Block D Lecture 1: Humoral and Antibody Mediated Immunity Flashcards

1
Q

What are the 2 times of acquired (specific) immunity?

A

Cell-mediated Immunity
Antibody-mediated immunity
(Slide 3)

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2
Q

What 2 factors decides what response the immune system takes against a pathogen?

A

Its size
Whether it’s extra or intracellular
(Slide 4)

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3
Q

What are the 4 steps of the humoral activation phase?

A

Phagocytosis of pathogen by Antigen presenting cells (APCs)
Antigen processing / presentation
Education of naïve T cell
Clonal expansion of T cell
(Slide 5)

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4
Q

What are the 4 steps of the humoral effector phase?

A

Uptake of pathogen by B cell
Antigen processing / presentation
Interaction with antigen specific T-cell
Clonal expansion of B cells and differentiation to plasma cell
(Slide 6)

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5
Q

What 5 antigens can antibodies recognise?

A

Proteins
Carbohydrates
Nucleic acids
Glycolipids
Small inorganic molecules
(Slide 7)

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6
Q

How many identical light and heavy chains do antibodies have?

A

2 of each
(Slide 8)

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7
Q

What chain of the antibody determines the isotype class of antibody (E.g. IgA, IgD, IgE.. etc)?

A

The heavy chain
(Slide 8)

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8
Q

What makes up the antigen binding regions in an antibody?

A

The variable regions of both the light and heavy chains
(Slide 8)

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9
Q

How many antigen binding regions does an antibody have?

A

2
(Slide 8)

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10
Q

What does the Fc portion (the heavy chain constant regions) bind to?

A

A cell surface receptor
(Slide 8)

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11
Q

What 4 places is IgA antibody found?

A

Breastmilk
Lung and airways
Intestinal lumen
Urogenital tract
(Slide 11)

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12
Q

Where is IgE antibody found?

A

Connective tissue mast cells
(Slide 11)

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13
Q

What 3 places is IgG antibody found?

A

Blood
Maternal blood (to supply a foetus)
Extravascular tissues
(Slide 11)

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14
Q

Where is IgM antibody found?

A

Blood
(Slide 11)

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15
Q

What form of IgA can survive on mucosal surfaces?

A

The dimeric form
(Slide 12)

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16
Q

What is the most common type of primary antibody deficiency?

A

Selective IgA deficiency
(Slide 12)

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17
Q

Why can an IgA deficiency appear asymptomatic?

A

As IgM can compensate
(Slide 12)

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18
Q

What 2 pathogens is IgA important in defending against?

A

Intestinal pathogens
Virus particles
(Slide 12)

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19
Q

What is the main antibody in the secondary response?

A

IgG
(Slide 14)

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20
Q

What does IgG provide to a baby?

A

Neonatal protection until the baby’s immune system develops
(Slide 14)

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21
Q

How does IgG provide neonatal protection to a baby?

A

By crossing the placenta and into the Fetal bloodstream
(Slide 14)

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22
Q

Roughly what percentage of circulating immunoglobulins in the blood are IgG?

A

75%
(Slide 14)

23
Q

What 4 things does IgG mediate in?

A

Phagocytosis
Opsonisation
Antibody-dependent cellular cytotoxicity by NK cells
Degranulation of neutrophils, eosinophils and mast cells
(Slide 14)

24
Q

Where is IgD inserted?

A

Into the B cell membrane
(Slide 16)

25
Q

What does IgD act as after inserted into the B cell membrane?

A

The B cell receptor for antigens
(Slide 16)

26
Q

What is the half-life of IgD?

A

3 days
(Slide 16)

27
Q

What 2 pathogens is IgD thought to be protective against?

A

Mucosal and respiratory
(Slide 16)

28
Q

What antibody is the first antibody secreted in the primary response?

A

IgM
(Slide 17)

29
Q

What is natural IgM?

A

IgM which is present in babies
(Slide 17)

30
Q

What is adaptive IgM?

A

IgM produced in response to antigenic stimulation of B cells
(Slide 17)

31
Q

What 2 types of microbial components can IgM recognise?

A

Viral antigens and bacterial toxins
(Slide 17)

32
Q

What does the high avidity of polymeric IgM mean?

A

It can immobilise a target at a site
(Slide 17)

33
Q

What is IgE meant to protect against?

A

Worm infestations
(Slide 19)

34
Q

What is IgE associated with in 1st world countries?

A

Type 1 allergic reactions
(Slide 19)

35
Q

How is IgE mediated?

A

Through degranulation of granulocytes
(Slide 19)

36
Q

How does IgE release pre-formed mediators?

A

IgE-mediated activation occurs through FcεRI on mast cells and basophils/multivalent (having multiple sites to attach to an antibody) antigens cross-link the receptor-bound IgE to trigger degranulation and the release of pre-formed mediators
(Slide 19)

37
Q

What do the pre-formed mediators release by IgE result in?

A

Allergic reactions
(Slide 19)

38
Q

What does the pro-inflammatory response triggered by IgE induce?

A

A T helper 2 (Th2) immune response
(Slide 19)

39
Q

Where do specific IgE bound to mast cells recognise antigens?

A

In venom from stings / bites
(Slide 19)

40
Q

How can IgE activation inactivate venom from stings / bites?

A

By causing mast cell degranulation and release of enzymes which inactivate the venom
(Slide 19)

41
Q

What are the 6 antibody mediated effector functions?

A

Neutralisation
Agglutination (clump together antibody and pathogen)
Opsonisation
Activation of complement cascade
Antibody-dependent cell mediated cytotoxicity (ADCC)
Trigger degranulation of granulocytes
(Slide 21)

42
Q

Why are T-independent (T-cell independent) responses fast?

A

Because B cells are directly activated by antigens with certain types of structure
(Slide 23)

43
Q

Why is IgM the only class of antibody that can be produced in T-independent response?

A

As T cells are needed to help B cells class switch
(Slide 23)

44
Q

What is the disadvantage of T-independent response?

A

Short life-span and are therefore not protective
(Slide 23)

45
Q

Does T-independent response make memory cells?

A

No
(Slide 23)

46
Q

What are T-dependent (TD) antigens?

A

Antigens that require the involvement of T cells to start a strong immune response
(Slide 24)

47
Q

What 6 functions requires T lymphocyte (T cells) to B lymphocytes (B cells)?

A

B cell proliferation
Production of immunoglobulins
Immunoglobulin class switching
Rescue of B cells from apoptotic death
Germinal centre formation
Generation of B lymphocyte memory (Memory B cells)
(Slide 24)

48
Q

What 2 classes can T-independent (TI) antigens be divided into?

A

TI-1 (TI type 1)
TI-2 (TI type 2)
(Slide 25)

49
Q

What are TI type 1 (TI-1) antigens?

A

Polyclonal (derived from many clones) B cell activators
(Slide 25)

50
Q

What are TI type 2 (TI-2) antigens?

A

Antigens able to directly stimulate B cells
(Slide 25)

51
Q

What antibody is specialised to activate complement efficiently upon binding an antigen?

A

IgM
(Slide 28)

52
Q

What are the primary and secondary immune responses?

A

The primary immune response is the first time the immune system encounters an antigen and the secondary immune response is any subsequent times it encounters the antigen
(Slide 30)

52
Q

How do memory cells make the secondary immune response faster?

A

As they remember each antigen encountered
(Slide 30)