Allergy And Hypersensitivity

Front 1

Type 1:

Back 1

Immediate hypersensitivity-
- occurs in minutes
- mediated upon binding of IgE to allergen.
- genetic and environmental factors.

Front 2

Type 2:

Back 2

Antibody-dependent cell cytotoxicity; IgG, IgM. Cytoplasmic or cell surface antigen

Front 3

Type 3:

Back 3

Immune Complex mediated (igM and IgG. Soluble antigen

Front 4

Type 4:

Back 4

Delayed type hypersensitivity; Mediated by T cell.

Front 5

IgE is present where?

Back 5

Tissue mast cells and cirulating basophils.

Front 6

What is released from mast cells when it is bound to IgG?
IgG binding also causes the producion of what?

Back 6

GM-CSF, Eotaxin, histamine, serotonin, etc. These are inflammatory mediators. IL 3-6, PAF, LTC4, PGD2, LTB4

Front 7

Name clinical features of allergic reactions: (5)

Back 7

Acute urticaria, systemic anaphylaxis, rhinitis, asthma, food allergy.

Front 8

Through which routes are type 1 hypersensitivity achieved? (4)

Back 8

Skin Contact
Injection
Ingestion
Inhalation

Front 9

Type 2 hypersensitivity uses which antibodies?

What do the antibodies specify against? (2)

Back 9

IgM and IgG

IgM and IgG produced against intrinsic antigens and extrinsic Antigens.

Front 10

Antibody binding to the surface of host cells leads to: (4)

Back 10

Opsonization
Complement activation
NK cell activation
Activation or blockage of important cell receptors.

Front 11

ADCC destruction of host cells occurs through:

Back 11

NK cell binding to FC portion of IgG.
NK cell release of perforins and granzymes.

Front 12

Myathenia Gravis:

Back 12

Antbodies activate or block important cell receptors. Acetylcholine receptors.

Front 13

Diseases mediated by ADCC:

Back 13

ABO and Rh Blood group incompatibilities.

Front 14

Autoimmune diseases:

Back 14

Idiopathic thrombocytopenic purpura
Myasthenia gravis
Goodpasture's
Graves

Front 15

Type 3: disease pattern:

Back 15

Deposit of Immune complexes into various tissues. If they deposit into the capillaries: activation of classical complement pathway.

Front 16

Signs of inflammation:

Back 16

Heat, redness, swelling pain, loss of function.

Front 17

Immune complex is caused when what is more present?

Back 17

Antigen is in excess during antigen-antibody complexes

Front 18

Associated pathologies to Type III:

Back 18

Arthus reaction
Serum sickness
Immune Complex Glomerulonephritis
Extrinsic Allergic Alveolitis

Front 19

Arthus reaction:

Back 19

Local reaction resulting from subcutaneous injection of any soluble antigen for which the host has a significant IgG titre.

excess antigen with antibodies in the extracellular spaces.

Front 20

Serum sickness

Back 20

Leads to chills, fever, rash, arthritis and glomerulonephritis.

Occured before antibiotic development when people were injected with horse serum.

Front 21

Type 4:
What tests would you use to identify this? Why would you want to identify this?

Back 21

T-cell mediated.
Use tuberculin test.
In order to determine what you have been exposed to.

Front 22

Tuberculin test

Back 22

Injection of dead TB.
APC will present peptides to Th1-cells. Release of INF-gamma and TNF-beta.

Front 23

INF gamma and TNF beta (3 functions)

Back 23

Stimulates expression of adhesion molecules on endothelium
Increase local blood essel permeability
Attract and retain macrophage

Front 24

Poison Ivy: (3)

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Contact dermatitis
Lipid soluble antigen.
Binds to self peptides and MHC 1 presentation.

Front 25

IgE is produced by:

Back 25

Plasma cells

Front 26

IgE is bound on: (3)

Back 26

Tissue Mast cells
Circulating Bsophils
Activated eosinophils

Front 27

How are IgE bound to these cells ?

Back 27

Fc-Epsilon-RI

Front 28

Two types of Fc-Epsilon Receptors:

Back 28

RI: high affinity receptor for IgE.
CD-23 (Fc-Epsilong-RII): low affinity receptor for IgE. Enhances antibody response

Front 29

Mast cells release mediators at different body systems (3) and cause three different pathologies.

Back 29

GI tract: diarrhea, vomitting
Respiratory system: coughing, wheezing, and mucus production
Blood vessels: hypertension and arrhythmias

Front 30

Type 1 hypersensitivities are either localized or systemic based on: (3)

Back 30

Nature/quantity of allergen
Route of introduction of allergen
Other host factors: PAF (platelet activating factor)

Front 31

Production of IgE from B cells requires:

Back 31

1) Costimulator ligand CD40L on T cells.
2) Secretion of IL-4/IL-13 by mast cells/basophils/Th2. IL-4,13 receptors are heterodimers.

Front 32

IL-4, -13 receptors:

Back 32

Activate STAT6--> only factor important for IgE production.

Front 33

Celiac disease, what type of hypersensitivity?

Back 33

type 4

Front 34

Genetic cause of allergies: (3)

Back 34

Polymorphism in IL-4 region. Increased IL-4 production.

IL-4 receptor alpha constitutively active.

Haplotypes of MHC Class II which can present pollens to Th2 better.

Front 35

What is fillagrin?

Back 35

Prevents allergens from coming into skin. Skin barrier integrity.

Front 36

Critical window:

Back 36

to expose child to microbes in order to reduce atopic diseases. The age of three months!

Front 37

Mast cell release:
Immediate:
Minutes:
Hours:

Back 37

Imm: Histamine, TNF-alpha, Proteases, Heparin
Minutes: Prostaglandins and Leukotrienes
Hours: IL-4, IL-3

Front 38

Mast cells are derived from:

Back 38

CD34+ progenitor cells

Front 39

Where is the major site of differentiation for mast cells

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Connective tissue

Front 40

Major growth factor for mast cells:
Receptor for this factor:

Back 40

MGF: Stem-cell factor which acts on C-kit receptor

Front 41

Mast-cell cytosis occurs due to what:

Back 41

Mutation of C-kit receptor (gain of function). Cells are always active and have massive proliferation.

Front 42

Life span of Mast cell:

Back 42

Week to months.

Front 43

What are the two major subsets of mast cells: i.e. where are they found?

Back 43

Connective tissue mast cells
Mucosal mast cells

Front 44

Individuals with mutation in filaggrin are strongly predisposed to:

Back 44

Eczema

Front 45

Histamine and lipid mediators cause:

Back 45

Vascular/smooth muscle response: immediate reaction

Front 46

Cytokines mediate:

Back 46

Inflammation: late phase reaction

Front 47

All hypersensitivity cells derive from which common precursor?

Back 47

CD 34+ progenitor cells

Front 48

Eosinophils:
Site of maturation
Which IL influences it:
What type of receptor does it express?

Back 48

Site: Bone marrow
IL-5
FC-Epsilon-R1.

Front 49

How do eosinophils migrate? (What does it respond to?)

Back 49

It responds to Eotaxins.

Front 50

Eosinophil products: (3)

Back 50

Major basic protein
Eosinophil-derived neurotoxin
Eosinophil Cationic protein

Front 51

Eosinophils are important for what type of responses?

Back 51

Important for response against extracellular parasites.
Viral response, due to RNAses in granules.

Front 52

Eosinophils use what methods to respond to bacterial responses.

Back 52

Secretes IL-4 to help polarize lymphocytes towards Th2.
Ejects DNA in order to capture bacteria.

Front 53

Eosinophils are also important for what large scale alteration?

Back 53

Tissue remodelling.

Front 54

Basophils:
differentiating molecule

Back 54

IL-3/5, CM-CSF

Front 55

Different from Eosinophils:

Back 55

Always have high expression of Fc-Epsilon-RI

Front 56

Important role of Basophils:

Back 56

Modulating the secondary immune response since it produces large quantities of IL-4, IL-13.
Also expresses CD40L

Front 57

Late phase response occurs after what period of time:

Back 57

After a few hours, up to 12 hours.

Front 58

Immediate response due to:

Back 58

Histamine and prostaglandins.

Front 59

Histamine and prostaglandins cause: (2)

Back 59

Rapid increase in vascular permeability

Contraction of smooth muscle

Front 60

Late phase reaction caused by:

Back 60

Release of leukotrienes, chemokines, and cytokines

Front 61

Late-phase reaction causesL

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Recruitment of other leukocytes to the site of inflammation

Less marked than immediate response.