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Inflammation is an essential process in the immune defense against infections. It involves concerted, timed, and highly regulated activities of tissue-resident and infiltrating immune cells, their soluble messengers, and effector molecules to fight off an invasion as well as to support subsequent attempts of repair. Inflammatory processes can also develop under non-infectious conditions triggered by some endogenous factors and as a consequence of cell and tissue impairment. Here too, the initiation of activities, namely in innate immune cells, would primarily aim at damage containment, tissue protection , and recovery. However, excessive, chronic or maladapt-ed inflammation can precipitate destructive cascades, which can eventually result in organ failure or even lead to a lethal outcome. In this regard, the central nervous system (CNS) is extremely vulnerable. Neuroinflammatory processes as they follow and accompany not only viral and bacterial infections, trauma, or stroke, but also neurodegenerative and autoimmune diseases can have a devastating impact on neuronal as well as glial structures and impede their sophisticated functions often causing massive and lasting disabilities [1, 2]. Therefore, it has been of foremost interest to establish therapeutic strategies which would allow for moderating dysregulated inflammatory reactions, especially also those affecting the CNS [2–5]. However, some of the interventions can cause themselves undesired effects—increas-ing the need to develop improved anti-inflammatory compounds and, in addition, to identify novel targets within the (pro)inflammatory signaling and effector mechanisms. Now and again, studies unravel links and interactions between signaling systems which, at first glance, do not intimately cooperate. Some reveal new functions of proteins that reach beyond of what was making its way to the textbooks. The work of Przanowski and collaborators [6] combines both kinds of surprises by linking Janus kinase-signal transducers and activators of transcription (JAK-STAT) sig-naling elements closely to the world of Toll-like receptors (TLRs). Not enough, an enzyme known for removing methyl groups from lysine 27 residues in H3 histones, the H3K27me3 demethylase Jmjd3, appears to be a key element in this coop-eration—yet not by its enzymatic activity but as a transcription factor. The findings bear (neuro)inflammation-relevant novelty as they are at the core of innate immune functions in the CNS. Within the CNS, microglial cells represent the equivalent of a tissue macrophage [7]. While having contributions to the CNS development and functional maintenance, these myeloid cells also serve as sentinels of the tissue homeostasis constantly scanning their environment and being capable of instantly responding to signs …

Linking STAT and TLR signaling in microglia: a new role for the histone demethylase Jmjd3