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Immunology 7070 > Lecture 7 > Flashcards

Lecture 7 Flashcards

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1
Q

What is the definition of hypersensitivity?

A

The immune responses that cause tissue injury are hypersensitivity reactions. Diseases caused by these reactions are hypersensitivity diseases or immune mediated diseases.

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2
Q

How many different types of hypersensitivity are there? List them and their brief description. (1-2 words)

A

Type I - Immediate (atopic/anaphylactic)
Type II - Antibody dependent
Type III - Immune complex
Type IV - Cell mediated /delayed type

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3
Q

Describe type I hypersensitivity.

A

It is an immediate, atopic, or anaphylactic reaction provoked by the re-exposure to a specific allergen. This may be through injestion, inhalation, injection, or direct contact of mucous membranes.

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4
Q

How are type I reactions mediated?

A

IgE antibodies

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5
Q

What do IgE antibodies lead to in hypersensitivity?

A

The release of histamine, leukotrienes, prostaglandins by basophils and mast cells. Causes rapid vascular leakage and mucosal secretions leading to redness, itching, and swelling.

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6
Q

Describe the two forms of Type I reactions.

A

Local or systemic.

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7
Q

What is anaphylactic shock?

A

Sudden death due to hypersensitivity to an antigen.

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8
Q

What are the two phases of type I hypersensitivity?

A

Sensitization and reaction phases

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9
Q

Describe the sensitization phase of type I hypersensitivity.

A

First exposure to allergen
Activation of Th2 cells and stim of IgE class switching in B cells - IL4 and IL-13 secreted by Th2s.
Production of IgE
Binding of IgE to FcepsilonRI on mast cells and basophils

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10
Q

Describe the reaction phase of type I hypersensitivity.

A

Repeat exposure to allergen and binding of IgE
Activation of mast cell to release mediators (histamine, leukotrienes, prostaglandins, TNF, and IL-4.)
Vasoactive amine and lipid mediators and cytokines are liberated from the mast cell.
Vasoactive amine and lipid mediators are immediate reactions minutes after exposure
Late phase reaction from cytokines 6-24 hours after allergen exposure.

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11
Q

In which percent of the population do clinical manifestations of type I reactions occur?

A

10-40%

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12
Q

List a couple airborne clinical manifestations of type I hypersensitivity.

A

Asthma
Allergic rhinitis
Allergic sinusitis
Allergic conjunctivitis

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13
Q

What are hives AKA?

A

Urticaria.

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14
Q

List a few symptoms that may occur in type I hypersensitivity systemic reactions.

A 
Vascular dilation
Airway contraction
Laryngeal edema
Fall in blood pressure
Airway obstruction
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15
Q

What are the factors that may predispose someone to type I hypersensitivity?

A

Genetic factors, environmental factors (air pollutants, cigarette smoke, bacteria/virus infections), high levels of cytokine IL-4, mutation of p40 subunit = lower IL-12, etc.

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16
Q

How to diagnose type I hypersensitivity?

A

Skin test for immediate and late phase reactions.
Radioallergosorbest test (RAST) and ELISA for detection of allergen specific IgE
Nasal provocation testing
Bronchial challenge
Histamine release from basophils

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17
Q

What is a RAST test?

A

A type I hypersensitivity diagnostic test measuring the rate of binding of IgE to the allergen coated on a stick.

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18
Q

What is RAST usually replaced with now?

A

UniCap

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19
Q

What is the typical therapy for type I hypersensitivity?

A 
Avoidance
Pharmaceutical agents (topical lotions, antihistamines, epinephrine)
Immunomodulatory agents (humanized anti-IgE antibodies
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20
Q

Describe intrinsic and extrinsic antibodies.

A

Antigens recognized by autoantibodies may be intrinsic.

Extrinsic antibodies are absorbed onto cells during exposure to a foreign antigen.

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21
Q

Describe type II hypersensitivity.

A

Is antibody-mediated hypersensitivity regulated by IgG. Mediated by complement, phagocytes, neutrophils, and NK cells

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22
Q

How long does it take for type II reactions to take place?

A

Hours to a day.

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23
Q

Desribe type II effector mechanisms.

A

Induction of inflammation at the site of antibody deposition
Antibody deposition leads to opsoniztion by phagocytes
Antibody binding interferes with normal cellular function

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24
Q

How is induction of inflammation at the site of antibody deposition mediated in type II hypersensitivity?

A

Complement and Fc receptor mediated inflammation via neutrophil activation resulting in inflammation and tissue injury.

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25
How is opsonization and phagocytosis mediated in type II hypersensitivity?
Fc receptors of antibodies
26
How is the interference of normal cell function mediated in type II hypersensitivity?
Antibodies are able to stimulate the receptors of thyroid epithelials and muscle cells without the actual normal mechanism.
27
List the two diseases that are driven by the interference with normal cell function in type II hypersensitivities.
Graves disease and Myasthenia gravis
28
Name four antibody mediated type II hypersensitivity diseases.
``` Autoimmune hemolytic anemia Autoimmune thrombocytopenic purpura Goodpasture's syndrome Graves' disease Myasthenia gravis Pemphigus vulgaris Pernicious anemia Rheumatic fever ```
29
What is Goodpasture's syndrome?
hemmorhaging in the lungs caused by antibodies against lung membrane.
30
What is Bullous Pemphigus Vulgaris?
Skin blisters caused by antibodies against skin cells
31
What is masthenia gravis?
Antibodies block acetylcholine which causes voluntary muscles of the face to malfunction.
32
How can you diagnose type II hypersensitivities?
Detection of circulating antibodies against the tissues involved. Presence of antibody and complement in the lesions by immunofluorescence.
33
Describe the type III immune complex mediated hypersensitivity.
Type III hypersensitivities are driven by the interaction of pre-existing IgG or IgM anitbodies with soluble antigens which form small immune complexes in the blood and are deposited in the tissues. The complexes are not easily cleared and initiate immune reactions. The reaction takes hours to days to develop.
34
Give scenarios in which immune complexes may occur.
``` Autoimmune diseases (e.g. RA) Persistent infection (e.g. Hepatitis) Repeated inhalation of antigenic materials ```
35
On what does type III hypersensitivity depend?
On the size of the immune complex. If it is small enough to degrade then there will be no reaction but if it cannot be degraded then there is an issue.
36
What steps occur in the effector mechanisms within the first few hours of a type III hypersensitivity?
Ag is injected to a person with IgG antibodies. Immune complex formation activates complement pathway and C5a binds to mast cell. Immune complex binds FcgammaRIII on mast cell - degranulation Local inflammation increases fluid and protein release, etc.
37
Describe the ratio of antigen to antibody in the early, mid, and late stages of type III hypersensitivity.
Early - Excess antigen, little antibody Mid - comparative Ag/Ab Late - Excess Ab, little Ag
38
What kind of skin reactions can be caused by type III hypersensitivities?
Red, indurate bumps which develop within 4-8 hours (drug induced rashes)
39
What kind of pulmonary reactions can be caused by type III hypersensitivities?
Farmers lung: fungal hay spores Bird fancier's lung: pneumonitis by bird droppings Allergic brochopulmonary aspergillosis: Ag from fungus Aspergillus spp.
40
Describe the steps to the systemic reactions caused by type III hypersensitivities.
Circulating Abs bind Ag in blood Formation of small immune compexes Recirculation and accumulation n basement membrane of capillaries and blood vessels Tissue inflammation and cellular destruction
41
List two immune complex mediated diseases. | Bonus points to list their involved Ag.
Systemic lupus - DNA, nucleoproteins, etc. Polyarteritis nodosa - Hep B surface Ag Poststreptococcal glomerulonephritis - Strep cell wall Ag Serum sickness - various proteins
42
Describe serum sickness in brief.
It is a transient disease caused by the injection of a large dose of protein Ag into the blood leading to the deposition of Ag/Ab complexes in blood vessel walls esp in kidneys and joints
43
Describe the pathology of serum sickness in brief.
The pathology depends on the site of IC deposition. Can be vasculitis, nephritis, or arthritis.
44
Describe systemic lupus erythematosis and by what this disease is characterized. What is the result?
Lupus is a hypersensitivity to one's own DNA and nucleoproteins. The disease is characterized by the presence of autoantibodies which form immune complexes with autoantigens which are deposited in the kidney glomeruli. It is responsible for the inflammation of blood capillary vessels in the glomeruli.
45
How can you diagnose a type III hypersensitivity?
Detection of circulating Abs against the tissues involved. | Presence of antibody and complement in the lesions by immunofluorescence.
46
How would you be able to diagnose lupus?
By detecting the circulating antibodies against DNA - look for anti-nuclear protein autoantibodies (aka ANA)
47
Briefly describe type IV hypersensitivity.
Cell mediated/delayed type reactions which do not involve antibodies but mainly involve T cells and monocytes/macrophages. Reations take 2-3 days to develop.
48
What are the two phases of type IV hypersensitivities?
Sensitization and elicitation.
49
Describe the sensitization phase of type IV hypersensitivities.
Lagerhans cells (skin DCs) take up and process Ag. Migration to regional lymph nodes and T cell activation. Proliferation of T cells which migrate back to dermis.
50
Describe the elicitation phase of type IV hypersensitivities.
Mediated two ways: 1. th1 cytokines that lead to the activation of macrophages in tissues leading to inflammation (IL-1, TNFalpha) 2. by the direct killing of tissue cells by CD8+ t cells = cell lysis and tissue injury
51
Name three diseases/issues that could come of a type IV hypersensitivity and their effector cell.
``` M. tuberculosis - CD4+ cytokines IBD - CD4+ Contact dermatitis - CD4+ and CD8+ Asthma (late phase) CD4+ Th2 Graft rejection - CD8+ CTLs MS - CD4+ Th17s ```
52
What is a Montoux reaction?
It is a diagnostic test to see if an individual has previously been infected with M. tuberculosis. It is an intradermal injection of TB antigen. A reaction develops 24-72 hours after injection. Lesion is characterized by induration and erythema
53
How do Montoux reactions take place? What are the mechanisms?
Th1 cells enter injection site and recognize complexes of peptide on MHC II molecules on APCs and release inflammatory cytokines such as IFNgamma and TNFalpha. Recruitment of phagocytes and plasma causes edema and swelling.
54
A patient presents with a type IV hypersensitivity contact dermatitis. What mechanisms have led to this reaction? What reaction is taking place?
Activation of CTLs respond to sensitizing agent. The direct killing of cells that present the sensitizing Ag occur by IFNgamma. The skin gets lesions and blisters within 48 hours.
55
How are type IV hypersensitivities diagnosed?
In vivo diagnostics include the delayed cutaneous reaction (Montoux test). In vitro tests examine T cell response to measure IL-2 production.
56
How are type IV hypersensitivities treated?
Corticosteroids and other immunosuppressive agents.
57
Discuss the differences between hypersensitivity and autoimmunity.
Hypersensitivity reactions are not always autoimmune but use the immune system to respond. Hypersensitivity reactions are often linked to autoimmune diseases but not all (e.g. pollen/ragweed allergies). Many AI diseases have hypersensitivity as a part of the reaction.
58
``` What are the immune reactants in: Type I hypersensitivity? Type II hypersensitivity? Type III hypersensitivity? Type IV hypersensitivity? ```
1. IgE 2. IgG 3. IgG (can be IgM also) 4. Th1, Th2, and CTLs
59
``` What are the antigens involved in: Type I hypersensitivity? Type II hypersensitivity? Type III hypersensitivity? Type IV hypersensitivity? ```
1. Soluble antigen 2. Cell/matrix associated Ag or Cell surface receptors 3. Soluble antigen 4. Coluble/cell-associated Ag
60
``` What are the effector mechanisms in: Type I hypersensitivity? Type II hypersensitivity? Type III hypersensitivity? Type IV hypersensitivity? ```
1. Mast cell activation 2. Complement/FcR cells and Ab altered signalling 3. Complement proteins and phagocytes 4. Macrophage activation, IgE production, and cytotoxicity.
61
A child reacts to a mosquito bite. Several minutes after bite the skin is inflammed, red, and indurate. Eye starts to close shut and takes a week to disappear. What kind of hypersensitivity is this? What are the mechanisms? How can we diagnose this?
Type I hypersensitivity because it happened so quickly and they are immediate. IgE response leads to the degranulation of mast cells and inflammation RAST can be performed
62
A woman puts uses someone else's phone while speaking to someone and has it against her face. Two days later there is redness and hypersensitivity on her cheek. What kind of hypersensitivity is this? What are the mechanisms? How can we diagnose this?
Type IV contact dermatitis T cell response to the foreign antigen on the skin Patch test

Immunology 7070 (15 decks)

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