Immunology Flashcards
Explain what gene mutation is associated greatly with auto-immune disease
Gene mutation in FOXP3 can causes loss of T-reg cells so there is no control of activation of self-reactive T and B cells.
What are four environmental factors that can cause auto-immune disease?
Molecular mimicry
Intercurrent infections
Tissue damage
Super-antigens
Explain role of molecular mimicry is in autoimmune disease
cross-reactivity between ‘foreign’ antigens and self-antigens, molecular antigen looks a lot like self antigens hence you will start reacting to your own, acute rheumatic fever after strep infection)
Explain role of intercurrent infections is in autoimmune disease
Immune responses can potentiate ongoing autoimmune reactions, simply due to so many inflammatory mediators going around the body.
Explain the role of tissue damage in autoimmune disease
Release of previously hidden self-antigens, eye, testis or brain have antigens permanently hidden due to poor connection to lymphatic system, if self antigens are always hidden they are not available to train developing lymphocytes hence never kill auto reactive T cells.
Explain the role of super antigens in autoimmune disease
Bacterial super-antigens can activate T cells non-specifically, can activate every T cell going e.g. toxic shock syndrome.
Immunology of myasthenia gravis? What type of hypersensitivity reaction?
Type 2- Autoimmune disease in which auto-reactive antibodies (auto-IgG) bind with acetylcholine receptors on muscle cells.
Clinical presentation of myasthenia gravis?
Complaints are fatigue and progressive muscle weakness. Often first complaint is of drooping eye. Gets better with rest which is different from other diseases.
How do you diagnosis MG?
Laboratory Tests
Presence of anti-AChR IgG in serum
Repetitive nerve stimulation
Gradually reducing responses (smaller and smaller muscle response with each repetitive stimulus) indicates NMJ dysfunction
Treatment of MG?
Increase neurotransmission (first line treatment improve symptoms) Anti-cholinesterase agents (e.g. pyridostigmine)
Surgery (first line treatment, if indicated)
Thymectomy
Reduce autoimmune reactions (second line treatments)
Immunosuppressive drugs, corticosteroids