In the intact brain, IL-1β and IL-1ra are constitutively expressed at low levels [25], but the synthesis of both IL-1β and IL-1ra can be rapidly and strongly upregulated in discrete brain areas in response to e.g. systemic inflammation [26]–[29], excitotoxic- and ischemic brain damage [22], [24], [30], brain trauma and infections [31]. The gene discussed is IL1B; the disease is infection.