While the mechanisms underlying this effect are unclear, decreases in astrocyte number/activation may result from increased apoptotic death of this population following infection or could occur as a result of the compensatory production of suppressive mediators, such as IL-10 and IL-19, that have been shown to be produced in a delayed manner by B. burgdorferi- challenged microglia and/or astrocytes [14, 23]. The gene discussed is IL10; the disease is infection.