Interleukin-33 (IL-33) is a relatively newly discovered member of the IL-1 family. It is regarded as an alarmin located in the nuclei of barrier cells such as endothelial cells. Upon tissue damage or cell death, IL-33 is released into the extracellular space and initiates corresponding cascades in nearby cells for protective reactions. The role of IL-33 in immune responses is dichotomous, as both pro-inflammatory and anti-inflammatory properties have been reported under various conditions. While most of the literature focuses on IL-33 dynamics in the peripheral immune system, its function in the central nervous system (CNS) remains somewhat ambiguous.

Our group previously found that the cognitive impairment in 12-month-old APP/PS1 mice, an animal model of Alzheimer’s diseas...[ Read more ]

Interleukin-33 (IL-33) is a relatively newly discovered member of the IL-1 family. It is regarded as an alarmin located in the nuclei of barrier cells such as endothelial cells. Upon tissue damage or cell death, IL-33 is released into the extracellular space and initiates corresponding cascades in nearby cells for protective reactions. The role of IL-33 in immune responses is dichotomous, as both pro-inflammatory and anti-inflammatory properties have been reported under various conditions. While most of the literature focuses on IL-33 dynamics in the peripheral immune system, its function in the central nervous system (CNS) remains somewhat ambiguous.

Our group previously found that the cognitive impairment in 12-month-old APP/PS1 mice, an animal model of Alzheimer’s disease (AD), was improved after a 2-day treatment with IL-33. This beneficial effect of IL-33 on neurodegenerative disease models prompted us to explore the underlying mechanism of IL-33 in AD model mice. Therefore, the transcriptome of mouse brains was analysed by oligonucleotide microarray, and 4 candidate genes were examined further. Herein, CD11c was characterized in APP/PS1 mice. CD11c protein overexpression was confirmed by immunofluorescence in the microglia-like cells of 7.5-month-old APP/PS1 mouse brains and compared to that in wild-type (WT) littermates. In addition, CD11c mRNA expression increased in parallel with AD pathogenesis, but not with aging in WT mice. These findings implicate a possible new contributory factor to AD progression as well as a possible mechanism of IL-33 signaling effects in the AD mouse model. In the future, we will investigate the origin of CD11c or CD11c+ cells in the AD mouse brain as well as the interaction of IL-33 with CD11c+ cells.