Question

Alexa is a 25 year old graduate student who arranged an urgent appointment with her primary care provider because her ‘vision is blurry’ in her left eye. She states that two days ago her vision changed. She compares her visual field to looking through a fogged up window. Her provider interprets this to mean she has a decrease in contrast and brightness. Eye examination reveals a marked reduction of visual acuity of her left eye. A swinging flashlight test reveals an afferent pupillary defect (Marcus Gunn pupil) of her left eye (i.e., paradoxical papillary dilatation in response to increased light). Visual acuity and pupillary responses in her right eye are normal. Assessment of the retina and retinal vessels in both eyes is normal. Additional findings show patchy but consistent hypoesthesia (decreased feeling) to pin and light touch over her right limbs. On questioning, Alexia states that she experienced a self-limiting episode of numbness and tingling a few months ago. She also states that she has been experiencing fatigue, particularly at the end of the day. She denies depression, and her family history is unrevealing. The remainder of the physical exam in normal. Alexa is referred to an ophthalmologist who diagnoses optic neuritis (inflammation of the optic nerve). She begins corticosteroid treatment, and is referred to a neurologist who schedules a cranial MRI with gadolinium. The MRI reveals the presence of multiple deep white matter lesions scattered throughout the brain, suggesting multiple sclerosis. A subsequent lumbar puncture and analysis of Alexia’s cerebral spinal fluid (CSF) is consistent with possible multiple sclerosis. Further work-up rules out other possible causes. Ultimately, the neurologist diagnoses Alexia with relapsing-remitting multiple sclerosis.

1.One phenomenon that may facilitate the appearance of autoreactive cells in multiple sclerosis is referred to as ‘molecular mimicry.’ What is molecular mimicry and how might an infection lead to such mimicry in multiple sclerosis?

Answer 1

One of the most important demyelinating disease of nervous system (CNS) in human is multiple sclerosis (MS). The disease may be very debilitating with vision loss, motor and sensory disturbances, and cognitive impairment. The clinical course may also gift as a relapsing-remitting disease path, a modern disease course, or a combination thereof. The etiology of MS is unknown. Though many viruses were shown to be related to MS, no person virus has ever been tested to be the reason of MS. In addition, MS is concept to have an autoimmune component. Molecular mimicry is one hypothesis placed forth which can reconcile the numerous pathology and etiology of MS. Molecular mimicry takes place when peptides from pathogens share series or structural similarities with self-antigens. Infection with diverse pathogens, every with its character molecular mimic to a CNS antigen.

Molecular mimicry, also called epitopic and antigenic mimicry, is one of the main theories that try to provide an explanation for why the immune system activates its very own frame in autoimmune illnesses such as multiplesclerosis

immune system uses to recognise a specific foreign invader, such as a selected virus or bacteria, additionally takes place within the frame’s very own tissue. Thus in addition to attacking the invader, the immune machine also mistakenly attacks its very own body giving rise to autoimmune illnesses.

The immune system will makes use of antigen presentation to helper T cells. B cells will not launch their antibodies or clone themselves unless they can giveto a helper T mobile with an equivalent receptor. When this kind of T cellular additionally recognises the epitope, it sends a signal to the B cell to activate itself. This is referred to as costimulation.

body's proteins are expressed inside the thymus. The immune system might then be loose to provide lymphocyes that focus on epitopes on those proteins, one protein in myelin, the insulating sheath around nerve cells in the brain, called Myelin Oligodendrocyte Glycoprotein (MOG), has been shown now not to be expressed within the thymus they are cross reactive epitope.