## Abstract Forkhead transcription factor3 (Foxp3) is critical for generating CD4^+^CD25^+^ regulatory T cells. However, its role in microglia has not been identified. Here, we show that Foxp3 is expressed in microglia and is upregulated upon activation. In Foxp3 mutant mice (Foxp3^sf^), microglia
Activation of microglia: A neuroinflammatory role for CAP37
β Scribed by H. Anne Pereira; Xin Ruan; Padmasini Kumar
- Publisher
- John Wiley and Sons
- Year
- 2002
- Tongue
- English
- Weight
- 316 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0894-1491
No coin nor oath required. For personal study only.
β¦ Synopsis
Recent evidence suggests that inflammation and immune function in the central nervous system (CNS) may play a considerable role in the progression of many neurodegenerative diseases. It is known that microglia, the CNS equivalent of peripheral blood monocytes, may be instrumental in causing neurotoxicity. However, the mediator(s) that activates microglia to produce toxic substances that orchestrate cell death has yet to be elucidated. We have identified a novel inflammatory molecule, cationic antimicrobial protein of molecular weight 37 kDa (CAP37), to the brains of patients dying from Alzheimer's disease. CAP37 is known to be a potent activator and regulator of monocyte function in the systemic circulation. We hypothesize that CAP37, a mediator previously shown to recruit and activate monocytes in the systemic circulation, may also play a role in CNS inflammation by modulating microglial function. Here we demonstrate that CAP37 is a chemoattractant for microglia and that CAP37-treated microglia express class II major histocompatibility antigens and produce proinflammatory cytokines and chemokines. We conclude that CAP37 has the ability to activate microglial cells and suggest that it has the potential to serve as a neuroinflammatory molecule.
π SIMILAR VOLUMES
## Abstract ## Objective Phagocytosis is necessary to eliminate the hematoma after intracerebral hemorrhage (ICH); however, release of proinflammatory mediators and free radicals during phagocyte activation is toxic to neighboring cells, leading to secondary brain injury. Promotion of phagocytosis
## Abstract The microglial cell, after many years of neglect, has become recognized as the sole representative cell of the immune system that resides in the normal central nervous system. While normally dormant, microglia can be activated by secretory substances or signals associated with disease o
## Abstract Microglia are activated by lipopolysaccharide (LPS) to produce neurotoxic proβinflammatory factors and reactive oxygen species (ROS). While a multitude of LPS receptors and corresponding pathways have been identified, the detailed mechanisms mediating the microglial response to LPS are
## Abstract The aim of this study was to examine the homocysteine effect on phospholipase CΞ³2 (PLCΞ³2) activation and to investigate the signaling pathway involved. We found that homocysteine stimulated the tyrosine phosphorylation and activation of platelet PLCΞ³2. The tyrosine kinases p60src and p7