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Principles of dizzees > Hypersensitivity and autoimmunity > Flashcards

Hypersensitivity and autoimmunity Flashcards

1
Q

What is hypersensitivity?

A

A group of disorders in which the immune system responds in an exaggerated or inappropriate fashion to environmental antigens in a way which causes harm to the body, instead of protecting it

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2
Q

What are the 4 types of hypersensitivity

A

Type I - IgE mediated

Type II - IgG mediated cytotoxic response

Type III - IgG mediated - immune complex

Type IV - T cell mediated

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3
Q

What happens in the sensitisation stage of the type I hypersensitive response?

A

1) Allergen enters body
2) Allergen carried to lymph nodes by APC - presented to naive T cells
3) T cell primed and differentiates into a Th2 cell (in response to interleukins)
4) Th2 cells release various interleukins that activate B cells and eosinophils
5) B cell produces IgE antibodies that bind onto Fc receptors on mast cells - sensitises them

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4
Q

What are interleukins?

A

A type of cytokine

Small protein molecules

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5
Q
  • Type I -

What happens when interleukins activate eosinophils?

A

Interleukins stimulate proliferation of eosinophils

Eosinophils can then degranulate, killing parasites and host cells

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6
Q
  • Type I -

What happens in the second exposure to an allergen?

A

1) Body exposed to allergen
2) Allergen binds to IgE antibodies on surface of sensitised mast cell
3) Activates the mast cell which degranulates, releasing mediators and enzymes - leading to the allergic response

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7
Q

What are mediators?

A

Communicatory molecules

In the context of hypersensitivity; they are Pro-inflammatory molecules

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8
Q

Describe how an allergic response causes breathing difficulty and oedema

A

1) Sensitised mast cell binds binds to allergen
2) Sensitised mast cell releases various mediators (degranulates)
3) Histamine (a type of mediator) causes:
- Smooth muscle contraction in bronchi ∴ breathing difficulty
- Vasodilation + increased permeability ∴ oedema

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9
Q
  • Type I - early phase

What are the effects of the mediators and enzymes released by mast cells when they degranulate

(BIVVIT)

A

Bronchial constriction

Intestinal hypermotility

Vasodilation

Vascular leakage

Inflammation

Tissue damage

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10
Q
  • Type I - early phase

What 2 ways does degranulation of mast cells lead to tissue damage?

A

1) Degranulation releases enzymes such as tryptase that damage tissues
2) Degranulation releases mediators that attract eosinophils that degranulate - killing pathogens but also surrounding tissue

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11
Q
  • Type I - late phase

Several hours after an allergic reaction, Th2 cells, basophils and yet more eosinophils are recruited to the location of the allergen

What causes this?

A

Cytokines produced in early phase reactions:

  • Interleukins
  • Leukotrienes
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12
Q

What is atopy?

A

Predisposition to allergy

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13
Q

What is the main factor determining atopy?

A

Genetics

Allergies often run in families

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14
Q

What is type II hypersensitivity caused by?

A

Auto-antibodies binding to our own cells

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15
Q
  • Type II -

Describe the reaction mechanism that causes neutrophils to kill our own cells

A

1) C1 protein binds to Fc portion of antibody attached to cell
2) Compliment cascade initiated leading to production of C3a, C4a and C5a
3) These are chemotactic - attract neutrophils
4) Neutrophils degranulate - cytotoxic - leads to tissue damage

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16
Q
  • Type II -

Describe the reaction mechanism involving the membrane attack complex

A

1) C1 compliment protein binds to Fc portion on auto-antibody on cell
2) Compliment cascade initiated leading to production of MAC
3) MAC punches hole in cell - causing swelling and bursting (cell lysis)

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17
Q
  • Type III -

Describe the reaction mechanism involving opsonisation

A

1) C3b compliment protein binds to Fc region on IgG antibody on cell
2) This opsonises the cell
3) This causes phagocytes to phagocytose the cell in the spleen

18
Q
  • Type II -

Describe the mechanism behind antibody-dependant cell mediated cytotoxicity (ADCC)

A

1) Bound antigen-antibody complex on our own cells is recognised by NKCs
2) These release perforins and granzymes
3) Perforins create pores in the cell, granzymes enter the cell and cause apoptosis

19
Q
  • Type II -

Why does ADCC not cause surrounding inflammation to the reaction site?

A

Granzymes cause apoptosis

Only cells with antibody on the surface are killed - surrounding cells are fine

20
Q
  • Type II -

What is antibody-mediated cellular dysfunction?

A

Non-cytotoxic mechanism

Antibody gets ‘in the way’ of the cell it is bound to

Example - Myasthenia Gravis. ACh receptors at NMJ are blocked by antibodies

21
Q

What happens in type III hypersensitivity?

A

Antigen-antibody complexes are deposited in blood vessel walls

Causing inflammation and tissue damage

22
Q

What are immune complexes?

A

Antibodies bound to soluble antigens

23
Q

Why do immune complexes only form in type III reactions?

A

In other types, the antigen is attached to a cell ∴ not soluble

Antibody-antigen complexes that form in other types are not immune complexes

24
Q

If something is very immunogenic, what does this mean?

A

It is very attractive to phagocytes

A strongly immunogenic pathogen will be quickly engulfed

25
Q
  • Type III -

Describe the mechanism of type III hypersensitivity and what it’s effects are

A

1) IgG antibodies bind to soluble antigen ∴ immune complex forms
2) Travels in bloodstream until it attaches to basal lamina
3) Immune complexes activate the compliment system
4) C3a, C4a, C5a - anaphylatoxins ∴ increase vascular permeability ∴ oedema
5) C3a, C4a, C5a also attract neutrophils
6) Neutrophils arrive and degranulate ∴ inflammation and tissue damage

26
Q

What is the difference in compliment protein usage between type II and type III hypersensitivity

A

Type III uses large amounts whereas type II uses relatively small amounts

27
Q
  • Type III -

When neutrophils arrive to the adhered immune complex, they degranulate.

What is the name of the condition they cause?

A

Vasculitis

Inflammation of blood vessels

28
Q

What is the basic difference in the clinical symptoms shown by type II and type III hypersensitivity?

A

Type II reactions show symptoms where the immune complexes are formed

Type III show symptoms where the immune complexes are deposited

29
Q
  • Type III -

Where are immune complexes often deposited?

A

Kidneys - where blood is filtered. This causes glomerulonephritis

Joints - plasma filtered to make synovial fluid. Responsible for rheumatoid arthritis

30
Q

What is type IV hypersensitivity?

A

Delayed type hypersensitivity that is mediated by T cells

31
Q

What are the two mechanisms of type IV hypersensitivity?

A

Cytokine mediated inflammation

T cell-mediated cytotoxicity

32
Q
  • Type IV -

Describe the mechanism of cytokine mediated inflammation

A

1) Antigen engulfed by APC and presented to T cell
2) T cell activated and turns into Th1 helper cell
3) Th1 cell releases cytokines & proliferates
4) Cytokines activate phagocytes
5) Phagocytes release various molecules that cause inflammation and damage local tissue

33
Q
  • Type IV -

In cytokine mediated inflammation, phagocyte activation by T cells causes inflammation and tissue damage.

Explain how

A

Phagocytes release:

  • Pro-inflammatory cytokines: Oedema, redness and fever
  • Enzymes, Compliment proteins and Reactive oxygen species to destroy antigen: Damage local tissue
34
Q
  • Type IV -

In the cytokine mediated inflammation mechanism, CD4+ T cells can also differentiate into Th17 cells instead of Th1 cells.

What causes this, and what do these Th17 cells do?

A

Dendritic cells release cytokines that cause activated CD4+ to change into Th17 cells instead of Th1

These Th17 cells release specific cytokines that attract neutrophils

35
Q
  • Type IV -

How does the T cell mediated cytotoxicity mechanism work?

A

1) Cells in our body present an auto-antigen
2) CD8+ killer T cell binds to auto-antigen
3) Stimulated release of perforin and granzymes
4) Perforin creates holes in membrane and granzymes enter and induce apoptosis ∴ cell death

36
Q
  • Type IV -

Under normal circumstances, T cell mediated cytotoxicity is necessary to protect our body. Why is this?

A

They kill cells that are infected with viruses ∴ present virus antigen

They kill cells that have mutated DNA ∴ present different antigens

37
Q

What health conditions are associated with Type II hypersensitivity?

A

AIHA - Anaemia

ATP

Rheumatic fever

38
Q

What health conditions are asociated with type III hypersensitivity

A

SLE - (Lupus)

Rheumatoid arthritis

Glomerulonephritis

39
Q

What health conditions are associated with type IV hypersensitivity

A

Dermatitis

Rheumatoid arthritis

MS

Inflammatory bowel disease

40
Q

What is immunological tolerance?

A

State of non-reactivity of the immune system towards a specific antigen

that would normally cause an immune response

41
Q

What mainly causes immunological tolerance?

A

Prior exposure to the antigen

Principles of dizzees (28 decks)

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