Review articleNeuroimmune regulation of microglial activity involved in neuroinflammation and neurodegenerative diseases

- Interactions of microglia with neurons and astrocytes regulate neuroinflammation.
- Th1 and Th17 CD4 + T-cells constitute the engine of chronic neuroinflammation.
- Encephalitogenic regulatory T cells and Th2 cells exert neuroprotective effects.
- Modification of central nervous system constituents triggers loss of self-tolerance.
- We hypothesise that autoimmune response is a major component in neurodegeneration.

Neuroinflammation constitutes a fundamental process involved in the progression of several neurodegenerative disorders, such as Parkinson's disease, Alzheimer's disease, amyotrophic lateral sclerosis and multiple sclerosis. Microglial cells play a central role in neuroinflammation, promoting neuroprotective or neurotoxic microenvironments, thus controlling neuronal fate. Acquisition of different microglial functions is regulated by intercellular interactions with neurons, astrocytes, the blood-brain barrier, and T-cells infiltrating the central nervous system. In this study, an overview of the regulation of microglial function mediated by different intercellular communications is summarised and discussed. Afterward, we focus in T-cell-mediated regulation of neuroinflammation involved in neurodegenerative disorders.

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