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Immunology > hypersensitivity > Flashcards

hypersensitivity Flashcards

1
Q

what is hypersensitivity more commonly known as?

A

Allergy / autoimmunity Hypersensitivity is a growing problem

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2
Q

what is happening to the incidence of children with asthma in the population?

A

There is a large increase in children suffering from asthma.

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3
Q

what is happening to the amount of allergic diseases among adults in the population?

A

large increase in allergic diseases among adults

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4
Q

How is hypersensitivity a growing problem in the dental surgery in terms of the dental team?

A

Dentists and nurses are becoming increasingly sensitised to latex and dental materials.

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5
Q

How is hypersensitivity a growing problem in the dental surgery in terms of patients?

A

Patients are becoming increasingly sensitised to latex, dental materials and drugs used in the surgery

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6
Q

what are the 2 components of the immune system?

A

innate immune system and acquired immune system

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7
Q

what does acquired immunity consist of? (2)

A

Antibody response (humoral response) Cell mediated response BOTH are involved in hypersensitivity reactions.

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8
Q

How is MHC II involved in antigen presentation?

A

B cells present antigens to T Cells via MHC II.

  • mIgM (or mIgD) binds to the antigen (Ag)
  • phagocytosis occurs
  • a peptide is displayed on the surface with MHC II (these are molecules found on antigen-presenting cells)
  • TCR (T cell receptor) of naive T helper cells (CD4) binds to MHC II
  • lots of other co-stimulatory molecules are required.
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9
Q

How do T cells help B cells? Think about how they cause clonal expansion

A

APC eats Ag (extrinsic) and presents it to naïve CD4+ T cells (via MHC II)

These turn into Th2 cells

Th2 cells bind to B cells that are presenting Ag (via MHC II). This Ag has been captured using the mIgR on cell surface.

Th2 cell now secretes cytokines (IL-4, IL-5, IL-10 and IL-13 )

These cause B cells to divide – CLONAL EXPANSION and differentiate into Plasma cells (AFC = antibody forming cell) and Memory B cells (Bm)

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10
Q

What are the stages of the antibody response to a pathogen?

A
  • antigen uptake by cell
  • antigen processing
  • antigen presentation by an APC
  • B cell binds to APC
  • T cell help (involves cytokines)
  • B cells proliferate to form plasma cells.
  • Antibody is produced
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11
Q

How long does the antibody response take? Why is the antibody response often systemic/widespread?

A

It occurs quickly

This is because antibodies are soluble proteins that can reach most parts of the body quickly via:

Blood

Tissue fluids

Body secretions

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12
Q

Explain the stages of cell mediated immunity for both first and second exposures to the antigen?

A

1st exposure to antigen:

  • Antigen uptake
  • Antigen processing
  • Antigen presentation in the context of MHC
  • T cell receptor on the naive T cell binds to MHC on the antigen presenting cell.
  • T cell then becomes activated
  • This activated T cell proliferates to form many antigen specific memory T cells that patrol the body.

2nd exposure to antigen:

  • T cell recognises the antigen expressed on the target cell in the context of MHC.
  • The T cell can then respond by releasing cytokines / killing the target cell by apoptosis
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13
Q

How does Th1 (CD4) activation occur?

A

APC presents Ag with MHC II to naïve CD4 cell

Stimulation with high levels of IL-12 activate naïve cells to Th1 cells

Th1 cells go to secondary lymphoid tissue (spleen, lymph nodes)

Activated Th1 (CD4) cells proliferate (clonal expansion)

Th1 cell recognises Ag on infected cells (with MHC II) via TCR (CD4) Th1 secretes INFγ – stop virus spread (apoptosis)

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14
Q

What is cell mediated immunity directly mainly against? Are cellular immune responses fast or slow?

A

Cellular targets such as tumour cells, virally transformed cells and foreign cells.

Cellular immune responses tend to be localised, slow to develop and slow to resolve.

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15
Q

What if the immune system fails to produce an adequate immune response?

A

Immunodeficiency

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16
Q

what if the immune system produces an overactive, damaging response?

A

Hypersensitivity - allergy

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17
Q

What is hypersensitivity?

A

When the immune system responds in an exaggerated or inappropriate way resulting in harm.

Usually occurs on second or subsequent exposure to the antigen

Hypersensitivity is a characteristic of the individual (genetic susceptibility)

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18
Q

What are the 4 types of hypersensitivity?

Which are antibody-mediated and which are cell-mediated?

A

Type I - Immediate/anaphylaxis

Type II - Cytotoxic

Type III - Immune complex

Type IV - Delayed

Type I, II, III are antibody-mediated, type IV is cell-mediated.

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19
Q

What is type I / immediate hypersensitivity?

A

This is anaphylaxis. It has a rapid onset and is IgE mediated.

20
Q

What allergens are involved in type I hypersensitivity? Give examples?

A

Allergen is an antigen. Most of these are small (10-40kDa) proteins.

Examples:

Der p 1&2 - dust mite faeces

Fel d 1 - cats

Rat n1 - rats

Pollen - grass

21
Q

What can be used as a diagnosis of type I (immediate) hypersensitivity?

A

Wheal & Flare skin test

Apply small amount of Allergen just under skin using prick test.

Skin response is fast (5 min)

WHEAL (swelling) caused by extravasation of serum into skin due to histamine – angio-odema.

FLARE (erythematous red patch) caused by axon reflex.

Late Phase (6 h+) due to leukocyte infiltrate + more oedema

22
Q

What do type I hypersensitivity responses most commonly present as? (3)

A
  • Hayfever
  • Asthma
  • Acute allergic responses: angio-oedema / anaphylaxis, e.g:

—–> peanut, latex allergy, allergy to LA, bee venom

23
Q

What is the management of a type I hypersensitivity response? (4)

A

Adrenaline (epinephrine)

Antihistamines

Corticosteroids

Avoidance of allergen

24
Q

In type I hypersensitivity, what does the release of histamine cause?

A
  • Vascular dilatation
  • Increased vascular permeability i.e. oedema
  • Bronchospasm (bronchial tubes go into spasm - difficulty breathing)
  • Urticarial rash – nettle rash
  • Increased nasal and lacrimal secretions
25
Q

Under which conditions do you get an overproduction of IgE? How does this link to type I reactions?

A

High levels of IL4 = T0 cell will turn into Th2 cell = B cell gets skewed along a differentiation pathway to produce lots of IgE.

Overproduction of IgE occurs in very high levels of IL4 or very low levels of IL12

People susceptible to type I hypersensitivity have high IgE levels.

26
Q

What happens during the FIRST exposure to the allergen / antigen in type I hypersensitivity?

A

Main targets are mast cells and basophils.

These cells have lots of IgE receptors on their surface and contain lots of histamine granules.

IgE rapidly bind to these receptors, so the cells become saturated with IgE.

The problems come with the 2nd exposure to the allergen…

27
Q

What happens during the SECOND exposure to the allergen / antigen in type I hypersensitivity?

A

Problems occur

The allergen binds to IgE on the cell surface. This crosslinks the receptors causing the receptors to cluster.

This sends an intracellular signal telling the cell to degranulate. This causes the cell to release all its histamine into circulation (happens quickly)

It can also release IL-5 to cause eosinophil production to also drive hypersensitivity reactions.

28
Q

Along with histamine, what do mast cells release?

A

Histamine

IL-5

Enzymes - tryptase and chymase

29
Q

What is type II hypersensitivity?

A

Antibody-mediated hypersensitivity

Antibodies target cell surface self antigens (auto-antibodies)

Usually IgG or IgM

The antibodies induce:

  • cell damage
  • inflammation
30
Q

Explain the stages of the type II hypersensitivity response?

A

Antibodies target self antigen (auto-antibodies) - something is going wrong where we now recognise self as foreign.

  • Causes: could have a DNA mutation, chemicals ingested could cause it, or blood transfusions

These auto-antibodies activate either:

  • ADDC (antibody dependent cell cytotoxicity) - brings in T cells, neutrophils and macrophages. Causes inflammation and cell death (killing our own cells)
  • Complement - activation results in inflammation or cell death via the MAC (membrane attack complex)
31
Q

When are type II hypersensitivity responses important? (3)

A
  • Acute transplant rejection / blood transfusion
  • Haemolytic Disease of the Newborn
  • Autoimmune diseases e.g. pemphigus and pemphigoid
32
Q

How does haemolytic disease of the newborn occur?

A
  1. First Pregnancy - RhD+ foetal blood enters RhD maternal circulation
  2. Baby born BUT mother raises Ab to RhD
  3. Second Pregnancy – If foetus is RhD+ mother IgG crosses placenta and will destroy foetal erythrocytes
  4. SO – preformed anti-RhD Ab is given to Rh- mothers immediately after delivery of RHD+ infants.
33
Q

What happens in the autoimmune disease pemphigus?

A

pemphigus

  • Auto-antibodies against desmoglein-1&3
  • Ab prevents formation of gap junctions between epithelial cells
  • Epithelial shedding – mainly mucosal
34
Q

What happens in the autoimmune disease pemphigoid?

A
  • Auto-antibodies against hemidesmosomes
  • Ab prevents binding of epithelium with dermis at basement membrane
  • Epithelial shedding – skin and mucosal
35
Q

What is type III hypersensitivity and what happens?

A

Antibody-mediated hypersensitivity. This time we get immune complexes forming between antigens and antibodies.

When these combine they can form aggregates to form a precipitate.

These complexes can bind to the endothelium and stick out (get lodged). This often happens in small blood vessels, such as in:

  • Glomeruli
  • Lining of blood vessels
  • Lung

Because they can’t be cleared you get complement activation, leukocyte binding and inflammation. It is too large for a neutrophil to phagocytose, so it degranulates toxic substances which affects healthy neighbouring tissue = localised pathology

36
Q

Explain the stages of type III sensitivity?

A
  1. Immune complexes normally bind C’. This binds to CR1 on erythrocytes which are removed in the liver.
  2. In inflammation, immune complexes bind to blood vessels where they act on platelets and Basophils
  3. These are then activated and release vasoactive peptides (histamine)
  4. This increases vascular permeability
  5. Increased vascular permeability allows more immune complexes to be deposited
  6. Induced platelet aggregation and C’ activation – (C5a & C3a - leukocyte chemotaxis)
  7. Neutrophils attracted but cannot ingest complexes
  8. They secrete lysosomal enzymes causing further tissue damage
37
Q

When is immune complex mediated hypersensitivity (type III) important?

A

in immune complex mediated vasculitis

e.g.

Erythema multiforme

Systemic lupus erythematosus (SLE)

38
Q

What is the treatment for immune complex mediated hypersensitivity?

A

Immunosuppression with steroids

39
Q

What is erythema multiforme?

A

An e.g. of type III hypersensitivity

Common skin condition mediated by deposition of immune complex in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure.

Often has a classical “target lesion” appearance.

40
Q

What is type IV hypersensitivity? What are the consequences of it being a cellular response?

A

Cell-mediated immunity / delayed type hypersensitivity

Mediated by T cells

As the response is cellular, it is usually:

  • Slow to develop (12-48h)
  • Slow to resolve
  • Localised
41
Q

What happens during type IV hypersensitivity?

A

T cell recognises antigen expressed on another cell in the context of MHC

The T cell can then respond by:

  • Killing the target cell
  • Releasing cytokines
42
Q

What are cell mediated immune responses (type IV) important in? (3)

A

Delayed type hypersensitivity responses

Contact hypersensitivity – e.g. dermatitis

Lichenoid reactions to amalgam fillings and other materials

43
Q

Explain the sensitisation phase and elicitation phase of type IV hypersensitivity (for dermatitis)?

A

Sensitisation phase

  1. Ag gets into skin & is internalised by Langerhans cells – These are special APC in the epidermis
  2. These travel to lymph nodes and present Ag to CD4+ T cells.
  3. These form memory CD4+ T cells

Elicitation phase

  • Langerhans cells move from epidermis to lymph nodes
  • They present Ag to memory CD4+ T cells in lymph nodes
  • These are activated, travel to dermis and secrete IFNγ.
  • This increases expression of ICAM-1 and MHCII on Keratinocytes
  • And causes secretion of proinflammatory cytokines
  • More leukocytes are attracted to site
  • Second wave: neutrophils arrive after 4 h, monocytes and T cells after 12 h & secrete tissue damaging cytokines

Tissue damage seen at post 12h (delayed)

Tissue damage resolved if Ag removed

44
Q

How can we test for type IV cell mediated delayed hypersensitivity responses?

A

Samples applied to skin of back or arm for 72-96 hours

45
Q

What are some common allergens that cause a type IV hypersensitivity?

A

Nickel - can leach from watch straps.

Denture acrylic allergy - Red areas due to uncontrolled inflammation and tissue damage. Epidermal thickening due to leukocytes, inflammation & proliferating keratinocytes trying to repair damage

Lichenoid reaction to amalgam - This is a type IV contact hypersensitivity response to mercury or amalgam. Lesions are closely associated with amalgam fillings. Positive skin patch test response to mercury or amalgam. Lesion resolves on removing the filling.

Dendritic cells will pick these allergens up and take them to lymph nodes. Wherever the chemical resides the T cells will act against it and kill the epithelium.

Immunology (2 decks)

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