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Abstract
Multiple Sclerosis (MS) is a neurodegenerative autoimmune disorder of the central nervous system (CNS) characterized by the recruitment of self-reactive T lymphocytes, mainly inflammatory T helper (Th) cell subsets. Once recruited within the CNS, inflammatory Th cells produce several inflammatory cytokines and chemokines that activate resident glial cells, thus contributing to the breakdown of blood-brain barrier (BBB), demyelination and axonal loss. Astrocytes are recognized as key players of MS immunopathology, which respond to Th cell-defining cytokines by acquiring a reactive phenotype that amplify neuroinflammation into the CNS and contribute to MS progression. In this review, we summarize current knowledge of the astrocytic changes and behaviour in both MS and experimental autoimmune encephalomyelitis (EAE), and the contribution of pathogenic Th1, Th17 and Th1-like Th17 cell subsets, and CD8+ T cells to the morphological and functional modifications occurring in astrocytes and their pathological outcomes.
Highlights
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) affecting more than 2.5 million people worldwide, with a 2020 global prevalence of 35.9 per 100000 people [1]
We describe the main astrocytic changes occurring in Multiple Sclerosis (MS) and the role of the crosstalk between inflammatory T cells and astrocytes in amplifying CNS inflammation and MS progression (Figure 1)
Astrocytes play a crucial role in removing the excess of glutamate by using specific glutamate transporters such as glutamateaspartate transporter (GLAST) and glutamate transporter-1 (GLT-1), which uptake more than 80% glutamate released in the synaptic cleft
Summary
Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS) affecting more than 2.5 million people worldwide, with a 2020 global prevalence of 35.9 per 100000 people [1]. After the initial CIS, most patients have a second relapse and develop the relapsing-remitting MS (RRMS) form [2]. Relapses are characterized by CNS inflammation and confluent area of demyelination in the white and grey matter of the brain and spinal cord caused by the loss of oligodendrocytes and myelin sheaths [3]. One to two decades post-diagnosis, 15-30% of RRMS patients develop secondary progressive MS (SPMS) that is characterised by gradual neuroaxonal loss and brain atrophy, leading to patient disability and neurodegeneration [4]. About 15% of patients develop an irreversible primary progressive form (PPMS) from the onset characterized by chronic demyelinated lesions in the white matter, axonal loss, diffuse and focal demyelination of the grey matter and neurodegeneration [5]. Several studies performed in murine models of experimental autoimmune encephalomyelitis (EAE) to explain MS pathophysiology, validated the hypothesis that
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