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Microbiology And Immunology > Allergy And The Mechanisms Of Hypersentivity > Flashcards

Allergy And The Mechanisms Of Hypersentivity Flashcards

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1
Q

What is hyposensatvity?

A

An inappropriate immune response to non-infectious antigens that results in tissue damage and disease

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2
Q

What are the four type of hypersensitivity?

A

Type 1- immediate hypersensitivity

Type 2 - cytotoxic hypersensitivity

Type 3 - serum. Sickness and Arthur’s reaction

Type 4 - 44delayed-type hypersensitivity, contact dermatitis

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3
Q

What occurs in type 1 hypersensitivity (allergy)?

A

A immune reactant - IgE

Antigen - soluble antigen, eg. Allergen

Effector mechanism - mast cell activation and degranulation causing inflammation

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4
Q

What are some examples of type 1 hypersensitivity?

A

Allergic rhinitis

Asthma

Anaphylaxis

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5
Q

What is the prick test?

A

Test the allergic reaction by injection of antigen

And seeing what the immune response reacts to

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6
Q

Wat is systemic anaphylaxis?

A

A progressive inflammation

Severe loss of function

Progressive anaphylactic shock

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7
Q

What occurs in type 2 hypersenstivity?

A

Penicillin modifies rote is on human erythrocytes to create foreign epitopes - new areas antibodies can bind too.

Immune reactant - igG or anti drug antibodies directed at cell surface receptors

Antigen - drug ingested or a modified internal protein

Effector mechanism - antibody bound cells are cleared by complement + ffcgR+ cells such as macrophages - uncontrollable activation or blocking receptor function

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8
Q

What are some examples of type 2 hypersensitivity?

A

Some drug allergies

  • eg. Penicillin,
  • eg. Graves’ disease ,
  • eg. myasthenia gravis (antibodies block or destroy nicotinic acetylcholine receptors at the junction between the nerve and muscle
  • eg haemolytic disease of newborn
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9
Q

How can haemolytic disease of newborn occur?

A
  1. During fetal erythrocytes leak into maternal blood father breakage of the embryonic chorion
  2. Maternal B cells are activated by the Rh antigen an produce a large amount of antibodies
  3. Rh antibody titer in mothers blood is elevated after first exposure
  4. Rh antibodies are small enough to cross the embryonic chorion and attack the fetal erythrocytes
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10
Q

What occurs in type 3 hypersensitivity (serum sickness)?

A

Immune reactant - igG

Antigen - soluble antigen

Effector mechanism - igG and soluble antigen form immune complexes, which are cleared by phagocytosis

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11
Q

What are examples of type 3 hypersensitivity?

A

Arthur’s reaction following tetanus vaccination

Serum sickness

Farmers lung

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12
Q

What occurs during Arthur’s reaction?

A
  1. Local immune complex formation causes Activate mast cells to release inflammatory mediators
  2. Inflammatory cells invade the site and blood vessels permeability and blood flow are increased
  3. Platelets also accumulate, leading to occlusion of the small blood vessels, haemorrhage, and the appearance of purpura
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13
Q

What is serum sickness?

A

Caused by large doses of soluble antigens (drugs)

IgG antibodies produced from small immune complexes with the antigen in excess

Immune complexes deposited in tissues

Tissue damage is caused by complement activation an the subsequent inflammatory responses

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14
Q

What determines the pathology of type 3 hypersenstivity?

A

Antigen dose and route of delivery

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15
Q

What occurs in type 4 hypersenstivity (delayed type)?

A

Immune reactant - Th1, Th2 (antigen specific)

Antigen - soluble antigen

Effector mechanism - eosinophil activation (Th2), macrophage activation (Th1)

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16
Q

What are some examples of type 4 hypersensativity?

A

Tuberculin reaction

Allergic contact dermatitis

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17
Q

Describe what happens in type 4 hypersenstivity

A

Antigen is injected into subcutaneous tissue and processed by local antigen presenting cells

Th1 effector cell recognises antigen and releases cytokines that act on vascular endothelium

Recruitment of phagocytes and plasm to site of antigen injection causes visible lesion

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18
Q

What test s used to diagnose type 4 hypersensativity?

A

Mantoux test

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19
Q

Define a allergy (type 1 hypersenstivity)

A

Disease following a response by the immune system to an otherwise innocuous antigen

20
Q

What is IgE?

A

First line f defence against worms

Bin FcR1 receptor on mast cells

Pre-arms mast cells to react when in the presence of antigen

21
Q

Describe the simple model of allergen specific IgE production

A

First exposure to pollen

IL-4 drives B cells to produce IgE in response to pollen antigens

Pollen specific IgE binds to mast cells

22
Q

What causes allergic sensitisation?

A

Exposure to allergen is critical

Role of pro-allergic dendritic cells and cytokines

Genetic predisposition to allergy

23
Q

What are features of inhaled allergen that may promote the priming of Th2 cels that drive IgE responses?

A

Protein

Enymatically active

Low dose

Low molecular weight

Highly soluble - readily elated from particle

Stable - allergen can survive in desiccated particle

Contains peptides that bind host MHC class 2 - required for T cell priming

24
Q

What makes a dendritic cell pro-allergic?

A

Not known

One candidate protein is RSLP - may switch DC to pro-allergic state

25
Q

What is the role of filaggrin in allergens?

A

Flaggrin links skin integrity and allergy

Defective atopic dermatitis is greater and there are no flaggrin granules

26
Q

What is the structure of a resting mast cell?

A

Contains granules containing histamine and other inflammatory mediators

27
Q

What is the structure of a activated mast cell?

A

Multivalent antigen cross-inks bound IgE antibody, causing release of granule continents

28
Q

What mediates thee early and late phases of the allergic response?

A

Early educated by mast cells

Late response educated by T cells

29
Q

What occurs during the acute allergic response?

A

Primary allergen exposure occurs and causes IgE production

After second exposure

30
Q

What occurs during the chronic allergic reaction?

A

Primary allergen exposure occurs and causes IgE production

After second exposure

31
Q

What are the effector mediators produced by mast cells in the early phase?

A

Histamine - increase vascular permeability and cause smooth muscle contraction

Leuktrienes - increase vascular permeability and cause smooth uncle contraction and stimulates mucus secretion

Prostaglandins - chemoattractants for T cells eosinophils and basophils

32
Q

What are the effector educators produced by mast cells in the late phase?

A

Cytokines
- IL-4, IL-13 - promotes Th2 and IgE

  • TNF-a - promotes. Tissue inflammation
33
Q

What is the effect of mast cell activation in the GI tract?

A

Increased fluid secretion, increased peristalsis

Expulsion of GI tract contents

34
Q

What is the effect of mast cell activation in the airways?

A

Decreased diameter, increased mucus secretion

Congestion and blockage of airways

Swelling and mucus secretion in nasal passages

35
Q

What is the effect of mast cell activation in blood vessels?

A

Increased blood flow, increased permiability

Increased permeability

Increased fluid in tissues means more flow of lymph to lymph nodes

Increased cells and proteins in tissues means Increased effector response in tissues

36
Q

What are eosinophils?

A

Located in tissues

Recruited to sites of allergic reactions

Express FceRI upon activation

37
Q

What are the 2 effector functions of eosinophils?

A
  1. Release toxic granule proteins and free radicals upon activation to kill parasites and cause tissue damage in allergic reactions
  2. Synthesis no release prostaglandins, leukotrienes and cytokines in order to amplify the inflammatory response by activating epithelial cells and recruiting leukocytes
38
Q

What cels cause chronic allergic inflammation?

A

Th2

39
Q

What does the late phase of the IgE mediated allergic response depend on?

A

Allergen dose

Continued synthesis and release of inflammatory mediators

40
Q

What is asthma?

A

A state of reversible bronchial hyper-reactvity resulting from persistent inflammatory process in response to stimuli in a genetically susceptible individual

41
Q

What are examples of non-atopic asthma?

A

Occupational

Excerise induced

Nocturnal asthma

Post-bronchiolitic wheeze

42
Q

What are the characteristics of allergic asthma?

A

Episodes of wheezy breathing

Narrowing of airways

Rapid changes in airway obstruction

Severity varies

43
Q

what occurs in the acute response of allergic asthma?

A

Occurs within seconds of allergen exposure

Results in airway obstruction and breathing difficulties

Caused by allergen-induced mast cell degranulation in the submucosa of airways

44
Q

What occurs in the chronic is response of allergic asthma?

A

Chronic inflammation of airways

Caused by activation of eosinophils, neutrophils, T cells and other leukocytes

Mediators released by these cells cause airway remodelling, permanent narrowing of the airways and further tissue damage

45
Q

What is the treatment of allergy in the clinic?

A

Steroids - act directly on DNA to increase transcription of anti-inflammatory mediators and decrease transcription of pro-inflammatory mediators

Broncholators - reverse acute effect of allergy on airways

Immunotherapy - reverses the sensitisation to allergen by means of tolerating exposure

Inhibit effects of mediators on specific receptors - anti histamine

Inhibit mast cell degranulation - mast cell stabiliser

Inhibit synthesis of specific mediations - lypoxygenase inhibitors

Microbiology And Immunology (29 decks)

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