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Flashcards in Immunopath Deck (56):
1

What is type II hypersensitivity?

Antiobody mediated
IgM and IgG against cell-bound or extracellular matrix Ag

2

What is type III hypersensitivity?

Immune complex
IgM and IgG immune complex deposition

3

What is type I hypersensitivity?

Immediate type
IgE, mast cells and lipid mediators

4

What is type IV hypersensitivity?

Delayed type
CD4 mediated delayed type hypersensitivity

5

Which complement pathway are we interested in with regard to hypersensativities?

Classic

6

Complement pathway?

a

7

What does C3b do?

Binds to C3b receptor on phagocytes, opsonisation,! removal of immune ! complexes!

8

What does C5a do?

mediators of inflammation, phagocyte recruitment

9

What do C5b, C6, C7, C8, C9 do?

Membrane attack complex (MAC). Lysis of microbes and infected cells

10

What happens in type II hypersensitivity?

Binding of Abs to host antigens

11

What are the outcomes of type II hypersensitivity?

Injury due to activation of effector mechanisms

Abnormal physiological response (Graves & MG)

12

What does injury due to activation of effector mechanisms involve?

•  C’activation
•  Recruiment of inflammatory cells
•  Activation via Fc Receptor

13

what does abnormal physiological response (Graves & MG) involve?

•  Binding to receptors or proteins interfering with function
•  Activation or inhibition.

14

What is the classic type II hypersensitivity?

Type II hypersensitivity responses often target erythrocytes

15

What are ABO blood group antigens?

Carbohydrate antigens,

16

What happens if you transfuse the wrong blood type?

Cause lysis, shock and potentially dath

17

What is a less common type II hypersensitivity?

Type II mediated drug allergies (rare)
eg penicillin, quinidine, methyldopa

18

What happens in type II drug allergies?

The drug becomes bound to red blood cells or platelets, which are then the target of anti-drug antibodies

19

Where are cells which are bound to drugs lysed in type II drug sensativity?

Splenic macrophages phagocytose the cells, resulting in haemolytic anaemia or thrombocytopenia

20

What happens if a mother is rhesis negative and she has a child which is rhesus positive?

Maternal antibodies can target foetal blood.
Can be a particularly big problem form the second child

21

How do we prevent against the development of an immune response against a rhesus +ve foetus?

Anti-Rh antibodies within 24 hrs of delivery remove fetal RBC’s in maternal circulation
Haemolytic

22

Can type II hypersensitivity responses can target tissues?

Yes

23

What is Goodpasture’s syndrome?

Antibodies are made against a variant of collagen type IV, a major component of basement membranes

24

How does Goodpasture’s syndrome present?

Nephritis
(slowing down of movement of antibodies allow them to activate against collagen in the nephron)

25

what does the thyroid gland do?

Thyroid gland essential for regulating metabolism through the production of thyroid hormones

26

What does the thyroid gland do?

It produces thyroid hormones in response to thyroid stimulating hormone

27

What happens in graves disease?

Antibodies bind to the thyroid gland and stimulate the production of thyroid hormones. This shuts down the pituitary,
Get hyperthyroidism

28

What is myasthenia gravis?

Autoantibodies inhibit receptor function at muscle nerve interfaces
antibodies block the binding site of AcH and destroy the receptors

29

What is the outcome of myasthenia gravis?

Muscle wasting and eventually death

30

What happens in type III hypersensatvity?

Immune complexes composed of self antigen or foreign antigen
Occurs if complexes are excessively produced, and inefficiently cleared

31

What is the pathology of type III?

Pathology depends entirely upon where these complexes deposit

32

How is complement usually removed?

Immune complexes are usually removed in the spleen by resident macrophages

33

What makes up immune complexes?

RBC, C3b Receptors, antigens, antibodies

34

What is needed for immune complex formation?

High affinity IgG, need to fix C’

35

Why are large complexes good?

Large complexes not only activate complement better, they are better at binding FcR, so are removed from the circulation more efficiently by RBCs

36

What happens when there is a large amount of complex formed?

The mononuclear phagocyte system may be overloaded when large amounts of complex are formed, leading to a rise in circulating complexes

37

What is equivalence?

Large lattices, good complement activation

38

When are immune complexes not cleared/

–  Ag excess
–  Low affinity Ab
–  Inefficient C’ activation

39

What happens to complexes over time?

Get deposition on vessel walls Increase in concentration over time results in eventual C’ activation

40

What are the downstream effects of complement?

•  Generate anaphylotoxins (C5a, C3a) –  neutrophil, mast cell degranulation

•  Induce macrophage cytokine release

•  Immune complexes directly activate platelets, basophils and mast cells

•  Vasoactive amines –  increased vascular permeability

41

Where does type III hypersensitivity form/

Small tissues
Slow blood flow

42

What are common outcomes of Type III Hypersensitivity?

Vasculitis (deposition in blood vessel walls)

•  Glomerulonephritis (deposition in glomerular basement membranes)

•  Arthritis (deposition in joint synovium and vessels)

43

Farmers lung?

•  serum sickness,
•  nephritis in chronic hepatitis,
•  rheumatic fever and endocarditis,
•  autoimmune conditions including rheumatic fever and systemic lupus erythematosis (SLE)

44

Diseases resulting from immune complex deposition

Persistant infection
Autoimmunity
Inhaled antigen

45

What casues farmers lung?

Farmers lung is caused by localised immune complex formation in the lungs due to exposure to hay dust or bacteria resulting in alveolitis

46

What agent specifically causes farmers lung?

Actinomyces, a Gram positive environmental bacterium, found in mouldy hay, that stimulates production of IgG antibodies.
IgG containing immune complexes are formed in the alveoli, leading to inflammation and fibrosis

47

Who is affected more by lupus?

Females

48

What triggers lupus?

Unknown, thought to be UV damage

49

What happens in lupus?

Numerous autoantigens are involved and these are widely expressed

Multiple systems involved

50

How is lupus diagnosed?

Presence of anti-DNA autoantibodies and immune complex deposition in kidney

51

What causes the damage in lupus?

Immune complex deposition on basement membranes of the kidney

Activation of the complement cascade

Tissue injury is the result of leukocyte activation and inflammation

52

Why do patients with lupus present with red rashes?

Antibodies target the skin as well.
UV light causes cell death which can in turn trigger immune response

53

How do we create antibodies against self?

Immune system has inbuilt randomness. The immune system has developed mechanisms to remove self antibodies

54

What is negative selection?

if an immune self can bind to a self anitigen it is destroyed

55

What is central tolerance?

–  Occurs during development in primary lymphoid organs
–  Removes self-reactive lymphocytes during development

56

What other mechanisms (aside from central tolerance) prevent immunological tolerance?

Peripheral Tolerance
–  Occurs in the periphery
–  Controls self-reactive lymphocytes