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Immunology / Micro > Hypersensitivity > Flashcards

Hypersensitivity Flashcards

1
Q

What is the definition of hypersensitivity?

A

Normal molecular / cellular mechanisms produce an innappropriately vigorous innate or adaptive response to antigens posing little to no threat.

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2
Q

What is type 1 hypersensitivity?

A

Reactions initiated by interaction between IgE and multivalent antigens

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3
Q

When is IgE normally used and what is its abundance in plasma?

A

IgE is used against parasitic infections, and is the lowest level of any Ig class.

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4
Q

What are atopic people?

A

People who are genetically predisposed to developing antibodies against common environmental allergens

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5
Q

What are the three properties of allergenic antigens, and what macromolecule are they typically?

A

Typically protein or glycoprotein.

  1. Presence of protease activity that can disrupt epithelial cell junctions to activate complement / immune system
  2. Presence of PAMPs capable of interacting w/ innate immune system
  3. Enter at VERY LOW concentrations, which favors Th2 > Th1, leading to IgE secretion
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6
Q

What are the three phases of allergy?

A
  1. Sensitization
  2. Activation
  3. Effector phase
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7
Q

What happens in the sensitization phase of allergy?

A

Initial exposure to an allergen activates Th2 response, stimulating B cells to form IgE-secreting plasma cells. The serum half-life of IgE is low, but IgE binds receptors on mast cells and basophils

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8
Q

To what receptors do Ig’s to the allergen bind

A

Fc regions bind high affinity IgE receptor, but also small contribution of IgG binding the low affinity Fc receptors

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9
Q

What is the activation phase of allergy? What substances does this include?

A

Second exposure leads to multivalent allergen crosslinking IgE high-affinity receptors, triggering degranulation

Release of vasoactive amines from mast cells and basophils, including primary / secondary mediators.

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10
Q

What is the function of the low affinity IgG receptors on mast cells / basophils?

A

Activation will inhibit the immune response generated by the IgE receptors

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11
Q

During the effector phase of allergy, what are primary vs secondary inflammatory mediators?

A

Primary - preformed and stored in granules prior to mast cell / basophil activation
Secondary - Synthesized in target cells after Galphaq activation (Phospholipase C)

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12
Q

How do mast cells in the skin differ from mast cells in the intestinal mucosa / alveoli?

A

Skin / intestinal submucosa - contains tryptase, chymase, and carboxypeptidase

Intestinal mucosa / alveoli - tryptase-positive only (think alpha-1-antitrypsin)

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13
Q

What is the primary vasoactive amine of the allergic response, and what receptor does it utilize? What does this cause?

A

Histamine - H1 receptor

Causes:
Contraction of intestinal and bronchial smooth muscles (increasing fluid leakage between them)
Increased permeability of small veins
Increased mucous secretion

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14
Q

Under what pathway are prostaglandins / leukotrienes formed?

A

Phospholipase A2 cleaves arachidonic acid, leading to their enzymatic synthesis

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15
Q

What is thought to lead to the prolonged bronchospasm and buildup of mucus seen in asthmatics? Is this part of the early or late-phase response?

A

Leukotrienes, which are released 30-60 seconds following allergen stimulation, 1000 times more potent than histamine at stimulating vascular permeability and mucus secretion.

Still part of the early response

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16
Q

What cytokines mediate the late-phase response?

A

Th2 mediated and macrophage-mediated.

IL-5 = Th2-produced -> recruit eosinophils along with eosinophil chemotactic factor (produced by mast cells)
IL-8 = macrophage-produced -> recruit PMNs
TNFalpha / IL-1 = macrophage-produced -> inflammatory influx

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17
Q

What causes the most damage during the late-response phase?

A

PMN degranulation after recruit via IL-1/IL-8. They release more leukotrienes, platelet-activating factor, and lytic enzymes

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18
Q

How is the delayed-phase response different than the late phase response?

A

Starts 3 days post-antigen challenge, it is unique in that it requires the presence of BASOPHILS.

Basophils will act on fibroblasts which recruit more eosinophils and neutrophils to cause more tissue damage

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19
Q

What is the mechanism by which systemic anaphylaxis is created? What are the symptoms?

A

Antigen is absorbed through gut or injected into bloodstream, causing massive complement activation and C3a recruitment. Leads to massive degranulation of basophils and mast cells.

Bronchiolar constriction, vasodilation (blood pressure drops) and contraction of other smooth muscles can lead to defecation, urination, and asphyxiation

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20
Q

Why is epinephrine used to treat anaphylactic reactions?

A

Relaxes smooth muscle of airways by increasing cell cAMP levels, reduces vascular permeability, improves cardiac output, and preventing vascular collapse by constricting blood vessels

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21
Q

What is hay fever and what is one strange treatment of it?

A

Allergic rhinitis - treated with oral sodium cromoglycate which prevents mast-cell triggering, reducing histamine and vasodilator release.

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22
Q

What is the other name for allergic eczema, what age group is susceptible, and how does it differ from delayed hypersensitivity?

A

Atopic dermatitis
Young children are susceptible
Differs in that it is mediated by mast cells and Th2 rather than Th1 / macrophages

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23
Q

Why can food allergies cause vomiting? Hives in random places?

A

Vomiting due to upper or lower GI local smooth muscle contraction and vasodilation

Hives because the antigen can diffuse out of the GI system and cause a local anaphylactic reaction in skin.

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24
Q

What are the origins of childhood vs adult-onset asthma?

A

Childhood - extrinsic or atopic asthma, due to genetic predisposition
Adulthood - intrinsic or non-atopic

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25
Q

What is the main cause of asthma? Why does it get worse overtime?

A

Skewed Th2 responses to inhaled antigens, leading to activation and recruitment of effector cells.

Gets worse due to airway remodeling, leading to mucus cell hyperplasia, subepithelial thickening, and loss of epithelial integrity

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26
Q

What is a wheal and flare reaction?

A

urticaria / hives

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27
Q

What is the mechanism of action of sodium cromoglycate?

A

Blocks chloride channel activity and maintains cells in normal resting physiological state

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28
Q

What is omalizumab’s role in treating asthma?

A

Monoclonal antibody directed against IgE, treats astham in early and late phase, which are both IgE dependent

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29
Q

How does early vs late phase asthma reaction differ?

A

Early - mostly mast cells
Late - activation of alveolar macrophages which release eosinophil chemoattractants, maintaining their survival and action

30
Q

What are the two main proposed mechanisms of hyposensitization?

A
  1. Repeated exposure to low doses of allergen induces Treg cells to produce TGFbeta / IL-10.
  2. Increase in non-inflammatory IgG4 rather than IgE, competitively inhibiting IgE binding and activating inhibitory FcR2 receptors
31
Q

What is isoprenaline?

A

Inhaled corticosteroid (nonselective beta-agonist) used for treatment of asthma

32
Q

What is the problem with first generation antihistamines like diphenhydramine?

A

Binds muscarinic Ach receptors causing dry mouth, constipation, slow heartbeat and sedation

Also binds H1 receptors in brain (cross BBB) to induce drowsiness

33
Q

Why are second-generation antihistamines guddle? List two

A

Fexofendadine, loratidine

Less cross reactive with muscarinic receptors and do not cross BBB

34
Q

What is Type 2 hypersensitivity?

A

Reactions involving antibody-mediated destruction of cells (other than IgE)

35
Q

What are the three mechanisms of Type 2 hypersensitivity?

A
  1. Activation of complement (especially via IgM)
  2. Opsonization and phagocytosis
  3. ADCC - antibody-dependent cell-mediated cytotoxicity
36
Q

What is ADCC?

A

Antibody-dependent cell-mediated cytotoxicity

NK cells bearing Fc receptors bind to antibodies on target cells and kill them

37
Q

What is the primary RBC lysis mechanism of transfusion reactions?

A

complement-activation, since isohemagglutinins are IgM and directed towards carbohydrates of bacterial cell moeities

This is the immediate reaction

38
Q

What is the delayed reaction of transfusion reactions? What is the treatment and what are we trying to avoid?

A

Free hemoglobin detected in plasma and filtered through kidneys (hemoglobinuria). Need a diuretic to keep kidneys following and avoid “acute tubular necrosis” caused by oxygen radicals of heme

39
Q

What is the breakdown product of hemoglobin and what does this cause?

A

Bilirubin - bilirubinemia will cause fever, chills, and nausea, plus clotting of blood vessels and lower back pain (kidneys)

40
Q

Why is the isohemagglutinin reaction to Rh factor different than the AB antigens?

A

Uses IgG subclass which doesn’t activate complement as well. Mostly opsonization and phagocytosis lead to slower hemolysis 2-6 days after transfusion. Same symptoms but less free hemoglobin in blood.

41
Q

How are babies with erythroblastosis fetalis treated?

A

UV light to break down bilirubin since it can cross BBB when you are young and cause severe neurological damage.

42
Q

How can drug-induced hemolytic anemia, thrombocytopenia, or agranulocytosis occur?

A

Certain antibiotics and other drugs can adsorb to protein on blood cell members and induce Ab formation. Immune system will attack the adducted cell via complement or phagocytosis (Fc or C3b receptors).

Which one is caused depends on what cell the drug binds to

43
Q

What can cause purpura?

A

Thrombocytopenia, leading to hemorrhage into skin and mucous membranes

44
Q

Which drug can induce all four types of hypersensitivity reactions?

A

Penicillin

45
Q

Under what conditions are antigen-antibody complexes (Type 3 hypersensitivity) not fully cleared by the immune system?

A
  1. The lattices are extensive
  2. The complexes have high affinity for particular tissues
  3. The phagocytic system is compromised and cannot efficiently clear them
46
Q

What can happen if Ag-Ab complexes are not efficiently cleared?

A
  1. Complement activation
  2. Concurrent release of C3a and C5a anaphylatoxins which attract PMNs
  3. Formation of microthrombi via interaction of immune complexes with platelets
47
Q

How do neutrophils contribute to pathology in T3 hypersensitivity?

A

Secrete proinflammatory cytokines, prostaglandins, and proteases.

The proteases and oxygen radicals destroy extracellular matrix leading to localized necrosis

48
Q

What is T3 immune complex deposition referred to if it occurs in blood vessel, kidney, or joints?

A

Blood vessel - vasculitis
Kidney - glomerulonephritis
Joints - arthritis

49
Q

When was serum sickness first observed, and what were its symptoms?

A

Repeated injections of horse antibodies against diphtheria toxin, patients would develop arthritis, urticaria, and fever/LN enlargement

50
Q

When can serum sickness still be observed and how have we combatted this?

A

Treating cancer patients with mouse monoclonal antibodies.

We replace the constant region of the antibody via recombinant DNA to human Fc.

51
Q

What is an Arthus reaction?

A

Localized swelling, erythema, and bleeding approximately 4-10 hours post intradermal antigen to which large amounts of circulating Ab already exist.

(T3 hypersensitivity, localized)

52
Q

What causes elephantiasis?

A

Dead filarial worm Wuchereria bancrofti found in lymphatic vessels causes inflammation and block of lymph flow, causing massive legs

(Type 3 hypersensitivity)

53
Q

What two microbial infections, when treated rapidly, can lead to massive buildup of immune complexs and resultant erythema?

A

Leprosy - treatment via dapsone

Syphilis - treatment via penicillin

54
Q

How are glomerulonephritis cases characterized?

A

Via site of antibody deposition

55
Q

What types of glomerulonephritis are Lupus nephritis classes 1-5?

A 
1&2 = mesangial, similar to IgA neuropathy
3&4 = subendothelial
5 = supepithelial, causes massive proteinuria
56
Q

What is linear glomerulonephritis? Give one common example

A

Immune complex deposits in the glomerular basement membrane, as in Goodpasture’s syndrome (Type 4 collagen)

57
Q

What is anti-neutrophil cytoplasmic antibody (ANCA)?

A

A type of glomerulonephritis also known as pauci-immune which develops in the absence of immune complex deposits

58
Q

What are the hallmarks of a Type 4 hypersensitivity?

A
  1. Initiation via T cells (only purely cell mediated hypersensitivity)
  2. Delay required for reaction
  3. Macrophages are primary cellular component of the infiltrate surrounding the inflammation
59
Q

What is the most common type of Type 4 hypersensitivity?

A

Contact dermatitis

60
Q

How do many type of contact dermatitis’ happen, chemically?

A

An oil or metal ion can chelate or covalent bond carrier molecules (jewellry, poison ivy / sumac), and become an immune target

61
Q

How does initial sensitization of the DTH (delayed type hypersensitivity) happen?

A

APCs, especially Langerhaans cells, carry antigens to lymph nodes and clonally expand Th1, Th2, Th17, and CD8+ T cells against the antigen for 1-2 weeks

62
Q

What is the effector phase of the DTH response?

A

Second exposure leads T cells secrete a variety of cytokines, including IFNy and TNFb, which recruits and activates macrophages / other inflammatory cells

63
Q

Why is the response “delayed” during the effector phase?

A

Inflammation doesn’t become apparent until 24 hours later, and peaks at 48-72 hours because it takes time to induce localized influxes of macrophages and their activation (via inflammatory cytokines)

64
Q

What are the major of cells in the DTH response?

A

Only about ~5% are Th1 cells, rest are macrophages and related inflammatory cells which amplify the Th1 response

65
Q

If the antigen is not easily cleared, what can a prolonged DTH reactino cause?

A

Formation of a granuloma, in which macrophages adhere to one another and form a nodule / giant multinucleated cells. These displace normal tissue cells via high concentrations of lytic enzymes.

66
Q

What is a tubercle?

A

A granuloma formed in the lungs during Mycobacterium tuberculosis infection

67
Q

What is the Mantoux test and how do you run it?

A

TB-skin test

Run by injecting PPD, a protein derived from the cell wall of TB. Check for red, swollen, firm lesion indicating previous exposure (48-72 hours later)

68
Q

What can cause a false positive and false negative Mantoux test?

A

FP - previous exposure to BCG vaccine, not routinely performed in the US
FN - T cells of immunosuppressed individuals may not respond to PPD antigen

69
Q

What is the most specific way to test for past TB exposure?

A

Mixture of mycobacterium proteins not in the TB vaccine are used to stimulate patient’s T-cells to produce IFN-y. Test for amount of IFN-y via ELISA

70
Q

What is the treatment for mild and severe DTH?

A

Mild - topical / systemic corticosteroids

Severe - more aggressive immunosuppressive therapy

Immunology / Micro (56 decks)

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