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Flashcards in L10 - Immunol disease overview COPY Deck (18)
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i) give two reasons why the immune system may fail to control infection?

ii) give two ways that the immune system maay cause disease directly 

iii) who proposed a system to classify immunol mediated disease? what mechanisms does the classification refer to?

i) pathogen factors have evasion mechanisms
- host factors eg immundeficiency

ii) imm sys can directly cause disease by failure of tolerance (allergy/autoimm)
- or inapprop activation eg IBD/asbestos

iii) Gell and Coombes
- refers to immunol processes that are all normal functions but are inappropriately activated 



i) what is the mechanism of a Type I hypersensitivity reaction?what Ig is involved? give two examples

ii) what directly causes disease in Type II hypersens? give two examples

iii) what causes disease in Type III hypersens? give three egs

iv) which cells is inflammation directly mediated by in Type IV hypersens? give two examples 

i) type I - IgE antibody directeed against an allergen triggers mast cell degranulatin 
- seasonal rhinitis and cat allergy

ii) type II - pathogenic antibody directly causes disease
eg autoimmune haemolysis and haemolytic disease of newborn

iii) antibody-antigen complex causes disease
eg serum sickness, hypersens pneumonitis, SLE

iv) type IV - inflamm is directly mediated by T cells 
eg contact dermatitis and tuberculin reaction



i) which Ig mediates this reaction? which cells class switch to allow this?

ii) what process involving the Ig antibody and antigen activates mast cells? 

iii) what do mast cells release on activation? (2) what does this lead to in the affected organ? what is this believed to aid in health?


i) IgE 
- B cells class switch > secrete IgE which is taken onto surface of mast cells and basophils

ii) cross linking of allergen spec IgE antibody by allergen activates the mast cell

iii) mast cells release histamine > symptoms in affected organ
- in health - assist in parasite immunity 



i) what is this mediated by? give an example

ii) which antibodies to AB antigens on blood cells develop in first year of life? what type of antibody are these an eg of?

iii) where are these antigens also found apart from on red cells? how does the immune system respond to this?

iv) complete diagram 

i) mediated by antibodies eg mismatch of blood types in blod transfusion 

ii) develop IgM antibodies to antigens on blood cells
- eg of isoantibodies 

iii) body develops antibodies to antigens on gut bacteria that are also found on red cells 

iv) 1 - anti B
2 - anti A 



i) what type of hypersensitivity reaction is this?

ii) what is the D antigen?

iii) are the majority of the population D+ or D-? will they have anti-D antibody?

iv) give two instances where a mother may be sensitised to foetal red cells during pregnancy?

v) when may anti-D to fetal cells cause disease?

i) type II hypersensitivity 

ii) D antigen is found on the surface of RBCs

iii) most people are D+ so wont have Anti -D antibody

iv) mother can be sensitised during birth or trauma

v) anti-D may cause disease in subsequent pregnancies if baby is rhesus positive - antibods cross placenta and cause disease in baby 



i) how can this disease be described? name three consequences for thee baby?

ii) what resus status mother and partners are given Anti-D igG during pregnancy?

iii) what does giving anti-D do? at what week is it given? name three other events it may be given after?

iv) what does giving anti D reduce the risk of maternal sensitisaton from and to?

v) what type of immunisation is this? 

i) autoimmune haemolysis 
- growth retardation, CV failure, neurotox from high bilirubin levels 

ii) rh- mother and rh+ partner - usually given at 28 weeks
- binds to fetal cells entering circulation and prevents sensitisation and production of antibodies
- also given post accident/miscarriage/surgical delivery 

iv) giving anti D reduces risk of maternal sensitis from 16% to 0.1%

v) passive immunisation 



i) what type of hypersensitivity reaction is it?

ii) what happens in relation to macrophages? (extravascular) (3)

iii) what triggers intravascular AH?

iv) give two clinical signs 

i) type II

ii) spontaneous form antibodies against red blood cells
- antibodes bind RBC
- macrophages see opsonised red cell and destory it

iii) intravascular AH can be triggered by activating complement

iv) anaemia and jaundice 



i) what is it caused by? is this a physiological process?

ii) what happens to cause a type III hypersens reaction? (3)

iii) name four situations that may cause this reaction 


i) caused by complexes of antibody and antigen 
- this is physiological and happens all the time but usually soluble and removed by the spleen

ii) in a reaction - the complexes become insoluble, deposit in capillaries and cause disease 

iii) large quantity of antigen, large quantity of antibody, interac bet antigen and antibod is v strong, complexes are of a certain size 




i) what type of hypersensitivity reaction is it?

ii) what happens? why?

iii) name two conditions it may be seen in 

i) type III

ii) painful lesions in the fingertip pulp due to depos of circulating immune complexes
- local inflammation and necrosis

iii) may be seen in infective endocarditis (oslers nodes) and SLE 



i) what type of hypersensitivity reaction is it? what is it mediated by?

ii) what does it mainly result from? give an example of this?

iii) name four symptoms 

iv) is it transient or permanent?

i) type III
- mediated by immune complexes 

ii) results from injection of non humanised immunogenic drugs/anti sera produced by animals eg after a snake bits 
- inject venom to animal to raise high affinity IgG antibodies to venom > purify and inject 

iii) rash, fever, arthritis, glomerulonephritis 

iv) transient - once serum is cleared it will go away 



i) what is it also known as? what type of hypersensitivity reaction is it?

ii) what happens? what type of Ig is produced?

iii) where do immune complexes form? what does this cause (2)

iv) name two causative organisms

v) is it transient or permanent? what can occur if it repeatedly happens?

i) extrinsic allergic alveolitis
- type III hypersens reac 

ii) patient becomes sensitised to an environmental allergen by repeated exposure > prod large amounts of IgG antibod

iii) immune complexes form in the lung upon re-exposure
- causes shortness of breath and cough 

iv) caused by mould spores in hay (farmers lung) and pigeon feathers/stool

v) transient but get lung scarring with repeated exposure 



i) what type of hypersensitivity is it?

ii) what are reactions mediated by?

iii) how long does it take for the reaction to develop? why?

iv) what is it known as in the skin?

i) delayed type hypersensitivity 

ii) reactions mediated by antigen specific effector T cells

iii) takes at least 24hrs to develop as it takes time to process and present the antigen

iv) contact dermatitis in skin 



i) what type of agent is the sensitising agent? give two examples

ii) what does the agent react with and what is created? which cells mediate this?

iii) what is haptensiation? which cells process and present antigen on MHCII?

iv) how do some individuals respond to these complexes? which cells are activated and where do they travel?

i) highly reactive small molecules that can penetrate the skin
eg nickel and molecules in perfume/cosmetics

ii) agents reacts with self proteins to create a protein-hapten complex > picked up by langerhans cells and migrate to regional LNs

iii) haptenisation is when hapten (small molecule) cant produce an immune response by itself byt can bind to a protein to alter its immunogenicity
- langerhans cells process and present complex on MHC II in LNs

iv) some individuals recognise the complexes as foreign
- this activates T cells > migrate to the dermis 



i) when does this process occur? 

ii) what happens in terms of hapten and langerhans cells?

iii) what is already found in the body? what is subsequently released to cause a reaction?

iv) name three ways the body reacts (3) 

v) how can contact dermatitis be tested for? how long does it take for results to be read?

i) when the antigen is met again

ii) agent penetrates the skin > haptenisation > taken up by langerhans cells and presented to a T cell

iii) pre formed Th1 cells that produce IFNy > reaction

iv) cytokines such as IFNy and chemokines cause 
- inflammation, vasodilation and infiltration of inflammatory cells 

v) antigen impregnated patch test placed on back 
- impreg with nickel, chrome, cobalt, epoxy etc
- results read after two days as its a delayed hypersens reaction



i) what type of hypersensitivity reaction is this an example of? what is it used to determine?

ii) what happens in the test? 

iii) what happens if there has been previous exposure to MTB? how long does this take to develop? why?

iv) which cells mediate the reaction?

i) type IV hypersens reaction
- used to determine previous exposure to TB

ii) tuberculin (mixture of antigens from MTB) is injected intradermally 

iii) if prev exposure > local inflam response over 24-72 hours
- takes up to 72 hours as its a delayed response that involves T cells 

iv) Th1 cells mediate reaction 



i) what happens to the tuberculin once its injected to the skin? 

ii) what type of cells is it recognised by if there has been previous MTB exposure? what happens in this case? (2)

iii) what happens if there has been no prev exposure to MTB?

iv) is this a specific or non specific test? why?

i) tuberculin is processed by local APCs and presented

ii) if there has been previous MTB exposure then it will be recognised by Th1 cells
- get inflammation and recruit phagocytes

iii) no prev exposure = no reaction as wont have Th1 cells

iv) non specific test has tuberculin has cross reactivity with non TB mycobacteria eg found in soil 



i) how is the test set up? which two MTB peptides are used?

ii) if there has been previous TB expsoure - what happens? if there has not been previous exposure - what happens?

iii) which lab technique is then used? 

iv) what is the plastic well of the dish coated with? what is added? if there has been exposure to TB - what happens? 

v) what is the final step? what does this allow?

vi) name another method that can be used for detection

i) MTB peptides added to blood in the lab
- use ESAT-6 and CFP-10 (unique to MTB)

ii) if prev TB expos > memory Th1 cells recog antigen and release IFNy in short time frame
- if no prev expos then no IFNy is produced in the short timeframe 

iii) then use ELISPOT
- plastic well coated with catcher antibod to IFNy
- add blood cells and peptide 
- if cells have produced IFNy then it will be captured by the antibody on the plate 

v) then add a secondary antibody as a marker to produce a colour change if IFNy has bound to antibody > see spots on plate 

vi) can also use ELISA method > look for concentration of IFNy produced 



i) name two pros

ii) is it useful in clinical practice?

iii) name a con

iv) name three diseases that are not well described in this framework? why?

i) only sucessful attempt to classify disease by mechanism
- useful framework to describe and understand diseases

ii) not very useful in clinical practice

iii) con - oversimplifies immunology (usually there are lots of components of the immune system involved) 

iv) Rheumatoid arthritis, chronic asthma, inflam bowel disease
- involve multiple immunol effector mechs that arent well described in this framework