Document Type
Article
Publication Date
3-11-2024
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. The 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 the 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.
Recommended Citation
Anilkumar, Sudha and Wright-Jin, Elizabeth, "NF-κB as an Inducible Regulator of Inflammation in the Central Nervous System" (2024). Department of Medicine Faculty Papers. Paper 443.
https://jdc.jefferson.edu/medfp/443
Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 License.
PubMed ID
38534329
Language
English
Comments
This article is the author's final published version in Cells, Volume 13, Issue 6, March 2024, Article number 485.
The published version is available at https://doi.org/10.3390/cells13060485.
Copyright © 2024 by the authors