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IMM Exam 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Hypersensitivity

A

defect in regulation or targeting of the usually beneficial immune response

i.e. overreaction of normal immune response triggered by self/microbial/environmental antigens

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2
Q

Triggers of hypersensitivity

A

3 types of antigens

  1. “self” antigens -autoimmunity
  2. microbial antigens - excessive inflammation
  3. Environmental antigens - allergy/atopy
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3
Q

What are the 4 types of hypersensitivity?

A

Type I - Immediate hypersensitivity

Type II - Antibody-mediated

Type III - Immune complex-mediated

Type IV - T cell-mediated

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4
Q

Names for Type 1 Hypersensitivity

A

Immediate, IgE-mediated, allergy/atopy

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5
Q

Timing of Type 1 Hypersensitivity

A

within minutes (very rapid)

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6
Q

Mechanism of Type 1 Hypersensitivity

A

cross-linking of IgE triggering mediator release in mast cells

Involve antigen-specific IgE on effector cells

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7
Q

Various mediators in Type 1 Hypersensitivity

A

vasoactive mediators (e.g. histamine)

lipid mediators

cytokines

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8
Q

Most common type of hypersensitivity

A

Type 1

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9
Q

Allergy =

A

histamine

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10
Q

Examples of allergic diseases (Type 1 Hypersensitivity)

A
  • Allergic rhinitis (“hay fever”)
  • Atopic asthma
  • Anaphylaxis (food allergy, stinging insect allergy, drug allergy)
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11
Q

Potential causes of increase in Type 1 Hypsersensitivity prevalence within the past 50 years

A
  • hygiene hypothesis

- environmental factors

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12
Q

Similarities between Type II and III hypersensitivity

A

both mediated by antibodies (involve IgG and IgM)

frequently involve auto-antibodies (failure in developing or loss of self-tolerance)

less commonly involve foreign antigens

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13
Q

Type II Hypersensitivity

A
  • Injury related to antibody directly binding to target

- Antigens are specific cells or extracellular matrix

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14
Q

Differences between Type II and III Hypersensitivity

A

Type II: Local, tissue/cell specific (i.e. “targeted”)

Type III: Systemic

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15
Q

Type III Hypersensitivity

A
  • Injury related to immune complex deposition

- Antigens are present in circulation

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16
Q

Names for Type II Hypersensitivity

A

antibody-mediated, cytotoxic

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17
Q

Timing for Type II Hypersensitivity

A

couple days up to a week

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18
Q

Mechanism of Type II Hypersensitivity

A

3 mechanisms:

  • complement/Fc receptor inflammation
  • opsonization/phagocytosis
  • receptor activation
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19
Q

1st mechanism of Type II Hypersensitivity

A

“Complement- and Fc receptor-mediated inflammation”

Antibody binds antigens and attract neutrophils and/or complement which lead to inflammation and injury

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20
Q

Goodpasture syndrome

A

Anti-glomelular basement membrane disease

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21
Q

What are antibodies directed against in Goodpasture syndrome?

A

Abs against basement membrane in kidney and lung

Activate complement and Fc receptors (of neutrophils), leading to inflammation

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22
Q

Symptoms of Goodpasture syndrome

A

Blood in urine, Blood in lung, kidney failure and fatigue

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23
Q

2nd Mechanism of Type II hypersensitivity

A

Opsonization and phagocytosis

Ab coat the outside of cells and then phagocytes come and eat them up

24
Q

ITP (Idiopathic thrombocytopenic purpura)

A

Autoantibodies against platelets –> opsonization

25
Symptoms of ITP
- Recurrent nose bleeds - Easy bruising - Petechiae
26
AIHA (Autoimmune hemolytic anemia)
Autoantibodies against RBC membrane proteins Pts. have symptoms of anemia On blood smear, less RBCs; not donut shaped - vary in size; no central pallor
27
3rd mechanism of Type II Hypersensitivity
Abnormal physiologic responses without cell/tissue injury - Abs turn things on or off - Antibody stimulates receptor without hormone (e.g. Grave's disease: Ab against TSH receptor leads to hyper-stimulation of thyroid and production of thyroid hormones) - Antibody inhibits binding of NT to receptor (e.g.: Myasthenia Gravis: Ab bind ACh receptors, preventing ACh from signaling from nerve to muscle)
28
Why are Grave's disease and Myasthenia Gravis examples of Type II Hypersensitivity?
Autoantibodies are involved, and the Abs bind particular cells and disease is tissue specific
29
Clinical examples of Type II Hypersensitivity
- Acute rheumatic fever - Abs against myocardial Ags ( cross-reactive anti-strep Abs) - Pemphigus vulgaris - Abs against desmosomes - Pernicious anemia - Abs against intrinsic factor
30
Names for Type III Hypersensitivity
Immune-complex mediated
31
Timing for Type III Hypersensitivity
several days up to a couple weeks
32
Mechanism of Type III Hypersensitivity
1. Abs bind Ags forming complexes 2. Complexes not efficiently cleared 3. Deposit in vessels or tissue 4. Trigger complement/Fc receptor inflammation (e.g.: vasculitis)
33
Type III Hypersensitivity and diphtheria treatment from horse serum
- Horse injected w diphtheria toxin --> induce Abs - Anti-diphtheria horse serum injected into humans to treat diphtheria - Some patients receiving the anti-diphtheria horse serum developed (1) fever, (2) hives and (3) joint pain note: symptoms occured with anti-diphtheria horse serum AND with horse serum alone repeated exposure to horse serum led to quicker and quicker rxns because already had developed antibodies
34
Type III Hypersensitivity and SLE (systemic lupus erythematosus)
Multiple nuclear autoantibodies: dsDNA, ribo-nucleopreotins, histones
35
SLE also has examples of Type II Hypersensitivity with the blood issues
but joint pain, nephritis and vasculitis are classic of Type III
36
Clinical examples of Type III Hypersensitivity
Poststreptococcal glomerulonephritis - group A strep Ag Polyarteritis nodosa - Hep B surface Ag
37
Slowest Hypersensitivity type
Type IV
38
Names for Type IV Hypersensitivity
delayed type, cell-mediated
39
Timing for Type IV Hypersensitivity
1-3 days
40
Mechanism of Type IV Hypersensitivity
2 mechanisms: (both T cell mediated) - CD4 T-cell cytokine-mediated inflammation - CD8 T-cell direct cytotoxic killing
41
Type IV Hypersensitivity and antibodies
T-cell mediated rather than antibodies - not transferrable by serum
42
1st mechanism of Type IV Hypersensitivity (Cytokine-mediated inflammation)
CD4 indirectly causes injury by releasing inflammatory cytokines (e.g. IFNgamma)
43
What is FoxP3
TF associated with regulatory T cells
44
Suppressive cytokines secreted by Tregs
IL-10 and TGFbeta
45
Cytokine associated with allergy
IL-4
46
TB test is example of what type of hypersensitivity
Delayed-type hypersensitivity (DTH) Type IV Hypersensitivity since CD4+ T cells are involved
47
Clinical examples of Type IV Hypersensitivity (cytokine-mediated inflammation)
MS Type 1 diabetes IBD Rheumatoid arthritis
48
2nd mechanism of Type IV Hypersensitivity
T cell-mediated killing of host cells; direct tissue injury by CD8+ cytotoxic T cells
49
Examples of CTL mediated Type IV Hypersensitivity
poison ivy (contact dermatitis)
50
Poison ivy (contact dermatitis)
Urushiol - colorless oil - low molecular weight, lipid soluble so crosses cell membrane - modifies intracellular ksin proteins; presented on MHC Class I --> cells appear FOREIGN - CTLs trigger cell destruction by apoptosis delayed, develops over 12-48 hours
51
Poison ivy (contact dermatitis) onset
delayed, develops over 12-48 hours note: this is Type IV Hypersensitivity (not Type I so not immediate)
52
Treatment options for Types I-IV Hypersensitivity
- Antihistamines, epinephrine - Plasmapheresis, immune biologics (target specific cytokine) - IVIG (high doses lead to immune suppression) - Corticosteroids (reduce inflammatory cytokines produced)
53
Diseases involving Type II Hypersensitivity
Goodpasture, AIHA, ITP, Graves, Myasthenia gravis
54
Diseases involving Type I Hypersensitivity
Allergic diseases and anaphylaxis
55
Diseases involving Type III Hypersensitivity
Lupus, serum sickness, post-strep glomerulonephritis, polyarteritis nodosa
56
Diseases involving Type IV Hypersensitivity
TB, contact dermatitis

IMM Exam 2 (15 decks)

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