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Host Defense Exam 2 > IgE Immunity > Flashcards

IgE Immunity Flashcards

1
Q

Define allergy.

A
  • immune response to an environmental antigen

- Type 1 hypersensitivity reaction

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2
Q

Define atopy.

A
  • ability to transfer reactivity via serum
  • genetically predisposed to having multiple allergic response
  • hereditary
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3
Q

What is the central mediator of the allergic reactions?

A

IgE = itch (utricaria), sneeze (allergic rhinitis), and wheeze (asthma)

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4
Q

What are the common effector cells of allergy?

A
  • mast cells
  • basophils
  • eosinophils
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5
Q

List components of an allergic reaction.

A
  • IgE
  • allergen
  • mast cells/basophils
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6
Q

Define IgE.

A
  • antibody
  • high affinity binding to FcE receptors on mast cells and basophils
  • very low levels in serum
  • normally, respond to worms and parasites
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7
Q

Characterize the 2 types of mast cells.

A

McT (tryptase)

  • prominent in respiratory and GI tracts
  • increase with mucosal inflammation

McTC (tryptase and chymase)
- prominent in connective tissue

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8
Q

List mast cell mediators of the allergic response.

A
  • histamine
  • prostaglandins
  • leukotrienes
  • cytokines (IL-3-6, 8, 10, 13)
  • TNF-a
  • GM-CSF
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9
Q

What are properties of mast cells and basophils relevant to the allergic response?

A
  • constitutively express high levels of FcE receptor
  • cytoplasmic granules of vasoactive mediators, such as histamine and leukotrienes
  • different phenotypic markers and lineage, but derived from HSCs
  • basophils are circulating, mast cells are in tissue
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10
Q

Define allergen.

A
  • ubiquitous environmental proteins that can induce a hypersensitivity response in atopic individuals
  • induce IgE instead of IgA/G/M
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11
Q

List the types of allergens.

A
  • aero - pollen, ragweed, etc.
  • food - milk, egg, nuts, shellfish,
  • insect venom
  • drugs
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12
Q

Define chitin.

A
  • plant polysaccharide that is found in many allergens

- induces expression of chitinase, which can induce a degranulation

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13
Q

Describe the role of genetics in the allergic response.

A
  • children of 2 atopic parents are 50% likely to be atopic as well
  • a multiplicity of genes must act in concert to mount an allergic response (ex: Tbet (INFg, Th1), mast cell signaling, FcE receptor avidity, TLRs on APCs)
  • direct relationship between IgE serum levels, allergic reactions, and atopy
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14
Q

What context is needed to get an allergic response?

A
  • time (level of exposure, how long you’ve been exposed, when in life you were exposed)
  • route of entry (mostly mucosal)
  • genetic predisposition
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15
Q

Describe the mechanism of an allergic response.

A
  1. contact with allergen - mostly mucosal, cutaneous, or systemic
  2. allergen binds to TLRs on dendritic cells
  3. antigen presentation on a Class II MHC to a naive T cell
  4. IL-4 produced by mast cells, basophils, and DCs activate the naive T cell to differentiate into a Th2 cell
  5. Th2 produces IL4 and activates class switching and allergen-specific antibody production from the B-cell
  6. IgE antibodies bind to FcE receptors on mast cells and basophils
  7. mast cells produce IL4 and activate B cell to make more antibodies (upregulation of CD23 on mast cells increases production of IL4)
  8. allergen will bind to mast cell FcEs => cross linking => signal transduction => calcium influx => degranulation
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16
Q

Recall how Th2 differentiation occurs.

A
  • APC makes IL4 => GATA => Th2 makes IL4, 5, 10, 13

- must occur in absence of IL12

17
Q

Characterize the FcE receptor.

A
  • very high affinity binding

- the only Fc receptor that can bind to an empty antibody (no antigen required to bind)

18
Q

What happens during the immediate phase of an allergic reaction?

A
  • previous exposure and sensitization is required for this to occur
  • lasts 15 minutes
  • vasoactive mediator release from mast cells and basophils
  • synthesis and release of prostaglandins and leukotrienes
  • tryptase release from mast cells activates complement
19
Q

What is the function of tryptase in the allergic response?

A
  • direct complement activation

- used as serum diagnostic marker for mast cell activation during anaphylaxis

20
Q

What happens during the late phase allergic response?

A
  • occurs within 6-8 hours
  • requires T cell activation, IL3-5, 10, 13, TNFa, GM-CSF
  • Th2 and mast cells release IL5 that recruits neutrophils and more mast cells/basophils
  • IL5 also increases FcE receptor expression
  • eosinophils increase release of major basic proteins, leukotrienes, cationic proteins (inflammatory)
21
Q

Define anaphylaxis.

A
  • acute life-threatening reaction due to mast cell and basophil mediators
  • organ = multi-systemic
  • route of entry = stings, ingestion
  • allergen = drug, food, venom
  • Sx: shock, hypotension, wheezing, angioedema, urticaria
  • can be fatal
  • Tx: epinephrine shot (but in some people, can escalate response)
22
Q

Define allergic rhinitis.

A
  • inhalation of allergen
  • main organs = nose, eyes
  • route of entry = mucosa
  • allergen = pollen, dander, molds
  • Sx: itchy eyes, nasal discharge, sneezing, nasal airway obstruction, inflammation
23
Q

Define urticaria/atopic dermatitis.

A
  • due to mast cell degranulation and skin microvascular hyperpermeability to recruited eosinophils, etc.
  • main organ = skin
  • route of entry = contact, ingestion
  • allergen - various foods, drugs
  • Sx: hives, wheals, angioedema
  • most common in ages 20-40
  • can last for a few hours or days
24
Q

Define wheals.

A
  • pruritic edematous plaques
25
Q

Define asthma.

A
  • chronic disorder of the airways
  • due to episodic bronchoconstriction, increased bronchial airway sensitivity, inflammation, increased mucus secretion
  • main organ = lung
  • route of entry = inhalation
  • allergen = pollen, dander, mold
  • Sx: wheezing, coughing, SOB, chest tightness, dyspnea, tachypnea
  • episodic attacks
  • increasing prevalence
26
Q

Describe how genes and environment interact to from an allergic response.

A

Environment

  • right allergen at the right time
  • small family (less exposure to various URI antigens)
  • hyperhygiene (less exposure to antigens)
  • antibiotics
  1. Genes + environment => Treg deficiency => atopy
  2. atopy + triggers => IgE => allergy
27
Q

What can trigger an allergy response?

A
  • reexposure
  • virus
  • pollutants
28
Q

Describe the hygiene hypothesis.

A
  • children are not getting as sick, and if they are, it is happening later in life
  • large families and day care babies are exposed to more pathogens => more URIs => more Th1, downregulate Th2 => allergies are rare in these people
  • early exposure to pathogens establishes the proper Th1:Th2 ratio
  • worms are protective because they induce Tregs in the gut that can migrate and suppress allergy and autoimmune responses in other parts of the body later on
29
Q

How can we detect if someone has an allergy?

A
  • history
  • skin test (more sensitive than blood test)
  • RAST
30
Q

Define RAST.

A

RadioAllergoSorbent Test

  1. allergen bound to well
  2. add patient serum
  3. wash => if IgE against that antigen is present, then it will be bound
  4. add radiolabeled anti-IgE antibody to detect presence of antibody against that allergen
31
Q

What are the drawbacks to allergy testing?

A
  • skin, blood, and RAST testing can be positive for the allergen, but if the patient does not have symptoms then they do not have that allergy
32
Q

List treatments to allergy.

A
  1. avoid allergen
  2. pharmacological suppression via anti-histamines
  3. anti-IgE therapy (anti-IgE monoclonal antibodies)
  4. allergen immunotherapy (SCIT, SLIT)
  5. vaccines
33
Q

Define SCIT/SLIT.

A

SubCutaneous (Lingual) ImmunoTherapy

  • giving shots of allergen
  • causes redirecting of response
  • allergen induces Th1 activation, macrophages to destroy the allergen
  • allergen causes Th2 activation, and B cell makes IgG instead
34
Q

Define allergic gastroenteropathy.

A
  • main organ = GI
  • route of entry = ingestion
  • allergen = food
  • Sx: pain, bloating, vomiting, diarrhea
35
Q

Define the role of anti-IL5 drugs in allergy treatment.

A

anti-IL5 would stop the recruitment of eosinophils and downregulate the FcE receptor

36
Q

Dogs vs. cats. Who is best for immunity?

A
  • dogs expose humans to antigens => protective immunity against allergens
  • if allergic to cats = all cats
  • if allergic to dogs = some breeds

Host Defense Exam 2 (11 decks)

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