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

Lecture 17 (10A) - Hypersensitivity Flashcards

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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

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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

Study These Flashcards
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

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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

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A

A and B

but no A and B antigens

25
Type II | Type O+ Rhesus negative
universal donor of red cells
26
AB+
have A antigens have B antigens Rh cells
27
Blood type O
antigen - no A or B | antibodies - anti-A and anti-B
28
Blood A blood type
antigens - A | antibodies - anti-B
29
Blood B blood type
antigens - B | antibodies - anti-B
30
Blood AB blood type
antigens - A and B antigens | antibodies - no a or B antibodies
31
When red blood cells with eg group A antigens on their membranes are mixed with plasma containing antibodies to group 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
Hemolytic transfusion reaction
``` • donor - blood type A • recipient - type O with anti-A antibody --> severe intravascular hemolysis 1. transfusion 2. agglutination and complement binding 3. hemolysis ```
33
Type II hypersensitivity | Rhesus
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
Type III hypersensitivity
* 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
Type III hypersensitivity | antibodies in equilibrium with
antigen • antibodies in equilibrium with antigen • polyvalent antibody - multivalent antigen • big agglutination (immune complex), antigen + antibody structure
36
Type III forms
immune complex • antigenic determinant sites on antigen, antibody binds • IgG antibody as 2 arms/binding sites
37
Immune complex disease
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
Type III hypersensitivity forms immune complex deposition by
complement • immune complex sticks to vessels • neutrophils come
39
Phases of Type III hypersensitivity
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
Type III hypersensitivity reactions | immune complex glomerulonephritis
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
Type IV hypersensitivity
``` 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
Examples of DTH | Type IV
* manatoux reaction to PPD for TB * poison ivy * nickel sensitivity * intradermal injection * measure the tiameter
43
Delayed hypersensitivity can do
a lot of damage
44
Type IV | normal lung vs lung with TB
* macrophage in tissues (eg TB) * T cells recognize, bring macrophages * in and lung destroyed * TB aka consumption
45
Type IV | granuloma
macrophages wall off bacteria
46
Type IV | poison ivy elicits
DTH reactions
47
When antigen is injected into the skin, different hypersensitivities
``` 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
Type I hypersensitivity - summary
anaphylactic type • mediator IgE bound to basophils/mast cells • mechanism - mediator release • examples - anaphylaxis, allergic dermatitis, drug and vaccine reactions, parasite reactions
49
Type II hypersensitivity - summary
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
Type III hypersensitivity - summary
* 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
Type IV hypersensitivity - summary
* 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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