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FPP Weeks 1 & 2 > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

Hypersensitivity

A

Excessive or abnormal secondary immune response to a sensitizing agent

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2
Q

Allergen

A

IgE mediated disease, require sensitization
Affects only those that are sensitized to the allergen
Not dose-dependent

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3
Q

Irritants

A

Not mediated through IgE

Dose dependent response, affects all

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4
Q

Type I Hypersensitivity

A

Mast cell and/or basophil dependent (IgE-dependent)
Initial response is immediate (within 15 mins)
Degranulates releasing preformed mediators

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5
Q

Histamine

A

Short half-life
Only produced by mast cells and basophils
At least 3 receptors (H1-3R)

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6
Q

Role of H1/H2R

A

Toxic to parasites
Increases vascular permeability
Causes smooth muscle contraction

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7
Q

Heparin

A

Released by mast cells

Similar effects as histamine

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8
Q

Mast Cell Enzymes

A

Tryptase: Two forms (Alpha - Constitutively, Beta - Activated mast cell)
Identifiable in serum for up to 4 hours after release
Only mast cells make this protein
Single best marker of mast cell activation
Leads to remodeling of connective tissue matrix
Chymase, Cathespin G, Carboxypeptidase: Remodeling of connective tissue matrives

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9
Q

Mast Cell Cytokines

A 
IL-4/13: Associated with Th2 cells and lead to Ig class switching in B cells to the production of IgE
IL-3/5, GM-CSF: Promote the survival and activation
TNF: Activates endothelium and leads to adhesion molecule expression, some exists as preformed mediator
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10
Q

Mast Cell Chemokines

A

MIP-1a (CCL3): Chemotactic for monocytes/macrophages/neutrophils/T cells/eosinophils
RANTES (CCL5) and Eotaxin (CCL11): Chemotactic for T cells and eosinophils

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11
Q

Mast Cell Lipid Mediators

A

Leukotrienes C4, D4, E4: Eosinophil migration, smooth muscle contraction, vascular permeability, mucus hypersecretion
Platelet activating factor (PAF): Attracts eosinophils and other leukocytes; activates eosinophils, neutrophils, and platelets; increases production of lipid mediators

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12
Q

What reduces the threshold for histamine release?

A 
Cytokines/chemokines
Antigen exposure
Histamine-releasing factor
Autoantibody
Psychological factors
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13
Q

What increases the threshold for histamine release?

A

Corticosteroids
Antihistamines
Cromolyn (in vitro)

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14
Q

What results in elevated eosinophil count?

A 
Neoplasia
Asthma
Allergy
Connective tissue disease
Parasitic disease
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15
Q

What is CCR3 for?

A

Eosinophil receptor for Eotaxin (only known receptor) and RANTES (CCL5)

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16
Q

What do corticosteroids result in?

A

Induce rapid apoptosis of eosinophils
Inhibit the production of IL-5
Inhibition of AP-1 and NFkB via GRa

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17
Q

What produces IL-5?

A

Th2 lymphocytes and other cells

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18
Q

IL-5 effects in vitro on eosinophils

A

Prolongs survival, enhances leukotriene production, cytotoxicity for parasites
Augments B2 integrin-mediated adhesion and transendothelial migration

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19
Q

IL-5 effects in vivo

A

Infusion causes eosinophilia
Levels increased in some diseases with eosinophilia
Levels increased in fluids obtained from sites of experimental allergic late phase reactions

20
Q

Function of lysophospholipase

A

Degrades lysophospholipids

21
Q

Function of MBP

A

Mast cell activation, helminthotoxic

22
Q

Function of ECP

A

Same as MBP plus neurotoxic

23
Q

Function of EDN

A

Neurotoxin

24
Q

Function of PAF

A

Bronchoconstriction and activates platelets

25
Function of LTC4
Bronchoconstriction, mucus hypersecretion, edema
26
Examples of Type I hypersensitivity
Allergic Rhinitis Asthma Anaphylaxis Urticaria
27
What causes allergic rhinitis?
Due to cross-linking of IgE in nasal mucosa and ocular conjunctiva with specific antigen exposure Systemic symptoms are rare
28
Mechanism of Asthma
Symptoms are due in part to IgE mediated disease in lower airways Wheezing, shortness of breath due to increased airway constriction (prevents exhalation) Increased mucus secretion and production (mucus plugging)
29
Definition of Type II hypersensitivity
Antibody (IgG or IgM) binding to cell or matrix bound antigen
30
Mechanism of Type II hypersensitivity
Phagocytic or NK cells bind ot the antibody via their Fc receptor Target tissue is then destroyed Complement may be involved (increases binding via C' receptors on phagocytic cells)
31
Mechanism of drug based Type II hypersensitivity
IgG is formed against drug-cell antigen Erythrocytes and platelets are targeted resulting in spleen damage Only targets cell-bound drug
32
Examples of drug based Type II hypersensitivity
Penicillin, Quinidine, Methyldopa
33
Definition of Type III hypersensitivity
Antibody (IgG) against a soluble antigen
34
Mechanism of Type III hypersensitivity
Antigen-antibody complex activates complement Activate FcyR expressing cells and complement Large complexes cleared by phagocytes Small complexes precipitate on blood vessel walls where leukocytes bind and activate against them
35
Where is there high risk for Type III hypersensitivity?
Highly vascularized beds with narrow vessels, where the complexes are most likely to precipitate on the endothelial walls Specifically: Kidneys, vessels, joints, and skins
36
What cells are recruited with Type III hypersensitivity and what do they do?
Phagocytes (neutrophil predominant) release their lysosomal enzymes and cause tissue destruction
37
Arthus reaction
Type III reaction when skin being sensitized when exposed to specific antigen Involves activation of mast cell and other leukocytes via FcyRIII and not complement
38
Serum sickness
Type III systemic reaction from injection of large quantities of foreign protein
39
Timeframe of serum sickness
Reaction happens 7-10 days post exposure (time length for IgM to IgG) which is the peak of Ag-Ab complexes Ag drops below Ab post this point Next exposure will have a much shorter time course
40
Symptoms of serum sickness
Flu-like, urticarial rash, arthritis, glomerulonephritis
41
Farmer's lung
Alveolitis due to a type III reaction against hay dust or mold spores Inflammation in and destruction of the alveolar wall
42
Examples of systemic antigen excess situations (Type III)
Autoimmune diseases Infections: Viral hepatitis or subacute bacterial endocarditis Recurrent antigen production
43
Definition of Type IV hypersensitivity
Cell-mediated reaction (No antibodies)
44
Mechanism of Type IV hypersensitivity
Antigen enters the skin (typically target) and then binds to self proteins Bound antigen must be taken up and processed by APCs to T-cells 24-72 hour latency to reaction Involves CD4+ Th1 cells or CD8+ T cells
45
Mediators important in Type iV and role
IFN-y: Induces expression of adhesion molecules, activates macrophages TNFa and Lymphotoxin (LT): Local tissue destruction, induces expression of adhesion molecules IL-3 and GM-CSF: Stimulate monocyte production Chemokines: Recruit macrophages to site
46
Tuberculin response
Type IV hypersensitivity reaction where TB derived peptides are injected in skin Th1 mediated response develops in 48-72 hours for previously exposed individuals
47
What are contact hypersensitivity reactions and what is an example?
Chemical exposure to skin where compounds bind with self proteins and generate a response with extensive macrophage mediated inflammation Example: Poison ivy or Rhus Dermatitis (due to pentadecacatechol)

FPP Weeks 1 & 2 (18 decks)

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