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PoM > Immuno - Hypersensitivtiy > Flashcards

Immuno - Hypersensitivtiy Flashcards

1
Q

How do we get autoimmune diseases?

A

Immune system reacts to self antigens

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2
Q

How can autoimmune diseases be fatal?

A

Inflammation is generated via the immune response to self antigens therefore can generate toxic molecules and potentially cause fatal tissue damage

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3
Q

What do all hypersensitivity reactions require?

A

Pre-sensitisation of the immune system

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4
Q

What differs between all hypersensitivity reactions?

A

The elements which over-react or inappropriately react to the antigen recognised differ between the different reactions.

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5
Q

What are the phases of a T cell response to an antigen?

A 
Antigen recognition 
Activation 
Clonal expansion 
Differentiation
Effector functions
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6
Q

What is involved in antigen recognition?

A

Antigen presenting cell binds to the naive CD4 T helper cell and the Naive CD8 cytotoxic T cell

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7
Q

In T cell responses, what is involved in activation?

A

Binding of the antigen leads to activation whereby the cells release IL-2 and IL-2R

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8
Q

In T cell responses, what is involved in clonal expansion?

A

Interleukins and cytokines released by T cells to themselves causes rapid clonal expansion

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9
Q

In T cell responses, what is involved in differentiation?

A

Other cellular sources if cytokines leads to the T cells differentiating into different effector cells

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10
Q

In T cell responses, what is involved in effector functions?

A

Effector and memory CD4 cells, and effector and memory CD8 cells

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11
Q

Where does the T cell response to an antigen take place?

A

Lymphoid organs originally however effector functions take place in the peripheral tissues

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12
Q

What do effector CD4 T cells do?

A

Activation of macrophages, B cells and other cells

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13
Q

What do effector CD8 T cells do?

A

Killing of infected target cells as well as macrophage activation

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14
Q

What is the other name for type 1 hypersensitivity?

A

Immediate or anaphylactic hypersensitivity

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15
Q

What is type 1 hypersensitivity?

A

Allergic reaction due to the re-exposure of an antigen called an allergen

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16
Q

What mediates type 1 hypersensitivity?

A

Specific IgE antibodies which are made in response to parasitic infection or very potent venoms.

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17
Q

How does type 1 hypersensitivity differ in people with allergies?

A

The antibody produced is against common multivalent environmental antigens, meaning that it can bind to multiple sites of an antigen and can be produced multiple times

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18
Q

What can we use to diagnose allergies?

A

Allergen skin prick test where we prick the skin with allergens to see how the body would react.

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19
Q

What is the first step of type 1 hypersensitivity?

A

Initial sensitisation is complex and involves both genetic and environmental factors however the end result is Type 2 CD4 T helper cells along with B cell helper follicular CD4 T cells producing type 2 cytokines IL-4 and IL-13.

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20
Q

What is the second step of type 1 hypersensitivity?

A

Cytokines act on B cells causing them to produce specific IgE antibodies.

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21
Q

What is the third step of type 1 hypersensitivity?

A

IgE binds to mast cells and basophils to the Fc epsilon receptor 1.

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22
Q

What is the fourth step of type 1 hypersensitivity?

A

Allergen binds to the receptor found on the innate immune cells to cause cross linking of antibodies

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23
Q

What is the fifth step of type 1 hypersensitivity?

A

Cross linking leads to degranulation and thus release of inflammatory mediators such as histamine

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24
Q

What is the sixth step of type 1 hypersensitivity?

A

Along with histamine, many more cytokines are released to promote the further activation of helper T cells.

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25
Q

What is the role of leukotrienes?

A

Cause smooth muscle contraction thus airway narrowing

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26
Q

What happens in early phase type 1 hypersensitivity?

A

Small bioactive response produced directly by mast cells

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27
Q

What happens in later response type 1 hypersensitivity?

A

Early inflammatory response and molecules such as neutrophils are recruited

28
Q

What happens in late response type 1 hypersensitivity?

A

High frequencies of eosinophils are recruited and Th2 cells are present.

29
Q

What is another name for type 2 hypersensitivity?

A

Antibody mediated cytotoxic hypersensitivity.

30
Q

What is type 2 hypersensitivity?

A

Involves the destruction of APCs bound to IgM or IgG antibodies.

31
Q

What is an example of type 2 hypersensitivity?

A

Mismatching of blood donors and the mixing of maternal Rh+ blood with foetal Rh- blood leading to inflammation and subsequent tissue damage.

32
Q

What is an immune condition involving type 2 hypersensitivity?

A

Immune thrombocytopenia

Grave’s disease

33
Q

What causes sensitisation in type 2 hypersensitivity?

A

Due to non self antigens or self antigens.

34
Q

What are the 3 mechanisms through which antibodies cause disease in type 2 hypersensitivity?

A

Anti-receptor activity - blocking or activating its function
Antibody depends cell-mediated cytotoxicity
Classical activation of the complement cascade

35
Q

What is the classical pathway of the complement cascade?

A

Where an antibody binds an antigen on the cell surface

36
Q

What does the classical complement pathway lead to?

A

Antibody is bound to by complement components

37
Q

What else does the classical complement pathway lead to?

A

Formation of the membrane attack complex (MAC) which causes loss of osmotic integrity and subsequent cells death.

38
Q

What happens in ADCC?

A

Antibody-antigen complex on cell surface is bound by the Fc receptor expressed by granulocytes and natural killer cells, on IgM/IgG antibodies.

39
Q

What does binding in ADCC lead to?

A

Direct lysis of the cell, and the release of inflammatory mediators, chemokine and cytokines.

40
Q

What is the overall consequence of ADCC?

A

Multiple mechanism of tissue injury - local/systemic inflammation, cell depletion leading to a loss of function or imbalance in organ function

41
Q

What is another name for type 3 hypersensitivity?

A

Immune complex driven disease

42
Q

What is an immune complex?

A

Non cell bound antibody antigen complex which are normally cleared via the immune system

43
Q

What happens in type 3 hypersensitivity?

A

Antibodies react against self antigens such as nuclear DNA leading to an immune complex which are not cleared by the immune system, they then build up and cause tissue damage and inflammation

44
Q

What are some of the symptoms of type 3 hypersensitivity?

A

Fever, joint pain, raises or protein in urine.

45
Q

What is type 3 hypersensitivity in the kidney?

A

Glomerulonephritis.

46
Q

What is type 3 hypersensitivity in the joints?

A

Arthritis

47
Q

What are some autoimmune diseases involving type 3 hypersensitivity?

A

MS

SLE (systemic lupus erythematosus)

48
Q

What occurs in SLE?

A

Patient develops IgGs abasing proteins or DNA in the nucleus (nucleoproteins) leading to deposits.

49
Q

What hypersensitivity reaction is involved with serum sickness?

A

Type 3

50
Q

When might someone get serum sickness?

A

If a person is bitten by a snake and given anti-serum/

51
Q

What makes up anti-serum?

A

Foreign antibodies that neutralise snake venom proteins.

52
Q

Why does the second dose of anti-serum cause inflammation?

A

Our bodies will produce our own antibodies abasing the anti-venom antibodies, which will take a few weeks. However, if we are given a second dose of anti-serum, we will get an immune response to the anti-venom antibodies and thus rapid inflammation.

53
Q

What is another name for type 4 hypersensitivity?

A

Delayed type or T cell mediated hypersensitivity.

54
Q

When does type 4 hypersensitivity develop?

A

Due to prior sensitisation of dendritic APCs by naive T cells to become activated to specific memory T cells, which takes several weeks

55
Q

When is type 4 hypersensitivity triggered?

A

When we re-encounter the pathogen, we should get direct inflammation at the site of exposure due to memory T cell action

56
Q

Why is there a 2-3 delay with type 4 hypersensitivity?

A

T cell response of inflammation requires expansion and recruitment to the site of pathogen entry.

57
Q

What is an example of type 4 hypersensitivity?

A

Contact dermatitis caused by touching poison ivy.

58
Q

What is the molecule in poison ivy?

A

Urushiol

59
Q

What does urushiol do?

A

Acts as a hapten to drive a Th1 response however due to its small nature, this rarely leads to an antibody response

60
Q

What happens upon re-exposure of urushiol?

A

Memory cells have been formed so produce cytokines that are pro-inflammatory therefore we get macrophage activation, swelling and consequent formation of blister like regions on the site of contact

61
Q

What is an example of the cytokines involved in type 4 hypersensitive (poison ivy)?

A

IFN-gamma (Interferon gamma)

62
Q

What are some other examples of contact antigens?

A

Nickel salts

Hair dyes

63
Q

What does hair dye/nickel salts or intracellular pathogens like mycobacterium tuberculosis cause?

A

Similar Th1 based inflammation like urushiol

64
Q

What is involved in the tuberculin skin test?

A

Measures previous exposure of tuberculosis by injection of small amounts of tuberculin protein in the skin.

65
Q

What happens in a rejected skin graft?

A

CD8 cells can cause inflammation from a rejected skin graft, directly killing transplanted cells.

PoM (27 decks)

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