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Principles of Disease > Hypersensitivity and Autoimmunity > Flashcards

Hypersensitivity and Autoimmunity Flashcards

1
Q

What cells are involved in innate immunity

A 
Phagocytes
Eosinohpils
Basophils
Mast cells
APCs
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2
Q

What receptors are involved in innate immunity

A 
Fc
Complement
Toll-like
Mannose
Cytokine
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3
Q

What molecules are involved in innate immunity

A

Complement
Acute phase reactants
Inflammatory mediators
Cytokines

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4
Q

What cells are involved in adaptive immunity

A

B cells

T cells

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5
Q

What receptors are involved in adaptive immunity

A 
Ig
TCR
HLA
Cytokine
Complement
Toll-like
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6
Q

What molecules are involved in adaptive immunity

A

Immunoglobulins

Cytokines

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7
Q

What does immunity involve

A 
Recognition
Interaction
Response
Elimination
Control and regulation
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8
Q

What is hypersensitivity

A

A group of disorders where the normally beneficial components of the immune response act in an exaggerated or inappropriate fashion to environmental antigens which do not normally cause tissue damage.

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9
Q

What is responsible for the tissue damage caused by hypersensitivity

A

The exaggerated response directed at the antigen

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10
Q

How can humans come into contact with allergens

A

Inhaled
Ingested
Injected
Contact

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11
Q

Describe the pathogenesis of an allergen

A 
Allergen leaches on cell
Enters to form APC which has MHC, a class II protein and epitope
T helper cell helps B cells
IgE produced
IgE binds to inflammatory cell 
Causes clinical effects

(Allergen could attach straight to Fc epsilon receptor to cause a response)

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12
Q

What can T helper CD4 cells form

A

Th 1 - found in type IV (IL-2, gamma-IFN, TNF)

Th2 - found in type I (IL-4,6,10,13)

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13
Q

Define Atopy

A

A genetic tendency to produce IgE to normally innocuous, common environment allergens

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14
Q

How many people does atopy affect

A

About 40% of the population

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15
Q

Define allergy

A

A clinical expression of the atopic tendency

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16
Q

How many people does allergy affect

A

15-20% of the population

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17
Q

State some specifc IgE triggers

A 
Insect venom
Pollen
Mould spores
Animal dander
Food allergens
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18
Q

State some non-specific allergy and atopy triggers

A 
Exercise
Acetylsalicylic acid
Tobacco
Sulphur dioxide
Cold air
Temperature
Pressure
Water 
Food items
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19
Q

What are some of the symptoms of allergy and atopy

A 
Anaphylaxis
Asthma
Rhinitis and conjunctivitis
Urticaria
Gastrointestinal
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20
Q

What can cause allergy

A 
Genes
Environment (allergen)
Immune dysregulation
Environment (other)
Internal influences
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21
Q

What types of mast cell mediators are there

A

Preformed

Newly synthesised

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22
Q

Name some preformed mast cell mediators

A 
Histamine
Heparin
Tryptase
Chymase
Eosinophil/neutrophil chemotactic factors
23
Q

Name some newly synthesised mast cell mediators

A

Prostaglandins

Leukotrienes

24
Q

Describe the pathogenesis of type I hypersensitivity

A

Allergen exposure trigger mast cells and IgE
This causes degranulation of preformed mediators and synthesis of new mediators
Response includes: mucosal oedema, secretions, vasodilation, capillary leakage and smooth muscle contraction.

25
Q

When does an early phase response occur

A

Within minutes using preformed mast cell mediators

26
Q

When does a late phase response occur

A

Takes hours using newly synthesised mediators, Th2 cytokines and eosinophil mediators

27
Q

Describe type II hypersensitivity

A

IgG/IgM mediated and its target antigens are either found on the cell surface or fixed in certain tissues
Involves immune effectors/target cell interactions

28
Q

How can tissue damage arise in type II hypersensitivity

A

Complement activation
Fc binding of immunogloubin and stimulation of phagocytes
Antibody-dependent cellular cytotoxicity (ADCC)
Effects on target cell function (inhibition of function or stimulation)

29
Q

What is the function of the immune complex

A

When formed under normal/physiological conditions has protective mechanisms including opsonisation, transportation and destruction

When formed under pathological conditions it has antigen factors and host response factors

30
Q

How can the immune complex form

A

In circulation causing systemic deposition in tissues (serum sickness)
Locally in tissues (arthus reaction)

31
Q

What is type III hypersensitivity

A

When there is an excessive or abnormal immune complex formation causing complement activation and the recruitment of inflammatory cells which leads to tissue damage

32
Q

How long does it take for type IV hypersensitivity to occur

A

Over 24 hours

Th1 mediated

33
Q

How does type IV hypersensitivity occur

A

An exogenous hapten (low molecular weight antigen) and endogenous protein (carrier) or microorganism cause antigen presenting cells (HLA class II) to form this stimulates Th1 cytokine production and causes inflammation

34
Q

Define automimmunity

A

A large group of clinical disorders which are characterised by tissue or organ damage mediated through aberrant immunological mechanisms which are directed against autoantigens

35
Q

What type of selection does central tolerance have

A

Positive or negative selection

36
Q

What is peripheral tolerance dependent on

A 
Tregulatory cells
Antibody idiotype regulation
Immune complex formation
Oral tolerance
Th17 cells
37
Q

What causes autoimmune disease

A 
The interaction of:
Genetic factors
Immune regulatory factors
Hormonal factors
Environmental factors
‘Other’ factors
38
Q

What does MHC stand for

A

Major histocompatibility complex

39
Q

What type of effector mechanisms are there

A 
Cell - mediated
Antibody - mediated
Antibody + complement
Immune complex - mediated
Recruitment of innate components
40
Q

Describe how an autoimmune disease occurs

A

An event initiates the process (e.g. infection) coupled with genetic susceptibility
Causes the breakdown of self-tolerance
Auto-reactivity occurs to cause either a humoral or cellular response
Leads to tissue damage

41
Q

What can autoimmune diseases range between

A

Organ specific to non-organ specific

42
Q

Where can organ specific autoimmune diseases occur

A

Thyroid
Stomach
Adrenal glands
Pancreas

43
Q

Name some autoimmune thyroid diseases

A

Hashimoto’s thyroiditis
Primary myxoedema
Thyrotoxicosis

44
Q

Name an autoimmune stomach, adrenal and pancreatic disease

A

Stomach - pernicious anaemia
Adrenal - Addison’s disease
Pancreas - juvenile diabetes

45
Q

Where can non-organ specific autoimmune diseases occur

A

Muscle - dermatomyositis
Kidney - SLE
Skin - scleroderma
Joints - rheumatoid arthritis

46
Q

How many types of hypersensitivity mechanisms are there

A 
4
Type I
Type II
Type III
Type IV
47
Q

How are Types I, II and III hypersensitivity mediated

A

Through antibodies

48
Q

What is type IV hypersensitivity caused by

A

By the inappropriate actions of Th1 cells

49
Q

What is type I hypersensitivity also known as

A

Allergy

50
Q

How does type I hypersensitivity arise

A

Through inappropriate synthesis of IgE by the immune system

IgE is directed at allergens

51
Q

Why does type I hypersensitivity arise

A

Due to a combination of interacting genetic factors, environmental influences, hormonal and neurological influences and immune regulatory factors

52
Q

Where can the antigens triggering type II and III sensitivity be derived from

A

External (exogenous)

Self (therefore almost an autoimmune disease)

53
Q

How do clinical conditions arise in type III hypersensitivity

A

Due to abnormal:
Deposition of formed antigen (Ag)
Antibody (immune) complexes in tissues

54
Q

Where to immune complexes go once formed

A

Bloodstream - kept soluble in blood
Transported (usually attached to red cells) to the liver and spleen where fixed phagocytes (e.g. Kupffer cells) take up and destroy them

Principles of Disease (41 decks)

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