When the immune system goes wrong Flashcards
what is immediate hypersensitivity and what is it mediated by
allergy
mediated by IgE, mast cells and Th2 responses
What is the immediate hypersensitivity response due to
mast cell degranulation and histamine release. If in skin->wheal and flare
What is the Th2 response to allergenic disease
pollen taken up by APC->processed and presented as peptides to T cell receptors on CD4->activation leads to Th2 response->B cell activated->class switch to IgE and differentiate to plasma cells->when pollen arives, binds to IgE on surface mast cell->potent activation of stimulus for mast cells which degranulates all of inflammatory mediators diffsued out into local areas->symptoms=sneezing, wheal+flare
Common diseases and therapies
Diseases-asthma, perennial rhiniitis, allergic eczema
Therapies-antihistamines, beta 2 adrenoreceptor antagonist, corticossteroids
Rare diseases and therapies
Disease: anaphylaxis
Therapies: desensitisation, monoclonal antibody
Autoimmunity what
loss of immunological tolerance to self components
What are the two types of autoimmune diseases and give examples of it
organ specific-type 1 diabetes, grave’s disease
non organ specific-rheumatoid arthritis, systemic lupus erythematosus
What is autoimmunity
Loss of immunological tolerance to self components
what are serum antibodies used for
diagnostic tool, monitoring disease activity, predicting future disease, may be pathogenic
(usually IgG class)
What is the proof of autoimmunity
Passive transfer of disease by immune effectors (e.g. T cells, antibodies)
Clinical responsiveness to immune suppression or reestablishment of tolerance
How does grave’s disease work
usually thyroxine act as feedback to prevent excess TSH but thyroid gland keep making thyroxine in unregulated way->hyperthyroidism->bulging eyes, fast heart rate, weight loss, hyperactivity
How does myasthenia gravis work
patients develop autoantibodies against ACh receptor->damage receptor->transmission impaired, insufficient engagement with ACh receptor-> no or poor contraction causing muscular weakness and fatigue
How can autoantibodies be passed on from mother to child
if mother has grave’s disease, IgG antibodies against TSH receptor passed onto child. Same with myasthenia gravis
How is type 1 diabetes T cell mediated
B cell autoantigens taken up by APC and presented to CD4->activation of Th2->mediate inflammation
B cell present autoantigen directly to CD8->kills B cell
Failure Treg to suppress
Are primary and secondary immunodeficiencies inherited/acquired and are they rare/common
primary=inherited defect=rare
secondary=acquired defect=common