pro-inflammatory signaling and attenuate anti-inflammatory signaling by reactive astrocytes. For example, it is well-documented that reactive astrocytes can control and limit the spread of inflammation after traumatic injury, stroke and other conditions, particularly through Stat3-mediated signaling [11, 32, 65]. However, in the context of tumor formation, recent studies in mice show that reactive astrocytes may be co-opted by tumor cells to inappropriately suppress local inflammation via Stat3-mediated mechanisms and thereby, aid tumor growth and invasive spread [22, 23, 82, 83]. Stat3-mediated astrocyte suppression of local inflammatory responses and phagocytosis may also reduce amyloid clearance in mouse models of AD-like amyloid toxicity [84, 85]. Thus, reactive astrocyte dysfunctions and detrimental effects are regulated in very specific ways by definable molecular signaling events that are highly context specific. Beneficially modulating specific reactive astrocyte functions will thus require a detailed understanding of specific mechanisms that operate in different contexts, and which might potentially involve the induction of opposite effects for different scenarios.
