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Immunology > Ch. 15 Hypersensitivities > Flashcards

Ch. 15 Hypersensitivities Flashcards

1
Q

What is the word origin for the word “allergy”?

A 
Allos= "other"
Ergon= "reaction"
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2
Q

Why was research into type I hypersensitivities delayed for eyars?

A

free circulating IgE is usually very low in concentration in blood serum; experiments did not take place until discovery of IgE-producing myeloma

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3
Q

Describe the antigens that are usually repsonsible for type I hypersensitivities

A
  • most are proteins or glycoproteins
  • most possess many antigenic sites (epitopes) per molecule
  • often have intrinsic enzymatic proteins
  • many contain potential PAMPs, stimulating innate immunity through interactions with PRRs
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4
Q

What is the mechanism behind the development of type I hypersensitivity?

A
  • exposure to antigen activates TH2 cells and stimulates B cells to become IgE plasma cells
  • secreted IgE binds to FcεRs (receptors on granulocytes for IgE constant region)
  • second exposure to allergen crosslinks FcεRs/IgE complexes and induces degranulatioin
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5
Q

Summarize how the primary inflammatory mediator, histamine, contributes to the signs and symptoms of type I hypersensitivity.

A
  • effects within minutes
  • binds to one of four possible histamine receptors
  • H1: induces contraction of intestinal and bronchial smooth muscles, increased permeability of venules, and mucous secretion
  • H4: binding on mast cells promotes their chemotaxis to sites of finfection/allergy
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6
Q

Summarize how the secondary inflammatory mediators, leukotrienes and prostaglandins, contribute to the signs and symptoms of type I hypersensitivity

A

-initiated by mast cell degranulation
-initial contraction of bronchial and tracheal smooth muscles is by histamine
-after 30-60s, further contraction is activated by leukotrienes and prostaglandins produced by mast cell degranulation
considered to be major cause of bronchospasm and mucus buildup in asthma suffers

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7
Q

IL-$ and IL-3 secondary mediators

A

stimulate TH2 responses to increase IgE production by B cells

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8
Q

IL-5 secondary mediator

A

recruits and activates eosinophils

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9
Q

IL-8 secondary mediator

A

acts as a chemotactic factor, attracting other cells

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10
Q

GM-CSF secondary mediator

A

stimulates production and activation of more myeloid cells, including more granulocytes

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11
Q

Early Phase Type I hypersensitivity response

A
  • responses occur within minutes of allergen exposure

- mediated by mast cell granule contents (histamine, leukotrienes, prostaglandins)

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12
Q

Late Phase Type I Hypersensitvity response

A
  • responses occur hours later, a result of recruited cells

- often inflammatory cell types such as neutrophils

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13
Q

Why does an EpiPen work to halt anaphylaxis?

A

counteracts effects of histamine and leukotrienes, relaxing smooth muscles in airways and reducing vascular permeability
improves CO, avoiding vascular collapse during anaphylactic reactions

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14
Q

What types of gne products are implicated in a genetic cause of type I hypersensitivities?

A
  • proteins involved in generation and regulation of immune responsiveness (innate immune receptors, cytokines/chemokines, and their receptors, MHC proteins
  • proteins involved in maintaining epithelial barrier integrity (growth factors, proteolytic enzymes)
  • proteins involved in activating allergic responses (FCERI, growth factors, etc)
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15
Q

What types of environmental triggers can increase or decrease an individual’s risk for developing allergies?

A
  • air pollution (cigarette smoke, diesel truck exhaust, factor fumes)
  • exposure to a range of bacteria (decreases risk)
  • diet also linked to risks of developing allergy
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16
Q

Skin testing in allergy identification

A
  • injects small quantities of known allergens under skin

- swelling and redness indicate allergic response

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17
Q

4 types of treatment of allergy

A
  • drugs that reduce symptoms
  • medications that reduce allergic asthma and anaphylaxis
  • Immunotherapeutics
  • desensitization/immunotherapy
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18
Q

Drugs that reduce allergic symptoms

A
  • antihistamines, leukotriene antagonists, and inhalation corticosteroids
  • antihistamines bind and block H1 receptors on target cells
  • leukotriene antagonists work in a manner similar to antihistamines
  • inhalation corticosteroids inhibit innate immune cell activity in airways, treating asthma
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19
Q

Medications that reduce allergic asthma and anaphylaxis

A
  • block degranulation of mast cells or counter bronchoconstriction
  • epinephrine or epinephrine agonists (like albuterol)
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20
Q

Immunotherapeutics

A

Anti-IgE antibodies that bind to IgE and inhibit IgE binding to FceR molecules

  • one approved by the FDA, Omalizaumab, binds to IgE Fc region (blocking binding to FcerI)
  • high cost, no more effective than second-generation antihistamines and so is not often prescribed
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21
Q

Desensitization/Immunotherapy

A
  • Treatment by repeated exposure of gradually increasing doses of allergen
  • injection, application on skin or under tongue
  • after maintenance dose is reached (can take up to three years), allergy responses can be eliminated for several years, but not always
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22
Q

What makes up human blood groups?

A

carbohydrates

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23
Q

Why do we make antibodies for blood groups that are not our own, even if we haven’t been exposed to blood belonging to those groups at some point in our lives?

A
  • adults possess anitbodies to the blood types they do NOT have due to the similarities of these carbs with similar carb antigens on microbes
  • if they receive a transfusion of the “wrong” type of blood, their antibodies will quickly attach to the donor blood cells and trigger complement
  • the degraded RBC components can build to toxic levels
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24
Q

Explain the mechanism behind a type II hypersensitivity

A
  • massive intravascular hemolysis of RBCs
  • free hemoglobin cannot be filtered fast enough and accumulates
  • the porphyrin component of hemoglobin is degraded to bilirubin, which is toxic
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25
Q

What treatment is available for newborns that have bilirubinemia?

A
  • Exposure to UV light breaks down toxic products
  • Babies that show the telltale jaundiced appearance of toxin accumulation are treated in UV cribs
  • Mild cases associated with blood type incompatibility usually easily treated this way without transfusions needed
26
Q

Why is RhoGAM an effective preventative measure for hemolytic disease of the newborn? When is RhoGAM given as a treatment?

A

• Prevention of these reactions is by prescription of RhoGAM anti-Rh antibodies
o Given around 28 weeks as within 24048 hours of delivery
o Also given following amniocentesis
o Prevents mother’s B cells from “seeing” Rh factor

27
Q

Other than blood transfusions, what else can trigger a type II hypersensitivity?

A

• Drug induced
o Some drugs (such as penicillin, cephalosporins, streptomycin, ibuprofen) can adsorb nonspecifically to proteins on RBC membranes
 These drug-protein complexes may stimulate antibody production
 Antibodies then bind to RBCs when the drug is present, stimulating complement-mediated destruction

28
Q

Describe the mechanism behind a type III hypersensitivity response

A

• Interactions with antibody and soluble antigen generates immune complexes
• Usually, these complexes facilitate clearance of antigen by phagocytosis or binding on RBCs
o Sometimes these immune complexes can damage various tissues
o If immune complexes aren’t cleared effectively, they may deposit in tissues
• May trigger release of inflammatory mediators and activate mast cells, neutrophils, macrophages through Fc receptors
o Results in tissue damage

29
Q

Two examples of temporary cases of type III hypersensitivity

A

• Streptococcal antigen-antibody complexes can bind to the basement membrane of the kidney and cause type III responses, but once infection is cleared hypersensitivity clears
o Streptococcal glomerulonephritis
• Injections with horse antibody in the early 1900s to treat diptheria caused a systemic type III response, which resolved when antibody injections ceased
o Serum sickness 

30
Q

What is a localized type III hypersensitivity called? Provide two examples of diseases characterized by a localized type III hypersensitivity.

A

• Arthus reactions are a localized type III reactions
o An inflammatory reaction induced by injection of an Ag in an individual with high levels of circulating Ab specific to it
• Two examples:
o Insect bites
o Farmer’s lung from moldy hay
o Pigeon fancier’s disease from inhaling dried pigeon feces

31
Q

What types of antigens can trigger a chronic state of type III hypersensitivities?

A

• Autoantigens can be involved in immune complex-mediated reactions; results in chronic type III responses.

32
Q

What outcomes are the result of unresolved, or chronic, type IV responses?

A

• A prolonged DTH response can result in formation of destructive
o Multinucleate giant cells
o Granulomas
o Tubercles
• Seen in infections such as tuberculosis caused by Mycobacterium tuberculosis
• If cannot eliminate infection, walls off pathogen to contain it, but lytic enzymes damage the healthy tissue

33
Q

How does the tuberculin test work in identifying someone with a preexisting exposure to Mycobacterium tuberculosis? Why does vaccination make this test ineffective?

A

• Detected by skin test
o Inject a small amount of Ag under the skin
 If a red, slightly swollen, firm lesion develops in 48 hours and is large enough, the test is positive
• This indicates the individual has a population of sensitized TH1 cells against the Ag
• This does NOT indicate if the exposure was due to a pathogenic form or from a vaccination, which is used in some parts of the world
 Commonly used in the US to test for tuberculosis exposure
• We don’t vaccinate for TB for this reason

34
Q

Explain how contact dermatitis is the result of a type IV hypersensitivity after exposure of skin to a triggering antigen such as urushiol.

A

• Sensitization can occur if a reactive chemical compound binds to skin proteins
o Modified proteins are then presented to T cells
o Could be induced by pharmaceuticals, cosmetics, hair dye, industrial chemicals, metal ions, urushiol from poison ivy, etc.
 Quite common
• 15% affected by nickel allergycheap jewelry
 Can cause strong cell-mediated responses against skin cells, inducing blister-like lesions and rashes

35
Q

Provide an example of an antigen that is capable of causing all four types of hypersensitivity responses.

A

• Penicillin can actually induce all four types of hypersensitivities under the correct circumstances for each
o Type I: urticaria, systemic anaphylaxis
o Type II: hemolytic anemia
o Type III: serum sickness, glomerulonephtritis
o Type IV: contact dermatitis

36
Q

Infectious causes of chronic inflammation

A

o Intestinal microbes
o Continual microbial invasion can induce chronic inflammation
 Gum disease
 Unhealed wounds
 Failure of tolerance mechanisms to gut microbes
 Some microbes are ineffectively cleared, inducing chronic inflammation
• Certain fungal and mycobacterial infections

37
Q

Noninfectious causes of chronic inflammation

A 
o	Hyperglycemia/obesity
o	Autoimmune responses
o	Allergic responses
o	Organ transplantation
o	Damage-associated molecular patterns (DAMPs)
38
Q

What allergen triggers systemic anaphylaxis?

A
  • often initated by an injected or gut-absorbed allergen

- insect venom, drugs like penicillin, food: nuts, seafood, etc., latex

39
Q

What allergens trigger food allergies?

A

Food allergens are often water-soluble glycoproteins stable to heat, acid, and proteases, some of which can act as TH2 adjuvants

40
Q

H1 binding of histamine

A

induces contraction of intestinal and bronchial smooth muscles, increases permeability of venules, and mucous secretion

41
Q

H4 binding of histamine

A

promotes chemotaxis to sites of infection or allergy

42
Q

Systemic anaphylaxis initiated by

A

injected or gut absorbed allergen

ex. insect venom, penicillin, food, latex

43
Q

Symptoms of systemic anaphylaxis

A
  • drop in BP leads to anaphylactic shock
  • contractions of smooth muscle leads to defecation, urination and bronchiolar constriction
  • lead to death by asphyxiation within 2-4 minutes
44
Q

What causes systemic anaphylaxis?

A

rapid antibody mediated degranulation of mast cells

45
Q

What is the immediate treatment for systemic anaphylaxis?

A

epinephrine

46
Q

Symptoms of localized reactions

A
  • runny nose
  • sneezing
  • coughing
  • tearing
47
Q

Symptoms of localized reactions result from

A

release of mediators in immediate exposure area

48
Q

Food allergies are caused by what kind of allergens?

A

water-soluble glycoproteins stable to heat, acid, and proteases, some of which can act as TH2 adjuvants

49
Q

symptoms of food allergies

A
  • vomiting and diarrhea due to smooth muscle contraction and gut vasodilation
  • some individuals have oral hypersensitivity as well as tingling, angioedema of lips, palate, and throat
50
Q

___________ in gut can make gut more permeable, introducing allergen to blood.

A

mast cell degranulation

51
Q

Examples of air pollution that increases risk for allergy

A

cigarette smoke, diesel truck exhaust, factory fume

52
Q

atopic dermatitis

A

itching, weakens epithelial layers and lets more allergens across to stimulate

53
Q

Antibiotic use associated with ____ in food allegies

A

increase

54
Q

probiotic use associated with ____ in food allergies

A

decrease

55
Q

Mechanism of antihistamines

A

bind and block H1 receptors on target cells

56
Q

Mechanism of inhalation corticosteroids

A

inhibit innate immune cell acitivity in airways, treating asthma

57
Q

Symptoms of type III hypersensitivities

A

-fever, rashes, joint pain, lymph node enlargement, and proteinuria

58
Q

Type III hypersensitivities are mediated by

A

formation of immune complexes and deposition in tissues causing the release of inflammatory mediators and activation of mast cells, neutrophils, and macrophages through Fc receptors

59
Q

Streptococcal glomerulonephritis

A

-streptococcal Ag-Ab complexes can bind to basement membrane of kidney and cause type III responses, cleared once infection is cleared

60
Q

Serum sickness

A

injection of horse antibody serum to treat diptheria in early 1900s, resolved when injections ceased

61
Q

Arthus

A

inflammatory reaction induced by injection of an antigen in an individual with high levels of antibody specific to it

Immunology (17 decks)

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