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Immunology (Parham) > Chapter 14 > Flashcards

Chapter 14 Flashcards

Allergy and the immune response to parasites

1
Q

What characterises type I hypersensitivity reactions?

A
  • allergen with IgE (specific for that allergen)
    • bound to FcεRI on mast cells, basophils, eosinophils
      • release inflammatory mediators
  • immediate
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2
Q

What characterises type II hypersensitivity reactions?

A
  • IgG/IgM with chemically reactive mol bound covalently to components on membrane of human cells
    • chemical reaction => modification in structure creating new epitopes (seen as foreign)
    • fixed (bound to cell surface)
    • ex.: penicilin
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3
Q

What characterises type III hypersensitivity reactions?

A
  • small immune complexes: IgG and antigen
    • in walls of blood capillaries, lung alveoli, kidney glomeruli
    • activate complement
  • inflammation damages tissue
  • occurs when non human antibodies / proteins are given
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4
Q

What characterises type IV hypersensitivity reactions?

A
  • nickel allergy (or other) -> nickel binds to proteins’ histidine
  • presented on MHC as non-self
  • CD4 or CD8 T cells bind
  • delayed = effect seen after a few days
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5
Q

How is parasite infection fought?

A
  • too big for phagocytosis
  • multicellular organisms
  • antigen binds to IgE -> basophils, mast cells, eosinophils release granules
    • inflammatory reaction -> removes parasites from tissues
  • type 2 immunity (mediated by TH2)
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6
Q

What is the function of basophils in TH2 response?

A
  • initiate the response
  • IL-4 and IL-13 -> T cells into TH2
  • TH2 matures and interacts with B cells -> secretion of IgE -> binds to basophils
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7
Q

What happens to IgE at the end of the immune response?

A
  • binds to receptors on mast cells and basophils
  • memory cells -> secondary response is faster
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8
Q

What differentiates IgE from other immunoglobulins?

A
  • in tissue (not blood or lymph)
    • binds to FceRI on mast cells in absence of antigen
  • amino and carboxy terminal are closer to each other
    • when bound to receptor IgE is crooked -> more outwards to capture antigens
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9
Q

What are the characteristics of mast cell and IgE binding?

A
  • many FceRI receptors on mast cells -> binds many different IgE
    • can respond to many antigens
    • quick: granules are preloaded with inflammatory mediators -> when activated releases them immediately and starts rapid production
  • during infection precursors of mast cells recruited by TH2 cells from blood -> differentiate
  • long-lived, IgE on its surface come from previous infections
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10
Q

How do B cells bind IgE?

A
  • FceRII receptors
  • can be cleaved off => soluble
    • binds to B cell receptor and co-receptor -> stimulates differentiation to IgE plasma cell
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11
Q

What is one of the ways to inhibit allergic response?

A
  • treatment with high-affinity humanised monoclonal IgG
  • binds to IgE site which normally binds to FceRI
    • reduction of expression of FceRI
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11
Q

What is histamine’s role in allergic reaction?

A
  • released as a mediator by mast cell
  • binds to endothelium: increases permeability
    • inflammatory mediators access tissue with allergen
  • smooth muscle: contraction (constriction of airways)
  • endothelial cells also stimulated by TNF-a
    • produce more adhesion molecules -> leukocytes migrate to tissue
    • TNF-a also stored and released by mast cells
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12
Q

What are the steps of eosinophils reaction when fighting allergies?

A
  • activated by external stimulus
    • have FceRI
  • enzymes and toxins kill pathogens and parasites
  • followed by slower response
    • prostaglandins (vasodilation)
    • cytokines
    • inflammatory response
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13
Q

How is reaction of eosinophils controlled?

A
  • limited generation in bone marrow
  • migration into tissues controlled by chemokines (esp CCL11)
  • expression of FceRI regulated (only once inflammation starts, production starts)
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14
Q

How are allergens presented?

A
  • trapped in mucus -> presented by APCs
  • TFH2 cells bind to protein antigens -> helper T cells stimulating type 2 immune response
  • similarities to antigens from parasites
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15
Q

What is the timeline of IgE-mediated allergic response?

A
  • immediate reaction
    • degranulation of mast cells (IgE)
      • blood vessels permeable -> fluid leaks out causing edema
    • in asthma: airways inflamed, blocked with mucus
  • late-phase reaction
    • wide-spread swelling: leukotrienes, chemokines, cytokines released by mast cell
16
Q

What is systemic anaphylaxis?

A
  • allergen in the blood -> binds to IgE on mast cells around the body
    • edema
    • organ damage
    • constricted airways
    • swollen epiglottis
17
Q

How can epinephrine control anaphylaxis?

A
  • stimulates re-formation of tight junctions in vascular endothelium
    • less fluid lost
  • relaxes bronchial smooth muscle
18
Q

What are rhinitis and asthma?

A
  • inhaled allergens
  • allergic rhinitis = violent sneezing, runny nose
    • mucous membrane -> activation of mast cells there
    • edema, obstruction of nasal airways
    • the same condition but in conjunctiva of the eye = allergic conjunctivitis
  • allergic asthma
    • chronic shortness of breath
    • submucosal mast cells (lower airways)
    • can turn into chronic asthma -> occlusion by plugs of mucus -> hyperreactivity (type IV hypersensitivity)
19
Q

What are urticaria and angioedema?

A
  • allergic reactions in skin, effects of anaphylaxis
  • urticaria = itchy swellings
    • skin mast cells
  • angiodema = diffuse swelling
    • subcutaneous tissue mast cells
    • food / drug
20
Q

What is atopic dermatitis?

A
  • also known as eczema = prolonged allergic response in skin
    • skin redness, irritation (chronic)
    • skin barrier deficient -> allergens enter easily -> inflammation
21
Q

How can foods induce allergic reaction?

A
  • broken down in GI tract -> peptides presented on APCs
    • mucosal mast cells (GI tract)
    • fluid into gut lumen, muscle contraction: cramps and vomiting (stomach), diarrhea (intestine)
22
Q

What are 3 approaches to treat allergic reactions?

A
  1. modification of behaviour and environment -> no contact with allergens
  2. drugs
    • monoclonal anti-IgE
    • limitation of inflammation
    • antihistamines = reduces rhinitis and urticaria
    • low-dose steroids -> dilate bronchioles
  3. desensitisation = prevent production of IgE (change response from IgE to IgG)
    • injections with allergens (increasing doses)
    • IgG4 produced with IL-10 -> inhibition of effector cells

Immunology (Parham) (13 decks)

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