The Toll Pathway in the Central Nervous System of Flies and Mammals.

Neuromolecular Med

The Mina and Everard Goodman Faculty of Life Sciences, Bar-Ilan University, Ramat-Gan, Israel.

Published: December 2018

Toll receptors, first identified to regulate embryogenesis and immune responses in the adult fly and subsequently defined as the principal sensors of infection in mammals, are increasingly appreciated for their impact on the homeostasis of the central as well as the peripheral nervous systems. Whereas in the context of immunity, the fly Toll and the mammalian TLR pathways have been researched in parallel, the expression pattern and functionality have largely been researched disparately. Herein, we provide data on the expression pattern of the Toll homologues, signaling components, and downstream effectors in ten different cell populations of the adult fly central nervous system (CNS). We have compared the expression of the different Toll pathways in the fly to the expression of TLRs in the mouse brain and discussed the implications with respect to commonalities, differences, and future perspectives.

Download full-text PDF

Source
http://dx.doi.org/10.1007/s12017-018-8515-9DOI Listing

Publication Analysis

Top Keywords

central nervous
8
nervous system
8
adult fly
8
expression pattern
8
toll
5
toll pathway
4
pathway central
4
system flies
4
flies mammals
4
mammals toll
4

Similar Publications

The endocannabinoid system (ECS), regulating such processes as energy homeostasis, inflammation, and muscle function, centers around cannabinoid receptors, including CB1. These receptors are mainly located in the central nervous system and skeletal muscles. Hyperactivity of CB1 receptors is linked to metabolic disorders and chronic inflammation, highlighting their potential as therapeutic targets for muscle hypertrophy and metabolic health.

View Article and Find Full Text PDF

This proceedings article summarizes the inaugural "T Cells in the Brain" symposium held at Columbia University. Experts gathered to explore the role of T cells in neurodegenerative diseases. Key topics included characterization of antigen-specific immune responses, T cell receptor (TCR) repertoire, microbial etiology in Alzheimer's disease (AD), and microglia-T cell crosstalk, with a focus on how T cells affect neuroinflammation and AD biomarkers like amyloid beta and tau.

View Article and Find Full Text PDF

Background: Sudden sensorineural hearing loss (SSNHL) is associated with abnormal changes in the brain's central nervous system. Previous studies on the brain networks of SSNHL have primarily focused on functional connectivity within the brain. However, in addition to functional connectivity, structural connectivity also plays a crucial role in brain networks.

View Article and Find Full Text PDF

Objective: We aimed to evaluate the diagnostic accuracy of heparin-binding protein (HBP) in cerebrospinal fluid for the diagnosis of bacterial meningitis in patients with a suspected central nervous system infection.

Methods: This prospective multicenter cohort study determined the diagnostic accuracy of HBP in cerebrospinal fluid (CSF) for bacterial meningitis among a cohort of consecutive patients with a suspected central nervous infection. The final clinical diagnosis was considered the reference standard.

View Article and Find Full Text PDF

Microglial phagocytosis of haematomas is crucial for neural functional recovery following intracerebral haemorrhage (ICH), a process regulated by various factors from within and outside the central nervous system (CNS). Extracellular vesicles (EVs), significant mediators of intercellular communication, have been demonstrated to play a pivotal role in the pathogenesis and progression of CNS diseases. However, the regulatory role of endogenous EVs on the phagocytic capacity of microglia post-ICH remains elusive.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!