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Immunology > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is a hypersensitivity reaction?

A

An overreaction to harmless antigen; usually environmental

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2
Q

What is an allergen?

A

An antigen that causes overreactions

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3
Q

What is atopy?

A

The genetic tendency to develop allergic diseases, typically associated with heightened immune responses to common allergens, especially inhaled allergens and food allergens.

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4
Q

How can a chemical, like a drug, be an allergen?

A

Chemicals can penetrate outer layers of skin and bind covalently and non-specifically to proteins and modify self-proteins

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5
Q

What is the typical T-cell response type generated by hypersensitivity?

A

Th2

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6
Q

What is Type I hypersensitivity?

A

IgE mediated hypersensitivity

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7
Q

What is Type II hypersensitivity?

A

IgG/IgM mediated hypersensitivity

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8
Q

What is Type III hypersensitivity?

A

Immune complex mediated

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9
Q

What is Type IV hypersensitivity?

A

Cell mediated hypersensitivity; delayed type hypersensitivity

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10
Q

What type of hypersensitivity is not antibody mediated?

A

Type IV

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11
Q

What is the general goal of IgE?

A

To rid the body of large, multicellular organisms (parasites, helminths)

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12
Q

What is the prerequisite for Type I hypersensitivity response?

A

IgE must be produced upone first exposure to antigen

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13
Q

How many times must a person be exposed to an antigen before a hypersensitivity reactions occurs?

A

Hypersensitivity rxns occur after second exposure to the antigen

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14
Q

What triggers eosinophilic degranulation in a type I hypersensitivity reaction?

A

Cross-linking between FceR on eosinophils and IgE antibody on a parasite following a secondary exposure the parasite/antigen triggers degranulation

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15
Q

Which cytokines are used in promotion of a anti-parastic Th2 response?

A

IL-4, IL-5

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16
Q

What is the hygine hypothesis?

A

States that children are exposed to fewer, less heavy infections that their parents leading to an underdeveloped, un-educated, less experienced immune system, leading to a greater incidence of allergy

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17
Q

Where is IgE typically most concentrated?

A

In the tissues

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18
Q

True or False: IgE can bind to FceRI only with antigen bound

A

False- must be no bound antigen

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19
Q

On what cells are FceRI constiuitively expressed?

A

Mast cells and basophils and activated eosinophils

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20
Q

What is the relative affinity of IgE for FceRI?

A

Very high, almost irreversible affinity

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21
Q

Once the primary IgE response subsides, all IgE molecules that did not see antigen bind to FceRI on mostly what cell? WHy this cell?

A

Mostly to mast cells because they live longer than basophils

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22
Q

What makes up the antigen receptor on mast cells?

A

FceRI + IgE

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23
Q

True or False: A mast cell/ basophil can have antigen receptors of more than one specificity

A

True

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24
Q

How does secondary antigen exposure induce degranulation in a type I hypersensitivity response

A

IgE not complexed with the first encounter of the pathogen bind to FceRI receptors on mast cells, and with secondary exposure the antigen cross-links between the IgE-FceRI and signals degranulation

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25
Q

How does Omalizumab work?

A

Humanized MOAb specific for the sit on IgE that binds to FceRI, which inhibits binding of IgE to mast cells, prevents cross linking and stops degranulation

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26
Q

What are the two types of mast cells?

A

Mucosal and connective tissue mast cells

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27
Q

What are the beneficial functions of the mast cells?

A

Maintain tissue integrity, alert the immune system, facilitate repair of wounds

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28
Q

What are the preformed mediators released by mast cells?

A

Histamine, enzymes/ metalloproteases, TNF-alpha

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29
Q

What are secondary mediators released by mast cells?

A

Chemokines, cytokines, eicosinoids (leukotrienes and prostaglandins)

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30
Q

What are the effects elicited by histamine? Through what receptor?

A

Induces vessel permeability and inflammation, smooth muscle contraction, and secretion of mucus; H1 receptor

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31
Q

True or false: Eosinophils are less toxic than mast cells?

A

False

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32
Q

What eosinophilically released compound stimulates histamine release?

A

Major Basic Protein

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33
Q

What cytokine induces the activation/proliferation of eosinophils? What chemokine controls eosinophilic migration?

A

IL-5; CCL11

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34
Q

How do basophils stimulate a Th2 response?

A

Secretion of IL-4 and IL-13

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35
Q

How do basophils stimulate B cells to class switch to IgE/ IgG4 producing cells?

A

Basophils express CD40L

36
Q

What are the characteristics of allergens?

A

Low molecular mass, high solubility, and high stability

37
Q

What is a wheal and a flare in the context of allergy testing?

A

Clinicians test patient sensitivity by injecting small quantities of antigen into the skin; a wheal is edema at the site of infection, a flare is an area of redness

38
Q

What type of allergen are eliminated quickest? Longest?

A

Airborne quickest, blood/ connective tissue longest

39
Q

What type of allergen causes systemic anaphylaxis?

A

Blood antigens

40
Q

What are the possible symptoms of anaphylaxis?

A

Edema in many tissues, hypotension, irregular heartbeat, loss of consciousness, difficulties swallowing and breathing, stomach cramps and vomiting

41
Q

What is the most common cause of anaphylactic shock?

A

Penicillin or related drugs

42
Q

What is allergic rhinitis?

A

Caused by inhaled allergens, leading to localized edema and obstruction of nasal airways, histamine release irritates the nose, nasal discharge and fluid-blocked sinuses

43
Q

What type of hypersensitivity is chronic asthma?

A

Type IV

44
Q

What is urticaria?

A

The wheal and flare reaction— hives or welts

45
Q

What is angioedema?

A

Activation of mast cells deeper in the subcutaneous tissue

46
Q

What is atopic dermatitis?

A

A more prolonged allergic reaction in the skin causing chronic itching

47
Q

How are corticosteroids used in treatment of allergic reactions?

A

Prevent secondary mediators from contributing to the inflammation

48
Q

How does cromolyn sodium work? IN what medicines is it found?

A

Prevents degranulation of granulocytes

49
Q

How does albuterol work?

A

B- adrenergic receptor agonist

50
Q

What is the function of metalloproteases?

A

Breakdown of extracellular matrix proteins

51
Q

How can a drugs like penicillin lead to a Type II hypersensitivity reaction

A

The drug can go bad and modify RBC or platelets resulting in hemolytic anemia or thrombocytopenia

52
Q

What is the time frame of onset for a Type II hypersensitivity reaction?

A

Within hours

53
Q

What antibodies are typically involved in a Type II Hypersensitivity reaction?

A

IgG or IgM

54
Q

What is the process of a primary response in a hypersensitivity type II reaction?

A

A patient with bacterial infection has deposition of Cb3 on RBCs as a side effect of infection. When the patient is treated with penicillin it can bind to the RBC surface and form new epitopes, which are recognized by immune cells

55
Q

What occurs with subsequent exposures to penicillin (or initial drug) with a type II hypersensitivity reaction ?

A

When treated with the same drug again the antibody specific for the drug modified self-peptides binds to cells and activates complement and recruits macrophages to phagocytosis them or complement deposits on the surface resulting in lysis

56
Q

What type of hypersensitivity reactions are autoimmune diseases such as myasthenia gravis or type II diabetes?

A

Type II

57
Q

What type of hypersensitivity reaction is a incompatible blood transfusion reaction?

A

Type II

58
Q

What mediates Type III hypersensitivities?

A

Small immune complexes that deposit on the walls of blood vessels or alveoli

59
Q

How do small immune complexes cause problems in type III hypersensitivities?

A

Immune complexes will accumulate on tissue and then fix complement and initiate inflammatory reactions which leads to tissue damage

60
Q

What is the typical instigator of type III hypersensitivity reactions?

A

Antibodies derived from non-human species

61
Q

Are large or small immune complexes most efficient at eliciting a hypersensitivity III reaction? Why?

A

Small- large IC aggregations can more easily fix complement and be engulfed and cleared by phagocytes

62
Q

What is the arthus reaction?

A

A local, subcutaneous Type III reaction triggered in the skin of sensitized patients

63
Q

What are the series of events that yield and arthus reaction?

A

Decomposition of complement on immune complexes, recruitment of immune cells

64
Q

How does an arthus reaction present?

A

Erythema and swelling with induration

65
Q

What is the time frame for onset of the arthus reaction?

A

4-48 hours after injection

66
Q

What is serum sickness?

A

A systemic type III hypersensitivity reaction

67
Q

What is the time course for the incidence of serum sickness?

A

Symptoms occur with 7-10 due to deposition of IC in tissues

68
Q

What antibody mediates serum sickness

A

High affinity IgG

69
Q

What are the signs of serum sickness?

A

Vasculitis, nephritis, arthritis, glomerulonephritis

70
Q

What are the common instigators of serum sickness?

A

Drugs (i.e., penicillin), non-humanized monoclonals

71
Q

What autoimmune diseases cause Type III sensitivities?

A

Subacute bacterial endocarditis, systemic lupus erythematosus, chronic tissue organ rejection

72
Q

What mediates Type IV sensitivity reactions?

A

Antigen- specific T cells

73
Q

What is the time frame for the onset of Type IV hypersensitivities?

A

1-3 days after exposure to antigen

74
Q

What are the two types of damage caused by Type IV hypersensitivity?

A

CD4+ cell and macrophage- induced damage; CD8+ cytotoxic damage

75
Q

What type of hypersensitivity requires the most antigen?

A

Type IV

76
Q

What is the sensitization of a type IV hypersensitivity reaction?

A

Antigen is presented to and processed by the APC that migrate to the regional lymph node and activate naive specific T cells

77
Q

What occurs in the second exposure in a hypersensitivity IV reaction?

A

Antigen is recognized by few antigen specific T cells activated and they will release cytokines, chemokines, and initiated inflammatory response at site of secondary antigen introduction

78
Q

What are common items that can cause CD4 mediated contact dermatitis? What is the likely common instigator? How does it present

A

Coins, jewelry, and metallic objects; nickel; inflammation anywhere the body contacts nickel

79
Q

What compound in poison ivy/ poison oak is a powerful hapten?

A

Pentadecatechol

80
Q

How does a CD8 mediated contact sensitivity reaction happen?

A

Proteins of skin cells are degraded ad become altered peptides which are presented to CD8 via MHC I; sensitization CD8 T cells attack areas of skin in contact

81
Q

What is the immune response to in Celiac disease ?

A

Gluten

82
Q

How is celiac disease mediated?

A

CD4+ T cells react with gluten derived peptides in the GALT and activate tissue macrophages, secreting proinflammatory cytokines and causing inflammation in the small intestines

83
Q

What would be the result of continuous intake of gluten in a patient with celiac disease?

A

Atrophy of the villi, malabsorption of nutrients, and diarrhea

84
Q

What is the basis of the tuberculosis test?

A

A delayed type hypersensitivity reaction to tuberculin inject under the skin

85
Q

What is the cause of acute rheumatic fever?

A

Cross reactive antibodies between M protein of strep pyogenes and cardiac tissue

Immunology (13 decks)

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