NRROS (E4B2D) Rabbit mAb #58142

Reactive oxygen species (ROS) produced by phagocytes are critical for defense against microbial and fungal challenges. However, excess ROS can lead to tissue damage from inflammation and thus must be carefully regulated (1,2). Negative regulator of ROS (NRROS, LRRC33) limits ROS production in phagocytes during inflammatory responses (1-3). NRROS expression in phagocytes can be repressed by inflammatory signals (2,3). NRROS-deficient phagocytes produce increased ROS upon inflammatory challenge, and mouse phagocytes lacking NRROS show enhanced bactericidal activity (2,3).

NRROS has also been shown as a key regulator of transforming growth factor beta-1 (TGF-β1) required for microglia function in the nervous system (3,4). Microglia and other macrophages within the central nervous system (CNS) have roles in neural development, inflammation, and homeostasis (3,5). NRROS is required for normal gene expression driving microglial development and function (6-8). Mutation and dysregulation of NRROS in mouse models and humans leads to severe brain disease owing to oxidative tissue damage in the CNS (6-8). NRROS is also involved in Toll-like receptor (TLR) signaling. NRROS ability to inhibit NF-κB activation downstream of TLR activation and subsequent decreased cytokine production is likely related indirectly to its role in the TGF-β1 pathway (9).