Immunology Flashcards
What is innate immunity?
Rapid first response to infection (0-96 hours).
No immunological memory.
Non-specific.
What is acquired immunity?
Slow in response to infection (>96 hours).
Immunological memory - subsequent responses are more powerful and faster.
Specific for each antigen encountered.
Self-regulating through regulatory T cells.
Can distinguish self from non-self and should only react against non-self.
Which immune cell responds to APCs presenting phagocytosed microbes?
T helper lymphocyte by responding to antigen in association with MHC class II that is present on APCs only.
Which immune cell responds to obligate intracellular microbes e.g. virus replicating within infected cells that are shielded from antibody?
T cytotoxic lymphocytes respond to antigen in association with MHC class I that is present on the majority of body cells.
Which immune cell responds to extracellular microbes?
B lymphocytes secrete specific antibodies that bind antigen and make them easier targets for phagocytes and complement.
What is autoimmunity?
The presence of adaptive immune responses against self-tissue/cells.
How do autoimmune diseases develop?
People have a genetic susceptibility to them and undergo an initiating event that causes a breakdown of self-tolerance and loss of immune regulation.
This causes activation of auto-reactive T and B cells leading to hypersensitivity reactions that cause either autoimmune phenomena or disease.
What environmental factors can trigger autoimmune diseases?
Molecular mimicry - cross-reactivity between non-self antigens and self-antigens.
Intercurrent infections - immune responses can potentiate ongoing autoimmune reactions.
Tissue damage - release of previously hidden self-antigens.
Superantigens - bacterial superantigens can activate T cells non-specifically.
What is the immunological basis of myasthenia gravis?
Auto-reactive antibodies (auto-IgG) bind with postsynaptic acetylcholine receptors on muscle cells which induce T-helper-cell-mediated destruction of them.
These antibodies block binding of endogenous ACh to the receptors -> defects in nerve impulse transmission at NMJ.
Antibody-bound receptors are eventually internalised and destroyed, reducing number of AChR at NMJ.
AChR antibodies bind complement, leading to destruction of muscle endplate (type II hypersensitivity).
What is early onset myasthenia gravis associated with?
Increased adaptive immune responses in the thymus.
What is the treatment for myasthenia gravis?
Anti-cholinesterase agents - increase neurotransmission.
Immunosuppressive drugs, corticosteroids - reduce autoimmunity.
Plasmapheresis - reduce autoimmunity.
IV immunoglobulin - reduce autoimmunity.
Eculizumab - reduce autoimmunity; terminal pathway complement inhibitor.
Surgery - thymectomy.
What is the immunological basis for rheumatoid arthritis?
Type IV hypersensitivity response.
Infiltration of synovium by self-reactive CD4+ T cells.
Secondary involvement of activated B cells and auto-antibodies.
What is the management of rheumatoid arthritis?
Decrease inflammation.
Reduce B cell proliferation.
