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Review
, 215 (11), 2702-2704

Targeting Neuro-Immune Communication in Neurodegeneration: Challenges and Opportunities

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Review

Targeting Neuro-Immune Communication in Neurodegeneration: Challenges and Opportunities

Aleksandra Deczkowska et al. J Exp Med.

Abstract

Immune cells patrol the brain and can support its function, but can we modulate brain-immune communication to fight neurological diseases? Here, we briefly discuss the mechanisms orchestrating the cross-talk between the brain and the immune system and describe how targeting this interaction in a well-controlled manner could be developed as a universal therapeutic approach to treat neurodegeneration.

Figures

Figure 1.
Figure 1.
Brain–immune communication points during aging and neurodegenerative disease. In a young individual, the peripheral immune system promotes CNS immune surveillance via the CP. Immune activities are controlled by anti-inflammatory cytokines, T regulatory cell function, and checkpoint receptors and ligands (such as PD-1/PD-L1) expressed on T cells, antigen-presenting cells, and possibly on the CP epithelium itself. With aging, dysregulation of peripheral immunity (thymic involution, increase in the systemic levels of myeloid-derived suppressor cells (MDSCs), and exhausted T cells), and CP-specific mechanisms (IFN-I, decrease in local IFN-γ levels) hamper supportive brain–immune cross-talk and promote accumulation of damage in the brain (neurodegeneration).

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