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51 Cards in this Set

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  • Back
What are the four major types of hypersensitive rxns?
Type I – immediate type hypersensitivity

Type II – cytotoxic hypersensitivity

Type III – immune complex hypersensitivity

Type IV – delayed type hypersensitivity
Give an example of each type of sensitivity.
Type 1: allergy, asthma (IgE mediated)

Type 2: Rh mismatch (Ig mediated C' activation)

Type 3: serum sickness, vasculitis, Ag-Ab complexes

Type 4: TB skin test, hypersensitive pneumonitis--Tdth cells
What are the two phases of Type 1 hypersensitivity?
Sensitization phase

Effector phase
What happens in the sensitization phase of a Type I hypersensitivity rxn?
Sensitization phase:

exposure to antigen (allergen)

production of IgE

binding to mast cells and basophils via Fc episilon Receptor on these cells
What happens in the effector phase of a Type I hypersensitivity rxn?
Effector phase:

IgE binds allergen (antigen)

crosslinking of IgE results in degranulation of the mast cell

release of pharmacologically-active mediators
What chemicals must be released in order for IgE to crosslink on a mast cell?
1. activation of tyrosine kinases

2. 2nd messengers. cAMP levels rise then fall. @ fall get degranulation

3. Ca+2 mobilization = influx. stimulates breakdown of arachidonic acids into: prostaglandins and especially leukotrienes

4. microtubule assembly to move granules to cell surface.

5. epinephrine and theophylline keep cAMP levels high (so no degranulation--can use as Tx)
What determines IgE production?
Genetics and relative dosage of an allergen
Describe the interleukins involved in IgE activation and inhibition.
cytokines produced by APC

IL-4, IL-5 and IL-13 (Th2) switch factor for IgE

IL-10 (Th2) INHIBITS IFN gamma(Th1), thus inhibiting IL4 production
What does the dose of an allergen control?
production of IgG or IgE. IgG can be used in DEsensitization. IgE causes the allergic rxn.
What are the preformed chemical mediators of allergies?
HISTAMINE--increase vascular permeability and smooth mm contraction

proteases: mucous secretion, generation of complement split products.
What are NEWLY FORMED chemcial mediators of allergies?

How long do they take?
Takes 30-60 seconds to form leukotrienes an dprostaglandins from arachodonic acid.

LEUKOTRIENES--(SRS-A=slow reactive substance of allergies/anaphylaxis). increases vascular permeability and contraction of pulmonary smooth muscles.

platelet activating factor--platelet aggregation and contraction of pulmonary smooth mm.

protaglandin D2--vasodilation, contraction of smooth muscles.

Cytokines--chemotactic and inflammatory
What do leukotrienes do?
increase vascular permeability and contraction of pulmonary smooth mm.

SRS-A 30-60s
What are the symptoms of allergy and what are they dependent on?

--wheal and flare rxn; pruitis, erythema


mucous secretion

vasodilation; even shock
What does pruritis mean? urticaria? atopy?
pruritis (itchy)

urticaria (hives)

atopy (localized)
What are some examples of atopy anaphylaxis?
pruitis, urticaria

allergic rhinitis (hay fever)

asthma (atopic asthma)

eczema (atopic dermatitis)

food allergies
What % of US pop has allergic rhinitis?

What are the symptoms?

What is the Tx?

airborne allergens with mast cells of conjunctivae and nasal mucosa--localized

localized vasodilation and increased capillary permeability
mucous production

Tx: anti-histamines and desensitization
How does an anti-histamine work?
blocks histamine binding--does NOT block release of histamine and does NOT block IgE.
How does desensitization work?
stimulate the immune response to produce IgG instead of IgE
What are the two major branches of asthma and what are their causes?
allergic and intrinsic asthma.

Allergic: airborne allergins (dust, pollen, insect parts), blood borne allergens (viral Ag), degranulation of mast cells due to IgE cross linking. lower respiratory tract usually.

Intrinsic has nothing to do w/ IgE. not immune stimulated. Instead exercise induced, warm to cold climates, other cmpds producing granulation--not IgE.
What % of the US poplulation has allergic asthma?

What can allergic asthma lead to?

airway edema and mucous secretion, with subsequent exposures gets worse. Can even lead to airway obstruction.

Usually hypersensitive to allergens
Where are cytokine genes found in asthmatics?
5q23-33 (IL-3, 4, 5, 9, 13)

IgE switch, eosinophil recruitment, mast cell proliferation.
What are some hypotheses for the increasing incidence of asthma?
increasing in cases AND severity

maybe due to:

complex genetic disease (see previous slide)

environmental factors (cockroach implicated)
How are allergies Dx?
skin test--scratch or intradermal. could cause severe rxn.

radioimmunoassays--need purified allergens. detect allergen specific IgE.
What are the treatments for allergies?
Anti-histamine – for atopic allergies

Epinephrine – for quick response--relaxes smooth muscle contraction and causes vasoconstriction

glucocorticoids and leukotriene modifiers

Desensitization – stimulate “blocking” IgG
doesn’t always work
What is the initial rxn in Type II sensitivity?
Ab mediated cytotoxicity

C' activation and ADCC.

Abs bind cell surface and activate C' then lysis
What would happen if you inject type B blood into a type A individual?
Type A person has anti-B abs, therefore will cause C' and lysis
Besides checking for type of blood what other test should always be done?
cross matching blood. detect the presence of Abs in donor and/or recipient

person may have had a transfusion etc and may produce Abs that would lead to rejection of blood.
Do O blood types have Ags? Do they have Abs?
Type O blood has anti-a AND anti B Abs, but neither Ag.

Universal Donor!

they DO have sugars, just none corresponding to Ag
What is erythroblastosis fetalis?

How does this happen?

How can this be prevented or treated?
hemolytic disease of the newborn (HDN). Caused when Rh - mother has a Rh +; no complications w/ this pregnancy.

However the mother should be treated w/ RhoGAM w/in 24-48 hrs of delivery so that she will not harm her next fetus.

Other more invasive options are to remove mothers plasma and replace the Abs OR give fetus Rh- blood every 10-21 days until delivery.
How does a Type III hypersensitivity rxn work?

Where do they localize?

What can this cause?
Immune complex disease: Ex. serum sickness and lupus

large Ab-Ab complexes are formed; mostly IgG, some IgM

Localized in the KIDNEY, blood vessel walls, choroid plexus of the brain.

When localized in the kidney can lead to accumulation and complications
What is an example of a localized type III reaction?

Where does the immune complex form?
arthus rxn= local inflammation

insect bite: remember must have had first exposure in order to exhibit inflammation.

where ag is deposited is where the immune complex will form
What is an example of a generalized type III rxn?

What happens when Ag is in excess?
complexes circulate and get concentrated by phagocytosis--Ex. kidney

if Ag in excess--don't get clearance of complexes by phagocytosis
Do you see large immune complex formation in serum sickness on the first or second injection of foreign serum?
second injection see rash, arthritis, edema, glomerulonephritis.

Ex. bite, treat w/ horse Ab. 2nd bite then do not treat w/ horse Ab b/c human body saw that once as Ag and developed Ab against it. Treat w/ human Ab if possible, if not cow Ab etc. to avoid serum sickness.
Give 5 examples of immune complexes that contribute to pathology.

rheumatoid arthritis

penicillin rxn


What is vasculitis?

What is the mechanism of pathology?

What happens when Ag in excess?
inflammation and damage to blood vessels
immunopathogenic mechanisms

thought to cause the pathology

Ag excess get complexes deposited on blood vessels. leads to local or systemic (hep B, serum sickness, cutaneous vasculitis are exs.)
What type of immune rxns occur in Type III immune complexes?
complement ADCC (neutrophil can release immune factors AND granules)
What is type IV hypersensitivity?
Delayed type hypersensitivity

DTH response:
1. CD4+ T cell (Tdth) – cytokines stimulate inflammation (Th1 type cytokines)

2. influx of inflammatory cells (especially macrophages)

3. initial symptoms seen after ~24 hours and peaks between 48-72 hours

4. not always detrimental…can be useful to fight certain infections--
especially intracellular pathogens
What is the Tuberculin rxn?
inject PPD (purified protein derivative from M. tuberculosis)

if EXPOSED, MEMORY Tdth cells present and become activated. confirm w/ chest x-ray
What can DTH be used to monitor? How?
monitor immune status of AIDS patient

use previously exposed Ags and inject under the skin and look at response
What induces DTH response?
intracellular bacteria, fungi, parasites

viruses, contact Ag
Where do primary immunodeficiencies come from? secondary?
primary=inherited defects

secondary= due to infections, aging, malignancies
What is SCID?

What causes it?

What is the treatment?
Severe combined immunodeficiency (SCID)

2 causes:
1 defect in g-chain of IL-2 receptor (CD132)

Shared by IL-2, -7, -11, and 15

lymphocyte development is abnormal

2. Autosomal mutants
defect in RAG1, 2 or other enzymes that prevent development of NORMAL B and T cells

defect in alpha chain of IL2 receptor (CD25)

Treatment is by bone marrow transplant
What is Bare lymphocyte syndrome due to?
Bare lymphocyte syndrome:

MHC deficiency due to
defect in MHC class II transactivator protein gene (= lack of MHC II)


TAP gene defect (= lack of MHC class I)

Causes immunosupression
What syndrome is caused by congenital thymic aplasia/hypoplasia?

What happens?

What is the treatment?
Di George syndrome

defect in fetal development in the 6-10th wk.

due to unknown causes

Tx: thymic graft from early fetus--13-14wk--to prevent graft vs. host disease.
Which is the most common of all the primary immunodeficiencies?
IgA deficiency
Why are nude mice important?
good experimental models of immunodeficiency (athymic).
What are SCID mice?
RAG 1 or RAG 2 mutants

put human cells into mouse SCID/Hu mouse
What is HIV and infection of?
CD4+ tcells

eventually lose Th cells

become more susceptible to opportunistic infections

Note: graph= initial spike in HIV and dip in CD4 in acute phase. Chronic phase: CD4 rise then continual fall as HIV increases.
Why can you irradiate to get rid of HIV and then do a bone marrow transplant to regain T cells?
because HIV infects macrophages too. macrophages are resistant to radiation. So, if you did a bone marrow transplant at that point the HIV in the macrophages would attack the activated T cells and you'd be worse off
What is normal CD4 level?
What is the CD4 count in HIV?