Adult stem cells are tissue-resident undifferentiated and self-renewing cells responsible for tissue homeostasis. Under physiological conditions, stem cells co-exist in a reversible cell cycle-arrested state known as quiescence and an activated proliferative state, which results in the production of cell progeny through asymmetric division. Different types of injuries can activate stem cells to produce progeny that contributes to tissue repair, but the molecular triggers and regulators of this activation are barely known. Living organisms are constantly exposed to a variety of internal and external stimuli and some of them can be classified as danger signals. Upon detection, a complex response is set in motion that is aimed at eliminating the danger signals and eventually restoring tissue and organism homeostasis. This response is generically referred to as inflammation and is part of the ancient innate immune system present in all metazoans. Adult stem cells are sensitive to their niche as they behave by integrating actions of intrinsic regulators in response to signals emanating from their most immediate microenvironment, as well as from circulation. Inflammation has been shown to act on several stem cell niches, but the observation of changes in tissue turnover that could reflect both detrimental and beneficial effects has left the precise role of inflammation in tissue maintenance and regeneration as controversial. In the case of the central nervous system, experimental evidence has accumulated in the last decade indicating that inflammation can play a negative role in adult mammalian neurogenesis. This work has addressed the possibility that neural adult stem cells of the rodent brain could respond positively to certain inflammatory signals, a reaction that would be obscured by the more dramatic detrimental effects of inflammatory cytokines on neurogenesis. We have found that adult neural stem cells can sense and respond to remote peripheral lesions by shifting from a dormant quiescent state to an alert prone-to-activation one and that TNFR2 signalling, in response to cytokines, such as tumour necrosis factor alpha and progranulin, is mediating this process. The first finding is in line with recent data indicating that adult stem cells of different systems can react to distant injuries, suggesting a homeostatic control of their activity at the organismal level. The second one increases our understanding of the role of inflammation in the neurogenic process. Although the most accepted view is that acute or chronic inflammation plays a negative role in neurogenesis, our data uncover concomitant beneficial effects of inflammatory cytokines in at least a fraction of neural stem cells.