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Immunology #2 > Hypersensitivities 1 > Flashcards

Hypersensitivities 1 Flashcards

1
Q

Hypersensitivities

A

Abnormal immune reactions- inappropriately directed immune responses to inherently harmless environmental antigens (food, pollen, etc.)

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2
Q

Types of hypersensitivities

A
  • Type I (IgE mediated)
  • Type II (IgG mediated)
  • Type III (immune complex mediated)
  • Type IV (T cell mediated) – delayed hypersensitivity
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3
Q

Type I hypersensitivity

A
  • Immediate hypersensitivity
  • Mediated by IgE antibodies
  • Effector cells: mast cells, basophils, eosinophils
  • Includes both anaphylaxis and allergy
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4
Q

Anaphylaxis

A

Systemic and severe (life threatening)

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5
Q

Allergy

A

Localized and not usually immediately life threatening

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6
Q

Type I hypersensitivity antigen binding

A

IgE antibody will bind to Fc-receptor (Fc epsilon RI) on mast cells, basophils triggers cells degranulation

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7
Q

What causes the pathogenesis of tissue damage?

A
  • Due to the effects of the released granules
  • Results in vasodilation, pruritus, and bronchoconstriction
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8
Q

IgE structure

A
  • 2 heavy chains and 2 light chains
  • Similar to IgG
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9
Q

Where are IgE found?

A
  • Predominantly at body surfaces (skin, intestine, and lung)
  • Also found bound to mast cells and basophils
  • Most individuals produce very low levels if IgE (but will increase with parasite load)
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10
Q

IgE half life

A

11-12 days

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11
Q

What induces IgE?

A

parasites

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12
Q

What antibody causes Allergies ?

A

A result of IgE production to an antigen

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13
Q

Atopy

A

Condition in which IgE is produced at abnormally high levels to many antigens

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14
Q

IgE Receptors

A
  1. Fc(epsilon)RI
  2. Fc(epsilon)RII
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15
Q

Fc(epsilon)RI

A
  • receptors with very high affinity binding for IgE
  • found on mast cells and basophils and sometimes found on eosinophils
  • Also found on dendritic cells and monocytes of atopic patients
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16
Q

Fc(epsilon)RII

A
  • Receptor with much lower affinity for IgE
  • Found on NK cells, macrophages, dendritic cells, eosinophils, platelets, and some B cells
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17
Q

What does binding of antigen or IgE to dendritic cells and monocytes on atopic patients result in?

A

Binding to these cells results in increased cytokines and drives further IgE production

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18
Q

Mast cell response to encountering antigen

A
  • Cytokine synthesis and secretion
  • Granule exocytosis
  • Prostaglandin and leukotriene synthesis

OVERALL: acute inflammatory response

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19
Q

Mast cell response speed

A
  • Almost immediate response and release of immune mediators
  • Already visible at 5 seconds, and then very large, obvious release by 60 secs
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20
Q

Granule Exocytosis(seconds to minutes)

A
  • Histamine
  • Serotonin
  • Tryptase
  • Kallikreins
  • Proteases
  • Proteoglycans
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21
Q

Eicosanoid synthesis and secretion (mins)

A
  • Leukotrienes
  • Prostaglandins
  • Platelet activating factor
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22
Q

Effect of histidine

A

Smooth muscle contraction (bronchoconstriction), exocrine secretions (mucus, tears, saliva)

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22
Q

Cytokine synthesis and secretion (hours)

A
  • IL-4
  • IL-5
  • IL-6
  • IL-13
  • TNF-alpha
  • MIP-1alpha
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23
Q

Effect of serotonin

A

Vasodilation (edema)

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24
Q

Effect of proteases

A
  • Trypsin
  • Chymotrypsin
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25
Q

Effect of arachidonic acid

A

Prostaglandins, thromboxanes, leukotrienes
- Some effect on vessel tone and permeability

26
Q

Role of eosinophils

A

Are mobilized and activated in Type I hypersensitivities
- Mobilized by the IL5 from the Th2 response
- Eosinophil chemotaxis is also increased by mast cell degranulation/inflammation

Degranulation which is induced by IgE/antigen binding at FcRII and by Th2 cytokines

27
Q

Degranulation of eosinophils

A
  • Small vesicles of the secondary granules (crystalloid) bud off and move to the plasma membrane and release granule contents extracellularly
  • Results in killing bacteria and parasites but also causes tissue damage
28
Q

What is in the eosinophil granules?

A
  • Major basic protein
  • Eosinophilic cationic protein
  • Eosinophilic peroxidase
  • Eosinophilic- derived neurotoxin
29
Q

Eosinophils effect on mast cells

A

Will exacerbate the inflammation that is triggered by mast cells

30
Q

Phase of exposures

A
  1. Sensitization
  2. Re-exposure
31
Q

Sensitization

A
  • The phase of exposure to antigen that causes an IgE immune response
  • IgE is produced and will bind to the high affinity receptors on mast cells
32
Q

What factors affect sensitization?

A
  • Nature/dose of antigen
  • Site of exposure/antigen presenting cells
33
Q

Re-exposure

A

Phase of exposure where you are re-exposed to the antigen and results in cross-linking of the IgE on mast cells which triggers degranulation

34
Q

Steps of exposure

A
  1. Allergen enters mucosa. Dendritic cells phagocytose allergen
  2. Dendritic cell primes T cell in lymph nodes. Resulting in Th2 T cells and B cell activation (IgE antibodies)
  3. Plasma cell travels back to mucosa and produces allergen-specific IgE antibodies
  4. Allergen-specific IgE binds to mast cell and triggers mast cell degranulation
  5. At the same time, IL-5 from the mast cells and Th2, and binding of antigens/IgE to eosinophils results in their activation and degranulation
35
Q

Clinical manifestations of Type I hypersensitivities

A

** depends on number and location of mast cells affected
1. Anaphylaxis
2. Allergies

36
Q

Anaphylaxis

A
  • Can occur if antigen is administered systemically and rapidly and there is generalized mast cell degranulation
  • Symptoms vary with species but likely due to binding of vasoactive molecules to receptors on smooth muscles of vessels, bronchi, GI tract
37
Q

Anaphylaxis in cattle and sheep

A
  • Serotonin, kinins, leukotrienes- main target organ is lung
  • Results in dyspnea due to bronchoconstriction and pulmonary edema
38
Q

Anaphylaxis in horses

A
  • Serotonin and histamine- main target is lungs and intestine
  • Results in coughing, dyspnea and diarrhea
39
Q

Anaphylaxis in dog

A
  • Histamine, prostaglandin, leukotrienes- main target is liver
  • Results in weakness/collapse
40
Q

Anaphylaxis in pig

A
  • Histamine- main target is lungs
  • Results in dyspnea
41
Q

Anaphylaxis in cats

A
  • Histamines and leukotrienes- target organ are lungs and skin
  • Results in scratching of skin and dyspnea
42
Q

What often causes anaphylaxis?

A
  • Drugs- vaccines, hormones, penicillin, etc.
  • Parasites- blackflies, midges, stable flies, mosquitoes
43
Q

Symptoms of anaphylaxis from parasites

A

Symptoms vary from intense pruritus to acute death associated with allergy to saliva

44
Q

Allergies

A
  • Local type I events
  • Caused by inhalation, ingestion, or percutaneous exposure to the antigens
  • Site of symptoms does not always relate to the site of exposure
    »Most allergens result in skin manifestations irrespective of route of entry
45
Q

Histological lesions of allergies

A
  • Edema
  • Infiltration of mast cells and eosinophils
46
Q

Allergic disease of the skin

A
  • Degranulation of mast cells in the skin result in vasodilation, edema, and inflammation
  • Pruritis
47
Q

Allergen examples

A
  • Aeroallergens (dust mites, pollens, molds)
  • Ectoparasites
  • Food
  • Drugs
48
Q

Skin allergy conditions

A
  • Urticaria/angioedema
  • Atopic dermatitis
  • Flea allergy dermatitis
  • Eosinophilic granuloma complex in cats
49
Q

Urticaria

A
  • Hives
  • Acute local response manifest as wheals
    o Not usually pruritic, lesions confined to the dermis
50
Q

Angioedema

A

More generalized dermal edema which can progress to involve subcutaneous tissue
- Can progress to anaphylaxis

51
Q

What is typically the allergen in vaccines?

A

adjuvant

52
Q

Atopic dermatitis

A

Occurs in individuals that respond with IgE to variety of allergens (typically house dust mites, food, environment, antigens)
- Predisposed by genetics (ex. several breeds of dogs)

Sensitization exposure is usually percutaneous

Can be complicated by secondary infections and/or flea allergies

53
Q

Clinical signs of atopic dermatitis

A
  • Chronically inflamed and itchy skin
  • Pruritus
  • Self trauma
54
Q

Itch mediators

A
  • Histamine
  • Some prostaglandins and leukotrienes
  • Some neuropeptides
  • IL-31
55
Q

IL-31 role in atopic dermatitis

A
  • Itch mediator
    -Causes intense itching
  • Activates bronchial epithelial cells and plays a major role in respiratory allergies
  • Produced by both Th2 cells and mast cells in response to antimicrobial peptides
56
Q

Flea allergy dermatitis

A

Similar to pathogenesis to atopic dermatitis but the most important predisposing factor is repeated flea exposure
- Results in pruritis, self-trauma, secondary infections

Causative antigens are components of flea saliva (similar in black flies, black ant, cockroach)

May also be due to type IV reactions

57
Q

Food allergies

A

IgE responses to food (can also be associated with IgA deficiency)
- May manifest as either GI signs (diarrhea/vomiting 10-15%) or as pruritic dermatitis (most cases)

Signs are typically in 4-24 hours of exposure/re-exposure
- Symptoms mild to severe

Diagnosed to exclusion diet/symptoms on reintroduction

58
Q

Most common food allergens

A
  • Dogs: wheat, beef, soy, fish, chicken, dairy products
  • Pigs: fishmeal, alfalfa
  • Horses: wild oats, alfalfa, clover
59
Q

IgA deficiency cause

A

Failure of immune exclusion of dietary antigens

60
Q

Allergic Rhinitis/Asthma

A

Type I reactions to mold
- Occurs in cattle, cats, Basenji dogs, horses (component of COPD or heaves which is seen with heave line)
- Immediate effects of edema and bronchoconstriction, which results in dyspnea

61
Q

Treatment of allergies

A
  • Avoid the allergen
  • Treat secondary infections
  • Anti-inflammatory agents to prevent mast cell degranulation
  • Anti-pruritus agents (anti-IL31 monoclonal antibodies, Apoquel- decreases proinflammatory cytokines by JAK1 inhibition which is the signal pathway for itching)
  • Hyposensitization
62
Q

Hyposensitization

A
  • Repeated injection of allergen subcutaneously at increasing doses
    o Promotes switch to Th1 cytokines and IgG response and IFN gamma which results in less activation of mast cells
  • ~50-80% effective in dogs. Most dogs require lifelong therapy (injection every 2-4 weeks)

Immunology #2 (17 decks)

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