4.3. Autoimmunity in the brain: Multiple sclerosis
It is known that deregulation of the immune system plays a crucial role
in neurological disorders. This is particularly evident in diseases
where the underlying pathology is autoimmune-related. MS is a chronic
autoimmune disease in which self-reactive T cell clones attack the
myelin component of the CNS. In early MS, active lesions are
characterized by focal demyelination of white matter accompanied by
perivenular infiltrates of immune cells such as CD8+ T
cells, CD20+ B cells, plasmablasts, and macrophages
that form a typical perivascular cuff. This demyelination disrupts the
BBB and causes progressive loss of neurological function due to damage
to the myelin sheath around the neuronal axons (Frischer et al., 2009).
Genetic predisposition to MS is linked to specific HLA class II
haplotypes (HLA-DR15 and HLA-DQ6), which are thought to present
autoantigens to the adaptive immune system. Other immune-related genes
have also been implicated in the development of MS, such as those
encoding for IL-17 and IL-2. In addition to genetics, various
environmental factors, such as lifestyle, vitamin deficiencies, and
infections such as EBV, have been identified as risk factors for MS.
Studying the immune response in the experimental autoimmune
encephalomyelitis (EAE) model has provided insight into the role of T
cell phenotypes and their effector mechanisms in the pathology of MS
(Pilli, Zou, Tea, Dale & Brilot, 2017).