Inflammasomes in neuroinflammatory and neurodegenerative diseases.
Sofie VoetSahana SrinivasanMohamed LamkanfiGeert van LooPublished in: EMBO molecular medicine (2020)
Neuroinflammation and neurodegeneration often result from the aberrant deposition of aggregated host proteins, including amyloid-β, α-synuclein, and prions, that can activate inflammasomes. Inflammasomes function as intracellular sensors of both microbial pathogens and foreign as well as host-derived danger signals. Upon activation, they induce an innate immune response by secreting the inflammatory cytokines interleukin (IL)-1β and IL-18, and additionally by inducing pyroptosis, a lytic cell death mode that releases additional inflammatory mediators. Microglia are the prominent innate immune cells in the brain for inflammasome activation. However, additional CNS-resident cell types including astrocytes and neurons, as well as infiltrating myeloid cells from the periphery, express and activate inflammasomes. In this review, we will discuss current understanding of the role of inflammasomes in common degenerative diseases of the brain and highlight inflammasome-targeted strategies that may potentially treat these diseases.
Keyphrases
- immune response
- cell death
- dendritic cells
- white matter
- resting state
- cerebral ischemia
- traumatic brain injury
- inflammatory response
- toll like receptor
- spinal cord
- microbial community
- single cell
- oxidative stress
- bone marrow
- cancer therapy
- lipopolysaccharide induced
- nlrp inflammasome
- multiple sclerosis
- drug delivery
- signaling pathway
- mesenchymal stem cells
- subarachnoid hemorrhage