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Flashcards in Session 1 Deck (41):

Goodpasture’s syndrome

Systemic lupus erythematosus

Myasthenia gravis

Rheumatoid arthritis

Graves‘ disease

Haemolytic anaemia



The term hypersensitivity describes? (HE SAID THIS WILL COME UP IN THE EXAM) 


the antigen-specific immune responses that are either inappropriate or excessive  and result in harm to host

excessive e.g. Type 1 allergies 

mechanisms -> those used to fight infections

hypersensitivity reaction driven by innate -> septic shock 

hypersensitivity driven by adaptive (what we will discuss today)



What are the triggers for hypersensitivity reactions? 

Hypersensitivity to exogenous antigens

-Non infectious substances (innocuous) e.g. allergens

-Infectious microbes e.g. infective endocarditis

- Drugs (Penicillin)

Hypersensitivity to intrinsic antigens (autoimmunity lecture - more difficult to treat)

- Infectious microbes (mimicry) (when you are infected mount a immune reaction to foreign antigens and self antigens/cells)

- Self antigens (auto-immunity) (no known cause yet !!!! In exam)



Types of hypersensitivity reactions

What is the different between them all 

• Type I or immediate (Allergy)
• Environmental non infectious antigens 

• Type II or antiBody mediated 

• Type III or immune Complexes mediated 

• Type IV or cell mediated (Delayed)
(Environmental infectious agents and self antigens)

Type 1,2,3 are antibody 

Type 1 is IgE 

Tpe 2 cell antigen 

Type 2 & 3 and IgM and IgG

Type 2 cell antigen bound vs type 3 soluble antigen 


Common feature of hypersensitivity reactions



• Sensitization phase

First encounter with the antigen. Activation of APCs and memory effector cells. A previously exposed individual to the antigen is said to be “sensitized.”

• Effector phase

Pathologic reaction upon re-exposure to the same antigen and activation of the memory
cells of the adaptive immunity.

Can’t have a hypersensitivity reaction in the first encounter ->  you will have antigen specific antibody & antigen specific T cells. 



Type II hypersensitivity

Give the most 4 important facts and examples if they have any 


• Usually develops within 5-12 hr

• Involves IgG or IgM antibodies 

• Targets cell bound antigens

Exogenous: Blood group antigens, Rhesus D antigens 

Endogenous :  self antigens

• Induces different outcomes:

Tissue/cell damage 

Physiological change


Type II hypersensitivity : mechanisms


Individual already sensitised because it has the antibody 
Antibody will bind to trigger
Will activate the complement pathway 
Activate cell lysis membrane attack complex 
Recruit neutrophils - release toxins 

Innate cell called NKC bind to the antibody by the FC receptor and release toxins/ radicals on the target cells 


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Type II hypersensitivity : importance of complement pathways


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An example of disease caused by type II hypersensitivity (IgM)


Haemolytic transfusion reaction

• Life-threatening condition

• Shock, kidney failure, circulatory collapse, and death

Immune mechanism

• Incompatibility in the ABO group or rhesus D antigens

• Donor RBC destroyed by recipient’s immune system

• RBC lysis induced by type II hypersensitivity involving by the naturally occurring antibodies (IgM)

If you are blood type A natural autoantibody against b antigen is IgM 


An example of disease caused by type II hypersensitivity (IgG)


Mother does not have Rhesus factor 
Rh+ antigens from the fetus gets transported to the mother from the blood i.e. in birth -> mother becomes sensitised (antigen on the cell membrane and this is antibody mediated thus is type 2) -> mother becomes pregnant again now in the effector phase ->EFFECTOR PHASE  re exposure mother now has memory cells (can produce antigen) -> complement activation & Ab dependent cytotoxicity -> rhesus haemolytic disease of newborn -> maternal IgG can get to the baby via the placenta (only IgG can cross the placenta) within 72 hrs of delivery must give RHOGAM IgG against Rhesus factor -> bind to fecal RBC and prevent them from lysis and prevent the fecal RBC from sensitising the mother  

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Type II hypersensitivity : mechanisms


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Type II hypersensitivity : therapeutic approaches know for exam



E.g. prednisolone but stone side effect profile  

Humour always or spleen macrophages problem wont make distinction if antibody is bound to a microbe or a self cells.g. RBC or platelet with destroy everything - e.g. autoimmune haemolytic anaemia  

Immunodeficiency and now for autoimmune disease MOA unknown -> one thought  

Is something is missing you restore it or if something is excessive you reduce it 

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Type II hypersensitivity : Plasmapheresis therapy


explain what it is and what it is used for

Myasthenia gravis

Goodpasture’s syndrome

Grave’s disease

Plasma is discarded and patient is given substitution fluid -> removal of autoantibody 

Short term relief and allows healing of damaged tissue



Give 4 facts about Type III hypersensitivity


• Usually develops within 3-8hr

• Involves immune complexes between IgG or IgM and antigens

• Targets soluble antigens

- Foreign (Infection)

- Endogenous (self antigens)

• Tissue damage caused by immune complex deposition



Type III hypersensitivity : key factors affecting IC pathogenesis

- People with low affinity antibodies more likely to produce immune complexes 

-Immune complexes can activate complement 
C3b can bind to this complement 
RBC have C3b receptor and can bind to the complement and take it to the kupffer cells in the liver to be destroyed
Patient deficient in C2 & C4 have deficiency of C3b (c3 convertse). cannot remove complexes that well 
 T3 hypersensitivity reaction  

Pressure, filtration, which favour immune complex deposition 

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Type III hypersensitivity : Immune mechanisms 

Easily cleared large by complement C3b bind to RBC and taken to liver and destroyed
Small can be phagocytosed by macrophages, monocytes

Intermediate ones deposit, when the deposit they activate compliment C3b binds to tissue opsonisation of tissue C£a chmoattraction of neutrophils 
When neutrophils come binds to the tissue -> degranulation 

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Examples of diseases caused by type III hypersensitivity


Rheumatoid arthritis (self antigen)

Glomerulonephritis (infectious)

Systemic lupus erythematosus


Rheumatoid arthritis (self antigen)

Glomerulonephritis (infectious)

state what the antigen is in both of them and features of each and prognosis for RA 

Fc portion of IgG in the host (this is acting like an antigen) 
The antibody against this is IgM 

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Systemic lupus erythematosus

state the antigen and who and what it effects 


• Antigen = Ds-DNA

• Most prevalent immune complexes disease 

• Ratio female:male (9:1) 

• 40-60% patients with cardiac, respiratory, renal, joint & neurological features 

• Repeated miscarriage 

• Every patient is unique!!!!!!


Type IV hypersensitivity

State when it develops

What it involves

The different subtypes 


• Usually develops within 24-72hr

• Involves lymphocytes & macrophages 

Different subtypes

Contact hypersensitivity (48-72 hr)

- Epidermal reaction (eczematous rash)


Tuberculin hypersensitivity (48-72hr)

- Dermal reaction (induration and swelling)


Granulomatous hypersensitivity (21-48 days)

- Persistence of the antigens (tissue damage) 

- Wall off the infected cells


Low molecular weight antigen, that needs to bind to a host protein to illicit an immune response - Mostly in the epidermis only when they bind to host protein when they drive the hypersensitivity reaction 

T cell have come in contact with TB Positive TST positive for both  IRN positive for latent

 Most severe form will induce tissue damage usually an antigen which persists inside the body
Microbe persists inside the body way to seal of the cells but will be tissue destruction 
TB, sarcoidosis, Chrons microscopic 
Chronic granulomatous disease In this genetic condition phagocytes are unable to generate the free radical superoxide.  Bacteria are phagocytised but the phagocytes cannot kill them as they can’t generate an oxygen burst.  This results in many  chronic  infections in the first year of life.  Numerous granulomas (these will be described in the next session on chronic inflammation)  and  abscesses  affecting the skin, lymph nodes, and sometimes  the  lung, liver and bones occur, however they are ineffective at eliminating the infectious agents.

Depends on the organ involved[2]
Lungs: wheezing, cough, shortness of breath, chest pain


Type IV hypersensitivity : mechanisms of tissue destruction


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Diseases caused by type IV hypersensitivity to exogenous antigens


Granulomatous hypersensitivity:

• Tuberculosis • Leprosy (tuberculoid) • Schistosomiasis • Sarcoidosis

Contact hypersensitivity:

• Nickel • Poison ivy • Organic chemicals



Type IV hypersensitivity :
Give two examples of where it is used as a determination of the sensitization status


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1. What is this image showing?

2.Diseases caused by Type IV hypersensitivity to endogenous antigens?


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1. Type IV hypersensitivity :Granulomatous hypersensitivity

2. • Autoimmune disease

• Pancreatic Islet cells: Insulin-dependent diabetes mellitus

• Thyroid gland: Hashimoto’s thyroiditis

• Involvement of CD8+ T cells & antibodies

• IgG: rheumatoid arthritis (IgG)



Hashimoto’s disease (IV) versus Graves’ disease (II) MOA 


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Type III and IV hypersensitivity : Therapy



Anti-inflammatory drugs 

• Non-steroidals 

• Corticosteroids (oral prednisolone) 

• Second drugs as steroid-sparing agents (<10 mg oral steroid)

- Azathioprine (anti-proliferative immunosuppressant - antimetabolite)

- Mycophenolate mofetil 

- Cyclophosphamide (anti-proliferative immunosupressants - alkylation agent )

Monoclonal antibodies
• B Cells and T cells
• Cytokine network
• APCs

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Systemic manifestations of allergic reaction: anaphylaxis

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What is type 1 hypersensitivity? 

Not a disease is a mechanism 

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Type I hypersensitivity : Examples of allergens


Perennial- lasting long 

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Type I hypersensitivity : mechanisms



Should drive the TH1 response  not allergic resuts in IgG4 not a problem 
TH2 response -> b -cells produce IgE


IgE binds on surface of mast cell
Does not differentiate between harmless or not harmless Just works when IgE bound 
Lung asthma


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Why do people have allergies?


Large family everyone gets sick 
Rural home different animals and bacteria
Intestinal micro flora diversity in micro flora eat a variety of food 
Low antibiotic usage


1 of your parents 13% 

both 17% 

genetic susceptibility = atopy

- alter normal flora diversity -> DYSBIOSIS 


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Give examples that result in loss of microbiota diversity/dysbiosis 

C - SECTION x8 likelihood of developing an allergy  


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Mast cell progenitor made in bone and matures in bone

STEM CELL FACTOR important for survival

where are their strategic locations?

Strategic location
• Most mucosal and epithelial
tissues = gastrointestinal
tract, skin, respiratory
epithelium • In connective tissue
surrounding blood cells



Skin manifestation of allergic reactions and cause? LO 


Urticaria -> mast cell activation within the epidermis

Mediators = Histamine and leukotrienes/cytokines

If prolonged and chronic exposure = atopic dermatitis and eczema

raised erythema 


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Faces manifestations of allergic reactions? Cause? Mediators? Location of mast cells/effects which regions?



Caused by mast cell activation in the deep dermis

Mediators = Histamine and bradykinin

lip, eyes, tongue and upper respiratory airways


What is anaphylaxis 

Systemic manifestations of allergic reaction: anaphylaxis -> life threatening 



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Signs of anaphylaxis 

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1. Give examples of other allergic diseases 


Food allergies, asthma 

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Type I hypersensitivity : therapy

explain what the first one is and how it works 

Allergen desensitization or immunotherapy

“It involves the administration of increasing doses of allergen extracts over a period of years, given to patients by injection or drops/tablets under the tongue (sublingual)”

90% effective in patients with bee and wasp venom anaphylaxis

Potential mechanisms:

• CD4+CD25 Regulatory T cells

Shift from TH2 to TH1

• Inhibitory anti-inflammatory cytokines

Allergen specific blocking IgG


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• Type I hypersensitivity reactions are involved in a number of disorders

• A ? are considered as important factors for the development of allergic diseases

The immunological mechanisms involve a ?

• ? of antigen-specific IgE on mast cells represents the main trigger of the clinical manifestations of the allergic disorders

• Oral immunotherapy and anti-IgE represent both promising therapies for the treatment of anaphylaxis


reduced infectious burden coupled to changes in the microbial dysbiosis (environment)

TH2 response and the production of IgE against innocuous antigens