
Neuroinflammation within the central nervous system involves multiple cell types that coordinate their responses by secreting and responding to a plethora of inflammatory mediators. These factors activate multiple signaling cascades to orchestrate initial inflammatory response and subsequent resolution. Activation of NF-κB pathways in several cell types is critical during neuroinflammation. In contrast to the well-studied role of p65 NF-κB during neuroinflammation, the mechanisms of RelB activation in specific cell types and its roles during neuroinflammatory response are less understood. In this review, we summarize the mechanisms of RelB activation in specific cell types of the CNS and the specialized effects this transcription factor exerts during neuroinflammation.
Immunosuppression Therapy, Inflammation, QH573-671, Transcription Factor RelB, astrocytes, NF-kappa B, microglia, oligodendrocytes, Brain, RelB, Review, NF-κB, neuroinflammation, Animals, Humans, Cytology, Signal Transduction
Immunosuppression Therapy, Inflammation, QH573-671, Transcription Factor RelB, astrocytes, NF-kappa B, microglia, oligodendrocytes, Brain, RelB, Review, NF-κB, neuroinflammation, Animals, Humans, Cytology, Signal Transduction
| selected citations These citations are derived from selected sources. This is an alternative to the "Influence" indicator, which also reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | 31 | |
| popularity This indicator reflects the "current" impact/attention (the "hype") of an article in the research community at large, based on the underlying citation network. | Top 10% | |
| influence This indicator reflects the overall/total impact of an article in the research community at large, based on the underlying citation network (diachronically). | Top 10% | |
| impulse This indicator reflects the initial momentum of an article directly after its publication, based on the underlying citation network. | Top 10% |
