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Principles of Disease-Megan > 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-Megan (41 decks)

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