study, we show by RT-PCR and immunocytochemistry that microglia express IL-23R and IL-12Rbeta1 mRNA and protein, respectively. Additionally, microglia expressed a functional receptor for IL-23, as IL-23 enhanced the Interferon (IFN)-gamma-induced signal transducer and activator of transcription (STAT)1 phosphorylation and chemokine production. Thus, IL-23R expression does not discriminate peripheral macrophages from microglia. Moreover, since microglia produce IL-23, it may function in an autocrine manner to recruit inflammatory cells by inducing chemokine production.