Abstract
The field of neuroimmunology endorses the involvement of the adaptive immune system in central nervous system (CNS) health, disease, and aging. While immune cell trafficking into the CNS is highly regulated, small numbers of antigen-experienced lymphocytes can still enter the cerebrospinal fluid (CSF)-filled compartments for regular immune surveillance under homeostatic conditions. Meningeal lymphatics facilitate drainage of brain-derived antigens from the CSF to deep cervical lymph nodes to prime potential adaptive immune responses. During aging and CNS disorders, brain barriers and meningeal lymphatic functions are impaired, and immune cell trafficking and antigen efflux are altered. In this context, alterations in the immune cell repertoire of blood and CSF and T and B cells primed against CNS-derived autoantigens have been observed in various CNS disorders. However, for many diseases, a causal relationship between observed immune responses and neuropathological findings is lacking. Here, we review recent discoveries about the association between the adaptive immune system and CNS disorders such as autoimmune neuroinflammatory and neurodegenerative diseases. We focus on the current challenges in identifying specific T cell epitopes in CNS diseases and discuss the potential implications for future diagnostic and treatment options.
Highlights
With recent advances in single-cell technologies, the field of neuroimmunology has adapted the concept of ‘central nervous system (CNS) immune cell coexistence’ (Mundt et al, 2019a)
It is widely acknowledged that immune privilege is limited to the brain parenchyma and that immune reactivity in the meninges and cerebrospinal fluid (CSF)filled spaces is comparable to the periphery
As we describe below, increased infiltration of dendritic cells (DCs), monocytes, and T cells in the brain parenchyma has been reported in several age-related neurodegenerative diseases, such as Alzheimer’s disease (AD) and Parkinson’s disease (PD), and in multiple sclerosis (MS)
Summary
With recent advances in single-cell technologies, the field of neuroimmunology has adapted the concept of ‘CNS immune cell coexistence’ (Mundt et al, 2019a). Β-Amyloid-Directed Autoreactive Immune Responses antigens responsible for T cell infiltration in the brain during AD have not been identified, T cells with reactivities toward Aβ-derived epitopes were detected in the blood of middle-aged, elderly, and AD patients (Table 1; Monsonego et al, 2003).
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