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Basic Immunology > Lecture 17 (10A) - Hypersensitivity > Flashcards

Lecture 17 (10A) - Hypersensitivity Flashcards

1
Q

Immune reactions in the body have by-stander effects on normal tissues

A

neutrophils gobble up and kill bacteria, but they also secrete toxic molecules

  • free radicals
  • tissue-degrading enzymes (elastase, collagenase)
  • cytokines
  • chemokines
  • defensins
  • -> cell death of healthy cell
  • -> tissue damage

• toxins that kill bacteria also kill normal cells (get inflammation)

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2
Q

Immunological hypersensitivity

A

hypersensitivity to innocuous antigens causes diseases
• Gell and Coombs classification still useful
• eg coeliac disease (hypersensitive to gluten)
• calssified immune response by what cause them - 4 types

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3
Q

Type I hypersensitivity

A

immediate hypersensitivity
• allergies AKA atopy
• hay fever (allergic rhinitis) and nasal allergies
• allergies increasing in developed world

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4
Q

CD4 T cells can differentiate along 2 pathways

A

Th0

presented IL-12 by APC
–> Th1
makes IFNγ, TNFα
–> excess macrphage activation, tissue damage

presented IL-4 by mast cell
--> Th2
makes IL-4, IL-5, IL-10
--> IgE, allergies
(IL-4 drives differentiation of B cells to make IgE - so allergic T cells = Th2)
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5
Q

T cells tell B cells what type of antibody to make

A
  • T cells make IFNγ = class switching from IgM to IgG2 or IgG3
  • T cells make IL-4 = class switching from IgM to IgG2 or IgE
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6
Q

Class switching to IgE is driven by

A

IL-4
• IL-4 causes looping out of DNA
• get VDJ + IgE

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7
Q

Serum IgE is often raised in allergies, but

A
  • you can be allergic with normal IgE
  • you can be not allergic with high IgE

• allergic patients don’t always have high levels of IgE

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8
Q

IgE secreted into serum binds to

A

surface of mast cells in tissues
• IgE molecule has FcεRI binding site, and mast cell has FcεRI receptor
• lungs, airways, skin, gut
• so it is sequestered on mast cells in tissues
• sucks IgE out of serum and puts on cells

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9
Q

Mast cells have lots of granules containing

A

pre-formed mediators
• flow cyto into mast cells
• high side scatter because lots of granules

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10
Q

What happens when IgE on a mast cell binds an antigen (allergen)?

A
  • allergen in, binds and cross links IgE
  • granules pop out of mast cell = immediate hypersensitivity

• Fcε signals to the cell to release granules

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11
Q

Mast cells release

A

histamines when the allergen is encountered
• also release serotonin
• allergic = take antihistamines
• very bioreactive to cells in the tissues –> mast cells with no granules left

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12
Q

Mast cell mediators

A
  • make blood vessels leaky - edema
  • vasodilation
  • cause smooth muscle contraction
  • urticaria
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13
Q

Symptoms of immune response

anaphylaxis = severe allergic response

A
  • anaphylaxis
  • loss of consciousness
  • hives
  • swelling of tongue, inability to swallow
  • rapid swelling of throat tissues
  • need epinephrine so muscles relax and can breathe
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14
Q

The sting of anaphylaxis

A

• anaphylaxis is the medical term for an allergic reaction
• the only treatment to an allergic reaction is the use of epinephrine and other treatments
- epinephrine can be self-injected or administered by a doctor
• often intravenous fluids, oxygen, and other treatments are necessary as well
• it is very important to call for medical assistance immediately

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15
Q

Interleukin-5 (IL-5)

A

draws eosinphils into tissues and blood

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16
Q

Eosinophils - stain with dye

A

eosin - and granues show up

• granules toxic to cells

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17
Q

Lung has no

A

exit - only 1 way in/out

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18
Q

Type I hypersensitivity is involved in some kinds of

A

asthma (allercig asthma)

• walls thinner, need steroids to relax it

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19
Q

Summary of an allergic Type 1
immediate hypersensitivity
response

A
  1. antigen (allergen) crosses mucosal lining
  2. onto APC
  3. through TCR induced to TH2 cell
  4. releases IL-4 –>
  5. makes B make IgE
  6. bind to mast cell
  7. cross links
  8. release of granules
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20
Q

Skin prick testing

A

inject suspected allergen into skin-wheal and flare reaction
• put an antigen in sin, have IgE and mast cells –> get reaction
–> skin swelling like happens in airways

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21
Q

How do you treat allergies?

type I

A
  1. avoidance
  2. anti-histamines, mast cell stabilizers
  3. omaluzimab-anti-IgE
  4. antigen-specific desensitization
    - dose they can tolerate goes up, give small amount of antigen, try to induce tolerance
    - immunosuppression mediated by regulatory/suppressor T cells
    (T cells suppress IgE responses)
22
Q

Type 1

A

antibody mediated hypersensitivity (IgE)
• type II is also antibody-mediated (IgM, IgG)
• type III is also antibody-mediated (IgG)

23
Q

Type II hypersensitivity reactions

A
  • also quick but not mediated by IgE
  • mediated by Igm and IgG natural antibodies in serum
  • also antibody-mediated
24
Q

Type II

Type O blood has natural antibodies to

A

A and B

but no A and B antigens

25
Q

Type II

Type O+ Rhesus negative

A

universal donor of red cells

26
Q

AB+

A

have A antigens
have B antigens
Rh cells

27
Q

Blood type O

A

antigen - no A or B

antibodies - anti-A and anti-B

28
Q

Blood A blood type

A

antigens - A

antibodies - anti-B

29
Q

Blood B blood type

A

antigens - B

antibodies - anti-B

30
Q

Blood AB blood type

A

antigens - A and B antigens

antibodies - no a or B antibodies

31
Q

When red blood cells with eg group A antigens on their membranes are mixed with plasma containing antibodies to group A

A

the antibodis cause the blood cells to clump, or agglutinate

give wrong type, get clumps of RBC - fingers fall off - because make antibodies against

32
Q

Hemolytic transfusion reaction

A 
• donor - blood type A
• recipient - type O with anti-A antibody
--> severe intravascular hemolysis
1. transfusion
2. agglutination and complement binding
3. hemolysis
33
Q

Type II hypersensitivity

Rhesus

A

Rh+ father with RH- mother carrying her first RH+ fetus
• Rh atigens from the developing fetus can enter the mother’s blood during deilvery
• in response to the fetal Rh antigens, the mother will produce anti-Rhh antibodies
• if the woman becomes pregnant with another Rh+ fetus, her anti-Rh antibodies will cross the placenta and damage fetal blood cells

baby Rh+
mothers Rh- –> make anti-rhesus antibodies
next baby –> kill baby’s RBC (anemia)

34
Q

Type III hypersensitivity

A
  • mediated by IgG antibodies and their specific antigen which form immune complexes
  • when they form in the skin after injection of the Ag-Arthus reaction
  • when they form in the blood and deposit in the kidneys and joints - serum sickness
  • also antibody-mediated - IgG
  • immune complex in skin - artnus, blood –> kidneys - serum sickness
35
Q

Type III hypersensitivity

antibodies in equilibrium with

A

antigen
• antibodies in equilibrium with antigen
• polyvalent antibody - multivalent antigen

• big agglutination (immune complex), antigen + antibody structure

36
Q

Type III forms

A

immune complex
• antigenic determinant sites on antigen, antibody binds

• IgG antibody as 2 arms/binding sites

37
Q

Immune complex disease

A

Immune complex disease

drug reactions
• allergies to penicillin and sulfonamides

infectous diseases
• poststreptococcal glomerulonephritis
• meningitis
• hepatitis
• mononucleosis
• malaria
• tyrpanosomiasis

• can make antibodies against antibodies

38
Q

Type III hypersensitivity forms immune complex deposition by

A

complement
• immune complex sticks to vessels
• neutrophils come

39
Q

Phases of Type III hypersensitivity

A

Phase I - immune complex formation
• antigen in circulation, B cell to plasma cell to antibody, antigen-antibody complex

Phase II - immune complex deposition
• inflammatory cell makes cytokines

Phase III - complex-mediated inflammation
• complement, neutrophil attacks the complexes, neutrophil lysosomal enzymes

40
Q

Type III hypersensitivity reactions

immune complex glomerulonephritis

A
  1. deposition of immune complexes
  2. activation of complement
  3. chemotactic attraction and activation of PMNs (neutrophils)
  4. release of proteases and oxygen radicals with tissue damage (neutorphil act)
41
Q

Type IV hypersensitivity

A 
delayed type hypersensitivity
• 24-48 hours to manifest, mediated by T cells and macrophages
• only  not mediated by antibodies
• T cell makes INF, TNF
blood monocyte --> increase adhesion
42
Q

Examples of DTH

Type IV

A
  • manatoux reaction to PPD for TB
  • poison ivy
  • nickel sensitivity
  • intradermal injection
  • measure the tiameter
43
Q

Delayed hypersensitivity can do

A

a lot of damage

44
Q

Type IV

normal lung vs lung with TB

A
  • macrophage in tissues (eg TB)
  • T cells recognize, bring macrophages
  • in and lung destroyed
  • TB aka consumption
45
Q

Type IV

granuloma

A

macrophages wall off bacteria

46
Q

Type IV

poison ivy elicits

A

DTH reactions

47
Q

When antigen is injected into the skin, different hypersensitivities

A 
happen at different rates
skin swelling
• type I high at 3 hours
• type III high at 8-10 hours
• type IV high between 12-24
48
Q

Type I hypersensitivity - summary

A

anaphylactic type
• mediator IgE bound to basophils/mast cells
• mechanism - mediator release
• examples - anaphylaxis, allergic dermatitis, drug and vaccine reactions, parasite reactions

49
Q

Type II hypersensitivity - summary

A

antibody dependent cytotoxic
• mediator - IgG/IgM directed cytotoxicity or dysyfunction
• mechanism - cytotoxicity mediated by complement or NK cell
• expamples - autoimmune hemolytic anemia, infections hemolytic anemia (anaplasmosis, babesiosis, EIA), myasthenia gravis (dysfunction)

50
Q

Type III hypersensitivity - summary

A
  • immune complex type
  • mediator - IgG and IgM
  • mechanism - immune complexes deposited with activation of complement and mediator release
  • examples - immune complex glomerulonephritis, immune complex vasculitis, extrinsic allergic alveolitis
51
Q

Type IV hypersensitivity - summary

A
  • cell mediated
  • mediator - CD4+ and CD8+ T-cells
  • mechanism - cell mediated immunity with lymphokine mediated effects and CD8-mediated cytotoxicity
  • examples - tuberculosis, contact dermatitis, transplant rejection

Basic Immunology (15 decks)

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