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MICR3305 > 17 - Hypersensitivity > Flashcards

17 - Hypersensitivity Flashcards

1
Q

Type 1 / immediate hypersensitivity

A
  • Allergies
  • Caused by the release of mediators from mast cells
  • Depends on the production of IgE against environmental antigens and binding of IgE to mast cells in various tissues
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2
Q

Type 2 hypersensitivity

A

Caused by antibodies directed against cell or tissue antigens

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3
Q

Type 3 hypersensitivity

A
  • Caused by antibodies against soluble antigens in blood forming immune complexes
  • Immune complexes deposit in blood vessels in various tissues causing inflammation and tissue injury
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4
Q

Type 4 hypersensitivity

A

T cell-mediated hypersensitivity reactions mainly due to autoimmunity and exaggerated or persistent responses to microbial or ther environmental antigens

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5
Q

Atopic

A

People prone to type 1 hypersensitivities (high levels of IgE)

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6
Q

Steps of type 1 hypersensitivity

A
  • Activation of Th2 and IL-4 secreting Tfh cells, which stimulate production of IgE
  • Binding of IgE to IgE specific Fc receptors of mast calls (FcεRI)
  • On subsequent exposure to antigen, cross linking of the bound IgE activates the mast cells to release various mediators
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7
Q

Mast cell mediators in type 1 sensitivity

A
  • Immediate reaction: Rapid increase in vascular permeability and smooth muscle contraction
  • Late phase reaction: Recruit neutrophils and eosinophils to site of reaction
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8
Q

When does immediate reaction occur

A

Minutes after exposure to antigen

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9
Q

When does late phase reaction occur

A

6-24 hours after exposure to antigen

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10
Q

Common types of allergies

A

hay fever, food allergies, asthma, and anaphylaxis.

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11
Q

Activation of mast cells

A
  • Cross-linking of IgE on a mast cell by an allergen
    stimulates phosphorylation of immunoreceptor tyrosine based activation motifs (ITAMs) in the signalling chains of the IgE Fc receptor (FcεRI)
  • Initates multiple signalling pathways
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12
Q

What do signalling pathways activated by IgE cross linking stimulate

A
  • Release of mast cell granule contents (amines, proteases)
  • Synthesis of arachidonic acid metabolites (leukotrienes)
  • Synthesis of various cytokines
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13
Q

Effects of release of mast cell granule contents (amines, proteases)

A
  • Vascular dilation, smooth muscle contraction
  • Tissue damage
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14
Q

Effects of synthesis of arachidonic acid metabolites (leukotrienes)

A
  • Vascular dilation
  • Smooth muscle contraction
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15
Q

Effects of synthesis of various cytokines

A

Inflammation (leukocyte recruitment)

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16
Q

Anaphylaxis

A

Shock caused by vascular dilation and airway obstruction due to laryngeal edema

17
Q

Steps of type 2 hypersensitivity

A
  • Typically IgG antibodies causing disease by binding to their target antigens in different tissue
  • Most often autoantibodies against self antigens
  • Cause disease by IOI
18
Q

What does IOI stand for in antibodies causing disease

A

I: Inducing inflammation at site of deposition
O: Opsonising cells for phagocytosis
I: Interfering with normal cellular functions (e.g. hormone receptor signalling)

19
Q

Diseases caused by type 2 hypersensitivity

A
  • Haemolytic transfusion reaction (HTR)
  • Haemolytic disease of the newborn
  • Myasthenia gravis
  • Graves disease
20
Q

Haemolytic transfusion reaction

A
  • Blood from a type A donor is administered to a patient with type B blood
  • Anti-A antibodies in the recipient bind to and agglutinate the incoming donor type A red blood cells
  • Bound anti-A antibodies activate the classical complement cascade, resulting in destruction of the donor red blood cells
21
Q

Haemolytic disease of the newborn

A
  • If an Rh− woman carries an Rh+ baby to term, the mother’s immune system can be exposed to Rh+ fetal red blood cells.
  • Problems occur in subsequent pregnancies if foetus is Rh+
  • Treated with anti-Rh antibodies which inactivate foetal Rh antigens before they stimulate immune response in mother
22
Q

Myasthenia gravis

A

Autoantibodies against the acetylcholine receptor inhibit neuromuscular transmission, causing paralysis

23
Q

Graves disease

A
  • Autoantibodies to TSH receptor stimulate receptor without hormone
  • Thyroid produces excessive amounts of thyroid hormones, which regulate metabolism
24
Q

Steps of type 3 hypersensitivity

A
  • Antigen-antibody complexes (produced during normal immune responses), cause disease when they are formed in excessive amounts and not efficiently removed by phagocytes, and become deposited in tissues
  • Causes vasculitis
25
Q

Vasculitis

A
  • Immune complexes deposit in blood vessels, activating complement and binding Fc receptors on neutrophils, causing them to release damaging proteases and ROS
  • Leads to renal disease if occurs in kidney glomerulus
26
Q

Diseases caused by type 3 hypersensitivity

A
  • Systemic Lupus Erythematosus (SLE)
  • Serum sickness
  • Arthus reaction
27
Q

SLE

A
  • Immune complexes of anti-DNA antibodies and DNA can deposit in the blood vessels of almost any organ, causing vasculitis and impaired blood flow, leading to a multitude of different organ pathologies and symptoms
  • Causes by susceptibility genes and external factors (e.g. UV radiation)
28
Q

Serum sickness

A

Can occur as a complication of any therapy involving injection of foreign proteins, such as antibodies against microbial toxins, snake venoms and T cells, that are usually made in goats or rabbits

29
Q

Arthus reaction

A
  • Formation of immune complexes at the site of antigen injection and a local vasculitis.
  • Vaccine recipients who have previously been vaccinated or already have antibodies against the vaccine antigen, a painful swelling that develops at the injection site
30
Q

Two main mechanisms of type 4 hypersensitivity

A
  • Inflammation may be triggered by cytokines produced by CD4 T cells, causing tissue injury by activated inflammatory cells
  • Direct killing of target cells mediated by CD8 CTLs
31
Q

Delayed type hypersensitivity reaction in the skin

A
  • Occurs 24 to 48 hours after an individual previously exposed to a protein antigen is challenged with the antigen
  • Delay due to time taken for circulating effector T lymphocytes to home to the site of antigen challenge and respond to the antigen at this site.
32
Q

What are DTH reactions manifested by

A
  • Infiltrates of T cells and blood monocytes in the tissues
  • Increased vascular permeability in response to cytokines
  • Tissue damage induced by leukocyte products, from macrophages and neutrophils (that are activated by the T cells)
33
Q

Examples of diseases caused by type 4 hypersensitivity (DTH)

A
  • Chronic inflammation and tubercular granuloma
  • Type 1 diabetes
34
Q

Chronic inflammation and tubercular granuloma

A
  • In TB, a T cell–mediated immune response develops against protein antigens of Mycobacterium tuberculosis
  • Response becomes chronic because the infection is difficult to eradicate.
  • The resultant granulomatous inflammation causes injury to normal tissues at the site of infection.
35
Q

Tuberculin reaction

A
  • Sensitised for DTH by infection or injection of protein antigens
  • Subsequent exposure to same antigen elicits the reaction (testing for IFN-gamma)
36
Q

Example of tuberclulin reaction

A

Purified protein derivative (PPD), a protein antigen of Mycobacterium tuberculosis, elicits the tuberculin reaction
when it is injected into individuals who have been exposed to M. tuberculosi

37
Q

Type 1 diabetes

A
  • Activated B cells interact with CD4+ and CD8+ T cells, as well as dendritic cells (DCs)
  • Antigen presentation by B cells and DCs drives the activation of β-cell-specific CD8+ T cells.
  • In addition, the exposure of B cells to β-cell autoantigens leads to the production of islet-targeting autoantibodies,

MICR3305 (25 decks)

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