Demyelinating Disorders of the CNS

Although many suspected autoimmune diseases are thought to be T cell-mediated, the response to therapy indicates that depletion of B cells consistently inhibits disease activity. In multiple sclerosis, it appears that disease suppression is associated with the long-term reduction of memory B cells, which serves as a biomarker for disease activity in many other CD20+ B cell depletion-sensitive, autoimmune diseases. Following B cell depletion, the rapid repopulation by transitional (immature) and naïve (mature) B cells from the bone marrow masks the marked depletion and slow repopulation of lymphoid tissue-derived, memory B cells. This can provide long-term protection from a short treatment cycle. It seems that memory B cells, possibly via T cell stimulation, drive relapsing disease. However, their sequestration in ectopic follicles and the chronic activity of B cells and plasma cells in the central nervous system may drive progressive neurodegeneration directly via antigen-specific mechanisms or indirectly via glial-dependent mechanisms. While unproven, Epstein-Barr virus may be an aetiological trigger of multiple sclerosis. This infects mature B cells, drives the production of memory B cells and possibly provides co-stimulatory signals promoting T cell-independent activation that breaks immune tolerance to generate autoreactivity. Thus, a memory B cell centric mechanism can integrate: potential aetiology, genetics, pathology and response to therapy in multiple sclerosis and other autoimmune conditions with ectopic B cell activation that are responsive to memory B cell-depleting strategies.

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Acute disseminated encephalomyelitis in a child with chikungunya virus infection

Das

Sarkar

Majumder

et al. 2015

J Pediatr Infect Dis

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An 8-year-old boy was admitted to the Pediatric ward with high fever and severe arthritis of 4 days duration. Chikungunya virus serology was positive. As he became afebrile one week after admission, he developed acute onset right sided hemiparesis and suffered from one episode of generalized tonic clonic seizure. The next day he developed flaccid quadriplegia, loss ot all sensory modalities below the C5 dermatome and urinary retention. After4 weeks of shock stage, spasticity appeared in all 4 limbs. Magnetic resonance imaging (MRI) brain and spine showed extensive areas of demyelination-suggestive of acute disseminated encephalomyelitis (ADEM). He was treated with intravenous methyl prednisolone for 5 days, followed by oral prednisolone for 6 weeks. He was left with gross neurodeficits, including confinement to a wheel chair, persistent sensory loss and need for bladder catheterization.

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Demyelinating Disorders of the CNS

Cited by 3 publications

References 40 publications

ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases

ACAID as a potential therapeutic approach to modulate inflammation in neurodegenerative diseases

Learning from other autoimmunities to understand targeting of B cells to control multiple sclerosis

Acute disseminated encephalomyelitis in a child with chikungunya virus infection

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