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102 Cards in this Set

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Type I hypersensitivity is ? mediated hypersensitivity.
Type I hypersensitivity is Ig-E mediated hypersensitivity.
Type II is ? or ? mediated hypersensitivity.
Type II is IgG or IgM mediated cytotoxic hypersensitivity.
Type III is ? mediated hypersensitivity.
Type III is complex-mediated hypersensitivity.
Type IV is ? hypersensitivity.
Type IV is cell-mediated hypersensitivity.
Type I is mediated by ? in response to ?.
Type I is mediated by IgE in response to allergens.
Responses to allergens are not seen when?
Not in the 1st exposure. Only 2nd and subsequent exposures. Your not allergic to anything the first time you come into contact with it.
In Type I hypersensitivity allergen specific IgE bind to what?
They bind to receptor on mast cell.
In type I hypersensitivity once degranulation occurs describe what happens to:
smooth muscle cells?
They contract
In type I hypersensitivity once degranulation occurs describe what happens to:
small blood vessels?
They dilate
In type I hypersensitivity once degranulation occurs describe what happens to:
blood platelets?
They clump
In type I hypersensitivity once degranulation occurs describe what happens to:
sensory nerve endings?
They get triggered
In type I hypersensitivity once degranulation occurs describe what happens to:
eosinophil?
Makes a lot of this.
List 4 different common components or Type I reactions.
1. Allergens

2. Reaginic Antibody (IgE)

3. Mast cells and basophils

4. IgE-binding Fc receptors
Describe some of the allergen components of type I reactions?
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.
The allergens in type I reactions have a strong ? component.
They have a strong genetic component. (On chromosomes 5,6 & 11).
List 2 common protein allergens associated with type I hypersensitivity.
1. Foreign serum

2. Vaccines
List 5 common food allergens associated with type I hypersensitivity.
1. Nuts

2. Seafood

3. Eggs

4. Peas, beans

5. Milk
List 4 common plant pollen allergens associated with type I hypersensitivity.
1. Rye grass

2. Ragweed

3. Timothy grass

4. Birch trees
List 4 common drug allergens associated with type I hypersensitivity.
1. Penicillin

2. Sulfonamides

3. Local anesthetics

4. Salicylates
List 5 common insect product allergens associated with type I hypersensitivity.
1. Bee venom

2. Wasp venom

3. Ant venom

4. Cockroach calyx

5. Dust mites
List some common environmental allergens associated with type I hypersensitivity.
1. Mold spores

2. Animal hair and dander

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

1. Fc-epsilon-RI (important)

2. Fc-epsilon-RII (CD23)
List the components and there purpose of the Fc-epsilon-RI receptor type that binds to the Fc region of IgE?
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.
Fc-epsilon-RII (with soluble CD23) is found in higher levels where?
Found in higher levels of atopic individuals on lymphocytes and macrophages, and higher levels of soluble form in serum.
cAMP is a what?
Key 2nd messenger.
Allergen and Fc-epsilon-RI display ? binding.
They display cross-link binding.
In allergies what kind of damage is caused by granules?
Tissue damage, if you don't take meds.
What are the principal mediators involved in type I hypersensitivity?
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)
What is the primary effect of histamine and heparin?
Increased vascular permeability and smooth muscle contraction.
What is the primary effect of serotonin?
Increased vascular permeability and smooth muscle contraction. (RODENTS)
What is the primary effect of eosinophil chemotactic factors (ECF-A)?
Eosinophil chemotaxis
What is the primary effect of neutrophil chemotactic factors (NCF-A)?
Neutrophil chemotaxis
What is the primary effect of proteases?
Proteases (like tryptase and chymase) cause bronchial mucus secretions; degradation of blood vessel basement membrane (tissue damage); generation of complement split products.
Type I rxns can be ? or ?.
Type I rxns can be systemic or localized.
What is systemic anaphylaxis?
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.
What might cause systemic anaphylaxis?
It is severe and may be seen in Bee stings.
What is atopy?
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.
What is included under the category of atopy?
1. Allergic rhinitis

2. Asthma

3. Atopic dermatitis (eczema)

4. food allergies
What is the most common type of atopy?
Allergic rhinitis (hay fever)

It affects about 10% of the US population.
What causes allergic rhinitis?
Due to inhalation of common airborne allergens. They react with sensitized mast cells in conjuctivae and nasal mucosa.
What can asthma be triggered by?
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)
All asthma triggers respond to what?
They all respond to albuterol inhalers because these target beta-agonist.
Asthma sufferers may have abnormal levels of what?
Sufferers may have abnormal levels of receptors for neuropeptides (substance P)
What are the 2 responses seen in asthma?
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).
What is related to the seriousness of the late response in asthma?
The thickness of the basement membrane.
Food allergies involve what kind of cross-linking?
Allergen cross-linking of IgE receptors on mast cells along upper and lower GI tract.
Food allergies have localized what? What does this result in?
Localized smooth muscle contraction and vasodilation. This results in diarrhea, vomiting, and increased permeability of mucous membranes so allergen enters bloodstream.
The increased permeability of mucous membranes that allows allerge to enter bloodstream during food allergies is related to what?
Asthma attacks, hives, and atopic uticaria.
Atopic dermatitis is aka what?
Allergic eczema
In what population is atopic dermatitis usually seen in?
Young children
What kind of skin eruptions are observed in atopic dermatitis?
Erythematous skin eruptions from RBCs infiltrating the area.
What is contained in the skin lesions observed during atopic dermatitis?
Skin lesions contain Th2 and eosinophils.
When do late-phase rxns occur?
As hypersensitivity I subsides.
How long after hypersensitivity type I subsides do you see late phase rxns? How long does it persist?
Develops 4-6h post initial type I rxn. It then persist for 1-2 days.
Late-phase rxns involves the infiltration of what cell types into the site of the rxn?
Infiltration of neutrophils (30%), eosinophils (30%), basophils, macrophages, and Th2 cells. (for ex, in asthma these will be observed in the lung)
TNF-alpha and IL-1 increase what during late phase rxns?
TNF-alpha and IL-1 increase CAM expression on venular endothelial cells.
Explain the factors regulating Type I hypersensitivity?
1. Th1 cells reduce the response

2. Th2 cells enhance the response

(remember IgE causes the allergy rxns)
How do Th1 cells reduce the response to type I hypersensitivity?
INF-gamma inhibits type I response; decreases IgE production.
How do Th2 cells enhance the response of type I hypersensitivity?
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
Which factors involved in the regulaion of type I hypersensitivity by Th2 are being looked at as targets for asthma meds?
IL-4 and IL-13
Clinical testing of type I responses are usually done how?
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.
List 2 types of immunotherapy to treat hypersensitivity?
1. Hyposensitization

2. Humanized monoclonal anti-IgE
What is hyposensitization?
Repeated injections of increasing doses of allergens. Causes a shift toward IgG production
What is humanized monoclonal anti-IgE?
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.
List 5 drugs used to tx type I hypersensitivity?
1. Antihistamines

2. Cromolyn sodium

3. Theophylline

4. Epinephrine (adrenaline)

5. Cortisone
What is the action of antihistamine?
Block H1 and H2 receptors on target cells.
What is the action of cromolyn sodium?
Blocks Ca2+ influx into mast cells.
What is the action of theophylline?
Prolongs high cAMP levels in mast cells by inhibiting phosphodiesterase, which cleaves cAMP to 5'AMP.
What is the action of epinephrine (adrenaline)?
Stimulates cAMP production by binding to beta-adrenergic receptors on mast cells.
What is the action of cortisone?
Reduces histamine levels by blocking conversion of histidine to histamine and stimulates mast-cell production of cAMP.
Although cAMP rises transiently during mast-cell activation, ? is prevented if cAMP levels remain high.
Degranulation is prevented if cAMP levels remain high.
Type II hypersensitivity is aka what?
Cytotoxic hypersensitivity.
Cytotoxic hypersensitivity is ? mediated.
Ab-mediated destruction of cells.
Ab-mediated cytotoxic (type II) hypersensitivity involves the activation of what?
Activation of complement or ADCC.
List the 3 types of type II rxns?
1. Transfusion rxns

2. Hemolytic disease in newborns

3. Drug-induced hemolytic anemia
Drug induced hemolytic anemia may be caused by what?
It is caused by some antibiotics. (penicillin, cephalosporin, streptomycin)
Type I penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?
IgE (the clinical manifestations include: urticaria and systemic anaphylaxis)
Type II penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?
IgM, IgG (the clinical manifestations include: hemolytic anemia)
Type III penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?
IgG. (Clinical manifestations include: Serum sickness and glomerulonephritis)
Type Iv penicillin-induced hypersensitive rxns induces what antibody or lymphocytes? What is the clinical manifestation?
Th1 cells (clinical manifestation include: Contact dermatitis)
Type III hypersensitivity is aka what?
Immune complex-mediated hypersensitivity.
Type III hypersensitivity is due to the build-up of what?
Immune complexes of Ab/Ag that form near the site of Ag entry. (hence the name Immune complex-mediated hypersensitivity)
In type III hypersensitivity neutrophils attracted to the site of deposit result in what?
Tissue damage:

1. Blood vessel walls

2. Synovial membranes of joints

3. Glomerular basement membrane of kidneys.

4. Chloroid plexus of brain
What is an arthus reaction? List examples?
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.
Generalized type III rxns have ? ? ? in the blood stream. When is this often observed?
Circulating immune complexes in the bloodstream. This is often observed after administration of antitoxins containing foreign serum (horse anti-tetanus)
What is "serum sickness"?
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.
What diseases are associated with circulating immune complexes?
1. Automimmune diseases

2. Drug Reactions

3. Infectious diseases
List 3 autoimmune diseases associated with circulating immune complexes?
1. SLE

2. RA

3. Goodpasteur's syndrome
List some drug reactions that may be associated with circulating immune complexes?
1. penicillin

2. sulfonamides
List some infectious diseases associated with circulating immune complexes?
1. Meningitis

2. Hepatitis

3. Malaria

4. Mononucleosis

5. Trypanosomiasis

6. Poststrep glomerulonephritis
Type IV delayed type hypersensitivity is a result of what?
Activated Th cells encountering certain types of Ags and secreting cytokines that induce a localized inflammatory reaction.
In type IV delayed type hypersensitivity there are large influxes of what?
Large influxes of nonspecific inflammatory cells especially macrophages.
In most cases, type IV delayed type hypersensitivity ? ? is limited.
Tissue damage is limited.
What is a tuberculin rxn?
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.
What are the two main phases of the DTH response?
1. sensitization phase

2. effector phase
When does the sensitization phase of the DTH response occur?
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.
When does the effector phase of the DTH response occur? Describe it.
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.
Granulomas can form from ? DTH resonse.
Forms from prolonged DTH response.
A poison oak DTH response is mediated by ?.
Th1
What is released during a poison oak DTH reaction?
INF-gamma, MCP-1, MIF are released.
In the poison oak DTH reaction tissue damage is caused by what?
Lytic enzymes from activated macrophages.
Some rxns seen in poison oak DTH rxns?
TNP, nickel, formaldehyde, poison ivy, some cosmetics and hair dye, turpentine.