Immunology: Chapter 15: Hypersensitivity

Front 1

Type I hypersensitivity is ? mediated hypersensitivity.

Back 1

Type I hypersensitivity is Ig-E mediated hypersensitivity.

Front 2

Type II is ? or ? mediated hypersensitivity.

Back 2

Type II is IgG or IgM mediated cytotoxic hypersensitivity.

Front 3

Type III is ? mediated hypersensitivity.

Back 3

Type III is complex-mediated hypersensitivity.

Front 4

Type IV is ? hypersensitivity.

Back 4

Type IV is cell-mediated hypersensitivity.

Front 5

Type I is mediated by ? in response to ?.

Back 5

Type I is mediated by IgE in response to allergens.

Front 6

Responses to allergens are not seen when?

Back 6

Not in the 1st exposure. Only 2nd and subsequent exposures. Your not allergic to anything the first time you come into contact with it.

Front 7

In Type I hypersensitivity allergen specific IgE bind to what?

Back 7

They bind to receptor on mast cell.

Front 8

In type I hypersensitivity once degranulation occurs describe what happens to:
smooth muscle cells?

Back 8

They contract

Front 9

In type I hypersensitivity once degranulation occurs describe what happens to:
small blood vessels?

Back 9

They dilate

Front 10

In type I hypersensitivity once degranulation occurs describe what happens to:
blood platelets?

Back 10

They clump

Front 11

In type I hypersensitivity once degranulation occurs describe what happens to:
sensory nerve endings?

Back 11

They get triggered

Front 12

In type I hypersensitivity once degranulation occurs describe what happens to:
eosinophil?

Back 12

Makes a lot of this.

Front 13

List 4 different common components or Type I reactions.

Back 13

1. Allergens
2. Reaginic Antibody (IgE)
3. Mast cells and basophils
4. IgE-binding Fc receptors

Front 14

Describe some of the allergen components of type I reactions?

Back 14

Majority of people mount IgE responses only against parasites. Some people have atopy (allergies), they develop hypersensitivity rxns to environmental Ags. There is an IgE regulatory defect.

Front 15

The allergens in type I reactions have a strong ? component.

Back 15

They have a strong genetic component. (On chromosomes 5,6 & 11).

Front 16

List 2 common protein allergens associated with type I hypersensitivity.

Back 16

1. Foreign serum

2. Vaccines

Front 17

List 5 common food allergens associated with type I hypersensitivity.

Back 17

1. Nuts
2. Seafood
3. Eggs
4. Peas, beans
5. Milk

Front 18

List 4 common plant pollen allergens associated with type I hypersensitivity.

Back 18

1. Rye grass
2. Ragweed
3. Timothy grass
4. Birch trees

Front 19

List 4 common drug allergens associated with type I hypersensitivity.

Back 19

1. Penicillin
2. Sulfonamides
3. Local anesthetics
4. Salicylates

Front 20

List 5 common insect product allergens associated with type I hypersensitivity.

Back 20

1. Bee venom
2. Wasp venom
3. Ant venom
4. Cockroach calyx
5. Dust mites

Front 21

List some common environmental allergens associated with type I hypersensitivity.

Back 21

1. Mold spores
2. Animal hair and dander
3. Latex

Front 22

How many different receptor types bind the Fc region of IgE? List them.

Back 22

Two different receptor types bind the Fc region of IgE.

1. Fc-epsilon-RI (important)

2. Fc-epsilon-RII (CD23)

Front 23

List the components and there purpose of the Fc-epsilon-RI receptor type that binds to the Fc region of IgE?

Back 23

1. Alpha chain binds IgE
2. Beta chain involved in signaling
3. Gamma-chains are most important component in signaling.
4. Beta and Gamma chains contain ITAM motif.

Front 24

Fc-epsilon-RII (with soluble CD23) is found in higher levels where?

Back 24

Found in higher levels of atopic individuals on lymphocytes and macrophages, and higher levels of soluble form in serum.

Front 25

cAMP is a what?

Back 25

Key 2nd messenger.

Front 26

Allergen and Fc-epsilon-RI display ? binding.

Back 26

They display cross-link binding.

Front 27

In allergies what kind of damage is caused by granules?

Back 27

Tissue damage, if you don't take meds.

Front 28

What are the principal mediators involved in type I hypersensitivity?

Back 28

1. Histamine (primary one)
2. Heparin
3. Serotonin (rodents)
4. Eosinophil chemotactic factor (ECF-A)
5. Neutrophil chemotactic factor (NCF-A)
6. Proteases (tryptase, chymase)

Front 29

What is the primary effect of histamine and heparin?

Back 29

Increased vascular permeability and smooth muscle contraction.

Front 30

What is the primary effect of serotonin?

Back 30

Increased vascular permeability and smooth muscle contraction. (RODENTS)

Front 31

What is the primary effect of eosinophil chemotactic factors (ECF-A)?

Back 31

Eosinophil chemotaxis

Front 32

What is the primary effect of neutrophil chemotactic factors (NCF-A)?

Back 32

Neutrophil chemotaxis

Front 33

What is the primary effect of proteases?

Back 33

Proteases (like tryptase and chymase) cause bronchial mucus secretions; degradation of blood vessel basement membrane (tissue damage); generation of complement split products.

Front 34

Type I rxns can be ? or ?.

Back 34

Type I rxns can be systemic or localized.

Front 35

What is systemic anaphylaxis?

Back 35

A systemic type I Rxn. It is often fatal and occurs in minutes. It is usually initiated by an allergen introduced directly to the bloodstream, skin or gut. Causes systemic vasodilation and smooth muscle contraction.

Front 36

What might cause systemic anaphylaxis?

Back 36

It is severe and may be seen in Bee stings.

Front 37

What is atopy?

Back 37

This is a localized type I rxn and is more common than systemic anaphylaxis. It is limited to a specific target tissue or organ (usually epithelial surfaces). Afflicts about 20% of the population.

Front 38

What is included under the category of atopy?

Back 38

1. Allergic rhinitis
2. Asthma
3. Atopic dermatitis (eczema)
4. food allergies

Front 39

What is the most common type of atopy?

Back 39

Allergic rhinitis (hay fever)

It affects about 10% of the US population.

Front 40

What causes allergic rhinitis?

Back 40

Due to inhalation of common airborne allergens. They react with sensitized mast cells in conjuctivae and nasal mucosa.

Front 41

What can asthma be triggered by?

Back 41

Dust, mite Ag, pollen, viruses, exercise, and cold air. (exercise and cold air are not protein triggers)(exercise and cold air are not allergens just a bronchial trigger)

Front 42

All asthma triggers respond to what?

Back 42

They all respond to albuterol inhalers because these target beta-agonist.

Front 43

Asthma sufferers may have abnormal levels of what?

Back 43

Sufferers may have abnormal levels of receptors for neuropeptides (substance P)

Front 44

What are the 2 responses seen in asthma?

Back 44

1. Early response (occurs in minutes; involves histamine, LTC4, and PGD2 (LTC4 & PGD2 are possible targets for future drugs) 2. Late response (Occurs hours later; releases IL-4, IL-5, IL-6, IL-13, TNF-alpha, ECF (increased eosinophils), PAF (platelet activating factor).

Front 45

What is related to the seriousness of the late response in asthma?

Back 45

The thickness of the basement membrane.

Front 46

Food allergies involve what kind of cross-linking?

Back 46

Allergen cross-linking of IgE receptors on mast cells along upper and lower GI tract.

Front 47

Food allergies have localized what? What does this result in?

Back 47

Localized smooth muscle contraction and vasodilation. This results in diarrhea, vomiting, and increased permeability of mucous membranes so allergen enters bloodstream.

Front 48

The increased permeability of mucous membranes that allows allerge to enter bloodstream during food allergies is related to what?

Back 48

Asthma attacks, hives, and atopic uticaria.

Front 49

Atopic dermatitis is aka what?

Back 49

Allergic eczema

Front 50

In what population is atopic dermatitis usually seen in?

Back 50

Young children

Front 51

What kind of skin eruptions are observed in atopic dermatitis?

Back 51

Erythematous skin eruptions from RBCs infiltrating the area.

Front 52

What is contained in the skin lesions observed during atopic dermatitis?

Back 52

Skin lesions contain Th2 and eosinophils.

Front 53

When do late-phase rxns occur?

Back 53

As hypersensitivity I subsides.

Front 54

How long after hypersensitivity type I subsides do you see late phase rxns? How long does it persist?

Back 54

Develops 4-6h post initial type I rxn. It then persist for 1-2 days.

Front 55

Late-phase rxns involves the infiltration of what cell types into the site of the rxn?

Back 55

Infiltration of neutrophils (30%), eosinophils (30%), basophils, macrophages, and Th2 cells. (for ex, in asthma these will be observed in the lung)

Front 56

TNF-alpha and IL-1 increase what during late phase rxns?

Back 56

TNF-alpha and IL-1 increase CAM expression on venular endothelial cells.

Front 57

Explain the factors regulating Type I hypersensitivity?

Back 57

1. Th1 cells reduce the response

2. Th2 cells enhance the response

(remember IgE causes the allergy rxns)

Front 58

How do Th1 cells reduce the response to type I hypersensitivity?

Back 58

INF-gamma inhibits type I response; decreases IgE production.

Front 59

How do Th2 cells enhance the response of type I hypersensitivity?

Back 59

1. IL-4, IL-13 enhance class switching to IgE
2. IL-4, IL-9 enhance mast cell production
3. IL-5, IL-9 enhance eosinophil maturation, activation and accumulation

Front 60

Which factors involved in the regulaion of type I hypersensitivity by Th2 are being looked at as targets for asthma meds?

Back 60

IL-4 and IL-13

Front 61

Clinical testing of type I responses are usually done how?

Back 61

By skin testing. Intradermal injection of potential allergens (forearm or back) are widely used. Wheal and flare will occur in 30 minutes. Another method involves measuring serum level of total IgE which just indicates that you have allergies not which specific one you have.

Front 62

List 2 types of immunotherapy to treat hypersensitivity?

Back 62

1. Hyposensitization

2. Humanized monoclonal anti-IgE

Front 63

What is hyposensitization?

Back 63

Repeated injections of increasing doses of allergens. Causes a shift toward IgG production

Front 64

What is humanized monoclonal anti-IgE?

Back 64

A type of immunotherapy. Binds to IgE before it is bound to FC-epsilon-RI. Binds to the same site where IgE binds to FC-epsilon-RI.

Front 65

List 5 drugs used to tx type I hypersensitivity?

Back 65

1. Antihistamines
2. Cromolyn sodium
3. Theophylline
4. Epinephrine (adrenaline)
5. Cortisone

Front 66

What is the action of antihistamine?

Back 66

Block H1 and H2 receptors on target cells.

Front 67

What is the action of cromolyn sodium?

Back 67

Blocks Ca2+ influx into mast cells.

Front 68

What is the action of theophylline?

Back 68

Prolongs high cAMP levels in mast cells by inhibiting phosphodiesterase, which cleaves cAMP to 5'AMP.

Front 69

What is the action of epinephrine (adrenaline)?

Back 69

Stimulates cAMP production by binding to beta-adrenergic receptors on mast cells.

Front 70

What is the action of cortisone?

Back 70

Reduces histamine levels by blocking conversion of histidine to histamine and stimulates mast-cell production of cAMP.

Front 71

Although cAMP rises transiently during mast-cell activation, ? is prevented if cAMP levels remain high.

Back 71

Degranulation is prevented if cAMP levels remain high.

Front 72

Type II hypersensitivity is aka what?

Back 72

Cytotoxic hypersensitivity.

Front 73

Cytotoxic hypersensitivity is ? mediated.

Back 73

Ab-mediated destruction of cells.

Front 74

Ab-mediated cytotoxic (type II) hypersensitivity involves the activation of what?

Back 74

Activation of complement or ADCC.

Front 75

List the 3 types of type II rxns?

Back 75

1. Transfusion rxns

2. Hemolytic disease in newborns

3. Drug-induced hemolytic anemia

Front 76

Drug induced hemolytic anemia may be caused by what?

Back 76

It is caused by some antibiotics. (penicillin, cephalosporin, streptomycin)

Front 77

Type I penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?

Back 77

IgE (the clinical manifestations include: urticaria and systemic anaphylaxis)

Front 78

Type II penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?

Back 78

IgM, IgG (the clinical manifestations include: hemolytic anemia)

Front 79

Type III penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?

Back 79

IgG. (Clinical manifestations include: Serum sickness and glomerulonephritis)

Front 80

Type Iv penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?

Back 80

Th1 cells (clinical manifestation include: Contact dermatitis)

Front 81

Type III hypersensitivity is aka what?

Back 81

Immune complex-mediated hypersensitivity.

Front 82

Type III hypersensitivity is due to the build-up of what?

Back 82

Immune complexes of Ab/Ag that form near the site of Ag entry. (hence the name Immune complex-mediated hypersensitivity)

Front 83

In type III hypersensitivity neutrophils attracted to the site of deposit result in what?

Back 83

Tissue damage:
1. Blood vessel walls
2. Synovial membranes of joints
3. Glomerular basement membrane of kidneys.
4. Chloroid plexus of brain

Front 84

What is an arthus reaction? List examples?

Back 84

A localized type III reaction. Occurs in 4-8h. Involves localized tissue and vascular damage due to edema and erythemia at the site. Includes mild swelling to tissue necrosis.
Examples: Insect bites, farmer's lung; pigeon fancier's disease.

Front 85

Generalized type III rxns have ? ? ? in the blood stream. When is this often observed?

Back 85

Circulating immune complexes in the bloodstream. This is often observed after administration of antitoxins containing foreign serum (horse anti-tetanus)

Front 86

What is "serum sickness"?

Back 86

It is involved with generalized type III rxns. It involves fever, weakness, rashes, edema, erythema, lymphadenopathy, arthritis, glomerulonephritis. It is most commonly seen today after antibiotic tx or vaccinations.

Front 87

What diseases are associated with circulating immune complexes?

Back 87

1. Automimmune diseases

2. Drug Reactions

3. Infectious diseases

Front 88

List 3 autoimmune diseases associated with circulating immune complexes?

Back 88

1. SLE

2. RA

3. Goodpasteur's syndrome

Front 89

List some drug reactions that may be associated with circulating immune complexes?

Back 89

1. penicillin

2. sulfonamides

Front 90

List some infectious diseases associated with circulating immune complexes?

Back 90

1. Meningitis
2. Hepatitis
3. Malaria
4. Mononucleosis
5. Trypanosomiasis
6. Poststrep glomerulonephritis

Front 91

Type IV delayed type hypersensitivity is a result of what?

Back 91

Activated Th cells encountering certain types of Ags and secreting cytokines that induce a localized inflammatory reaction.

Front 92

In type IV delayed type hypersensitivity there are large influxes of what?

Back 92

Large influxes of nonspecific inflammatory cells especially macrophages.

Front 93

In most cases, type IV delayed type hypersensitivity ? ? is limited.

Back 93

Tissue damage is limited.

Front 94

What is a tuberculin rxn?

Back 94

A localized skin reaction involved with type IV DTH that develops as a result of a localized inflammatory response when injected intradermally with a filtrate derived from mycobacterial culture.

Front 95

What are the two main phases of the DTH response?

Back 95

1. sensitization phase

2. effector phase

Front 96

When does the sensitization phase of the DTH response occur?

Back 96

1-2 weeks after contact with Ag. Involves the Ag-presenting cells: macrophages langerhans cells. Involves the DTH-mediating cells: Th1 (CD4) cells generally and CD8 cells occasionally.

Front 97

When does the effector phase of the DTH response occur? Describe it.

Back 97

It occurs following subsequent exposure to Ag. Th1 cells secrete cytokines to recruit and activate macrophages. Response peaks 48-72 h after second contact. Macrophages are primary effector cells of DTH.

Front 98

Granulomas can form from ? DTH resonse.

Back 98

Forms from prolonged DTH response.

Front 99

A poison oak DTH response is mediated by ?.

Back 99

Th1

Front 100

What is released during a poison oak DTH reaction?

Back 100

INF-gamma, MCP-1, MIF are released.

Front 101

In the poison oak DTH reaction tissue damage is caused by what?

Back 101

Lytic enzymes from activated macrophages.

Front 102

Some rxns seen in poison oak DTH rxns?

Back 102

TNP, nickel, formaldehyde, poison ivy, some cosmetics and hair dye, turpentine.