WEEK 10: 10.7 Autoimmunity & Hypersensitivity Flashcards
(17 cards)
Define hypersensitivity reaction
an inappropriate/exaggerated response to an antigen
What is the consequence of a hypersensitive reaction
over inflammatory response (acute/chronic) and destruction of innocent cells
What are the 4 types of hypersensitivity reactions, differentiate them based on name, onset of symptoms, antigen, Ig isotype, effector cells and examples
Immediate: 2-30 min, allergen, IgE, Mast cell, asthma/allergic rhinitis
Cytotoxic: 12-24 h, particulate antigen cell, IgM & IgG, ADCC, transfusion reactions/anemias
Immune complex: 24-36 h, soluble antigen (proteins), IgM & IgG, neutrophils and macrophages, rheumatoid arthritis
Delayed type hypersensitivity: >72 h, haptens/bacteria, no Ig isotype, T cells & macrophages, granulomatous diseases
Describe what kind of reaction type 1 is
atopic- predisposed toward generating high levels of IgE due to a complex combination of genetic and environmental factors
Why is there a predominance in IgE antibodies in type 1
the immune system of atopic patients are skewed to produce IL-4 and IL-5 cytokines in response to allergens
What do the granules contained within mast cells contain?
powerful pharmacologically active mediators that cause rapid symptoms to appear
Briefly describe asthma as a type 1 hypersensitivity reaction?
Asthma is a form of type 1 HS taking place deep in lung, eosinophils play a major role in the response, chronic inflammation results in permanent tissue damage and remodeling
What are treatment options for type 1 HS
avoidance
blocking of the histamine receptor
puffer
monoclonal antibody therapy
desensitization program
What kind of mechanism is type IV hypersensitivity reaction
cell-mediated:
t helper and macrophages
no antibody involvement (no immunoglobulin)
what is an example of type IV
contact dermatitis (poison ivy)
How does a granuloma form for type IV?
antigen is persistent
DTH becomes prolonged and chronic
hyperactivates macrophages to fuse and adhere
granuloma forms
How are TCR and BCR made sure to not recognise self antigen?
through screening
For TCR and BCR, what happens if they bind to self antigen?
they are apoptosed
What happens if TCR and BCR do not bind to self antigen?
TCR- lives and exits thymus, released into circulation (blood and lymph)
BCR: lives and exits bone marrow, released into circulation (blood and lymph)
Where are TCRs generated
in thymocytes
What is autoimmune disease caused by?
A breach in screening process that causes T and B cells that recognise self to escape, and causes self-reactive lymphocytes to be released into circulation, causing autoimmunity
Give me one example of autoimmunity
type 1 diabetes mellitus, in which the self antigen is pancreatic B cells, and the immune effector is auto antibodies and Th cells
