Review
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NF-κB as an Inducible Regulator of Inflammation in the Central Nervous System
Version 1
: Received: 31 January 2024 / Approved: 31 January 2024 / Online: 1 February 2024 (09:28:58 CET)
A peer-reviewed article of this Preprint also exists.
Anilkumar, S.; Wright-Jin, E. NF-κB as an Inducible Regulator of Inflammation in the Central Nervous System. Cells 2024, 13, 485. Anilkumar, S.; Wright-Jin, E. NF-κB as an Inducible Regulator of Inflammation in the Central Nervous System. Cells 2024, 13, 485.
Abstract
The NF-κB (nuclear factor K-light-chain-enhancer of activated B cells) transcription factor family is critical for modulating the immune proinflammatory response throughout the body. During the resting state, inactive NF-κB is sequestered by IκB in the cytoplasm. Proteasomal degradation of IκB activates NF-κB, mediating its translocation into the nucleus to act as a nuclear transcription factor in the upregulation of proinflammatory genes. Stimuli that initiate NF-κB activation are diverse, but are canonically attributed to proinflammatory cytokines and chemokines. Downstream effects of NF-κB are cell type specific and, in the majority of cases, result in activation of pro-inflammatory cascades. Acting as the primary immune responders of the central nervous system, microglia exhibit upregulation of NF-κB upon activation in response to pathological conditions. Under such circumstances, microglial crosstalk with other cell types in the central nervous system can induce cell death, further exacerbating the disease pathology. In this review, we will emphasize the role of NF-κB in triggering neuroinflammation mediated by microglia.
Keywords
NF-κB; inflammation; microglia
Subject
Biology and Life Sciences, Neuroscience and Neurology
Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
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