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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is the definition of hypersensitivity?

A

Excessive, undesirable reactions produced by the normal immune system

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2
Q

Who made the 4 types of hypersensitivity classification?

A

Coombs-Gell

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3
Q

Which one is an immediate hypersensitivity?

A

1

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4
Q

Which one is a distinct/delayed hypersensitivity?

A

4

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5
Q

Which hypersensitivity is triggered by antibody molecules (humoral immune response)?

A

1,2,3

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6
Q

Which hypersensitivity is triggered by T cells (cell immune response)?

A

4

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7
Q

Which antibody is most in type 1 hypersensitivity?

A

IgE (allergic)

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8
Q

What is the process of hypersensitivity 1?

A

Antigen met -> make IgE (instead of IgG)
crosslinking antigen w/ receptor and mast cell
mast cell + basophil make histamines + leukotrienes

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9
Q

What are the 4 phases of hypersensitivity 1?

A

Sensitization phase -> activation phase -> effector phase -> late stage phase

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10
Q

What is atopy? What is it caused by? Which exposure do you feel symptoms? best example?

A
  • Allergies
  • caused by: family tendencies + genetic predisposition
  • second exposure
  • hay fever
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11
Q

How do allergens enter?

A

Skin, Ingestion, Injection + Inhalation

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12
Q

What is the sensitization stage?

A

1st time: inject guinea pig -> make IgE but no primary response

2nd time: inject guinea pig -> allergen cross link IgE on cell surface -> neutrophil -> anaphylaxis + vasodilation (low BP) + bronchoconstriction

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13
Q

What is activation stage?

A
  • Allergen internalized by APC
  • APC breaks it down –> presents it with MHC class 2
  • this will then be recognized by T cell receptor
  • clonal expansion + differentiation (make TH0 -> TH2)
  • TH2 produce IL4,5,9,13
  • These Cytokines makes IgM to IgE
  • IgE will then bind to mast cell to Fc receptors
  • the allergen bind to IgE through antigen binding site (2 Ab bound to 1 antigen must happen)
  • binding= degranulation of mass cell
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14
Q

In activation stage- how many IgE should bind to an antigen molecule?

A

2

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15
Q

What is effector stage dependent on?

A

Method of allergy entry

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16
Q

Effector stage- what happens if it is in GI? lung? blood vessels?

A

If it enters GI… diarrhea + vomiting

If it enters lung… airway constriction + mucus hypersecretion + coughing + wheezing + phlegm

If it enters blood vessel… edema + > blood flow + > vascular permeability

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17
Q

What are preformed mediators + new molecules made in effector stage?

A

preformed: Histamine + eosinophilic chemotactic factors + IL8
new molecules: Leukotrienes + Prostaglandins + Platelet-activating factor

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18
Q

What is late stage?

A

24-48 hours later. (can last a few days)

Recruitment of eosinophils and neutrophils

19
Q

How to stop anaphylaxis?

A

Epi-pen

20
Q

What do these cytokines do in hypersensitivity 1: IL 4,5,6,13 + TNF

A

IL 4 + 13: Make TH2 cell + switching to make IgE
IL 5: Maturation, chemotaxis, activation + survival of eosinophil (prepare basophil for histamine + leukotriene release)
IL6: Mucus production
TNF: Pro-inflammatory cytokine= activate neutrophil + eosinophil + > monocyte chemotaxis

21
Q

What is clinical aspect of allergies?

A
  • Allergic rhinitis
  • Asthma
  • Atopic dermatitis
  • Food allergies
22
Q

How to detect allergies? Which way is qualitative and which is quantitative?

A

ELISA – checks IgE (quantitative)

SKIN PRICK TEST- wheal + flare reaction (arm or back) -> prick individual with all different allergens -> then you see erythema + edema (qualitative)

23
Q

What is the 4 ways to help to type 1 hypersensitivity?

A

Desensitization: instead of making IgE we teach it to make IgG -> you do this by therapy by small doses of allergen -> not 100% effective (should be controlled)

Monoclonal antibodies IgE (so we make an Ab to stop IgE so no cross linking occurs)

Bronchodilators

Avoid allergens

24
Q

What is the hygiene hypothesis?

A
  • The dirtier you are -> the less allergies you get

* You are exposed CONSTANTLY -> so you teach immune system to not react at everything

25
Q

What is Th1 vs Th2 balance in type 1 hypersensitivity?

A

> Th2

26
Q

What is type 2 hypersensitivity antibody?

A

IgG (can cross placenta)

27
Q

What is type 2 example?

A

hemolytic disease of newborn

28
Q

What is type 2 mechanism?

A

o Antibodies bind to self antigen on cell membrane
o This activates cascade (classical)
o Cell undergoes lysis
o Opsonization occurs by macrophage + C3b
o This leads to severe damage

29
Q

What is type 2 transfusion reaction?

A

Type O blood has anti a and anti B
If a type O is transfused with type A blood
IgM in blood of type O recognize donor blood -> activate complement -> lysis of RBC

30
Q

What Rh incompatibility/ Erythroblastosis fitalis or hemolytic disease of the newborn?

A

If mother is Rh- + fetus is Rh+
At first birth mother will make Ab that is against Rh antigen -> make IgG
In second pregnancy -> IgG cross placenta
IgG coat fetal cell -> opsonize it.
Destoy fetus + new RBC + hemoglobin

31
Q

What is cure for Rh incompatibility/ Erythroblastosis fitalis or hemolytic disease of the newborn?

A

Pregnancy: Inject mother with Anti-Rh Ab shortly before delivery (26-28 weeks)-> prevent sensitization (should be IgM)

After birth: give for 72 hours after delivery

Therapy: Rhogam -> makes IgM instead of IgG + bind to D antigen

32
Q

What is ABO hemolytic disease of newborn? Is it as severe as Rh incompatibility?

A

Less severe than Rh incompatibility
Fetal RBCs express less ABO antigens compared to adult
ABO antigens are expressed on a variety of fetal cells reducing the chance of antibodies binding to antigens

33
Q

What is type 3 hypersensitivity? is it systemic/localized? is it endogenous/ exogenous? At what time does the reaction start? What is the treatment? Which antibodies found here?

A
  • Fc of antibody binds to phagocytic cells + RBC -> go to liver and get phagocytosed and destroyed
  • is both systemic + localized
  • both endogenous (SLE) + exogenous
  • 3-8 hours after exposure (arthus reaction)
  • anti-inflammatory agents
  • IgG + IgM
34
Q

Where is immune complex deposited in type 3? What do lesions contain?

A

kidneys, joint, skin + blood vessels

PMN (macrophage), deposits of immune complex and complement

35
Q

What is the mechanism of hypersensitivity 3?

A
  • Immune complex formed
  • C3a + C5a made (classical pathway)
  • > vascular permeability -> neutrophil come
  • Autolysis of neutrophil -> lysosomal enzymes release -> damage to the glomerular basement membrane
  • Immune complex activates complement cascade which activates basophils or mast cells
  • Mast cell + basophil -> Histamine + leukotrienes made -> activate platelet
  • vasoactomines released -> retraction of endothelial cells -> increase in permeability
  • Immune complexes get deposited on sites such as kidney or joints
  • Persistent inflammation
36
Q

What is problem with hypersensitivity 3 in size and in Integrity of mononuclear phagocytic complex?

A

Size of complex
o If big = easily removed by phagocytes
o If small = bind less avidity
Integrity of mononuclear phagocytic complex= Overload

37
Q

What is serum sickness? The process? The symptoms?

A

injection of foreign protein/ serum (Treatment of diphtheria and tetanus with antisera from horses)
Process: antibodies made for foreign Ig
Symptoms: Fever, pain in joint (arthralgia) + skin eruption

38
Q

What is arthus reaction? due to? process?

A
  • What: due to moldy hay -> respiratory distress
  • Due to occupation.
  • Process: IgG made against spores -> complex + inflammation in lung
39
Q

What is activated in type 4 hypersensitivity/delayed type hypersensitivity ? how long is this hypersensitivity?

A

T cell + chemokine + cytokine

48-72 hours

40
Q

What are the stages in type 4 hypersensitivity?

A

SENSITIZATION STAGE:
o Antigen enter -> recognized by T cell -> make TH1

ELICTION STAGE:
o TH17 + TH1 -> Pro-inflammatory cytokine made
o Recruit plasma cell + macrophage (non specific leukocytes)

41
Q

What is contact dermatitis target organ? characterized by? example + symptoms?

A
  • Target organ: skin
  • Characterized by: eczema
  • Example: Poison ivy dermatitis -> Urushiol penetrates the skin and form hapten-carrier conjugates -> Persists on the initial site of contact
  • Symptom: Blister formation + Mononuclear infiltrates + Separation of epidermal cells
42
Q

What is treatment for type 4 hypersensitivity?

A

Corticosteroids: topical or systemic

43
Q

Why do we have type 4 hypersensitivity?

A

Protective:
• Intracellular bacteria which does not respond to antibody production
• They grow inside macrophages
• Presented in association with MHC II
• Activate Th1 cells -> IFN-gamma, TNF, MAF
• Activate macrophages

Damaging:
• Chronic infection (tuberculosis, leprosy)
• Bacteria are slow growing (several years)
• Following inhalation, alveolar macrophages get activated
• Ag is presented and Th1 cells are activated
• Recruitment of macrophages
• Bacteria is not efficiently cleared which leads to granuloma
• Damage to the lung

44
Q

What is leprosy caused by? What are the 3 responses- normal, no response + hyper response?

A
  • Caused by: Mycobacterium leprae
  • If individual mounts normal response then there is a small lesion and infection is well controlled
  • If individual fails to mount response: a lot of bacterial growth, blebs are full of bacteria and can be transmitted
  • Hyper response: Hardly any bacteria BUT the response is so strong that there is damage to the nerve endings -> loss of fingers

Immunology (8 decks)

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