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Immunity, Infection and Haematology > B Cell Block > Flashcards

B Cell Block Flashcards

1
Q

What are antibodies?

A

Glycoproteins that specifically bind target antigens, present in body fluids and external secretions but can also be found on specialised cells (e.g. IgE bound to mast cells)

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2
Q

What is an antigen?

A

Molecules that induce an immune response through the activation of antigen specific B lymphocytes and/or T lymphocytes

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3
Q

What is an epitope (antigenic determinant)?

A

The molecular structure recognised by the binding site of an antibody molecule or a T cell receptor

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4
Q

How many classes of human immunoglobulin are there?

A

5

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5
Q

What are the 5 classes of human immunoglobulin?

A

IgM, IgMG, IgA, IgD, IgE

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6
Q

What are the different classes of Ig defined by?

A

structure of the constant region of their heavy chains, which in turn determines function

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7
Q

How many subclasses of IgG are there?

A

4 - IgG1, IgG2, IgG3, IgG4

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8
Q

How many subclasses of IgA are there?

A

2 - IgA1, IgA2

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9
Q

On which chromosome are the genes encoding for the heavy chains of Ig located?

A

Chromosome 14

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10
Q

Structure of IgM

A

Heavy chain comprised of 4 constant domains
Expressed as a monomeric transmembrane molecule on B cells
Secreted by plasma cells as a pentamer (polymerisation facilitated by inclusion of J chain, a polypeptide produced within the plasma cell)

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11
Q

Structure of IgA

A

Heavy chains comprised of 3 constant domains
IgA1 has an extended, highly glycosylated hinge region
IgA present in plasma results from production in bone marrow, monomeric
IgA present in external secretions a product of the local immune system and is produced by plasma cells a dimer (includes a J chain)

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12
Q

How is secretory IgA formed? What is the process called?

A
  1. Dimeric IgA binds to poly-Ig receptor on the basal surface of epithelial cells
  2. Complex is transported to the apical surface where the receptor is cleaved to release the IgA dimer attached to a portion of a receptor (“secretory piece”)

Process called ‘transcytosis’

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13
Q

Structure of IgE

A

Heavy chain comprised of 4 constant domains

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14
Q

Structure of IgD

A

Heavy chain comprised of 3 constant domains and an extended, glycosylated hinge region
Expressed as a transmembrane receptor molecule on the surface of mature B cells

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15
Q

What does the Fc region do?

A

Mediate the effector functions of antibody - acts as a target for Fc receptor of phagocytes

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16
Q

What are the 6 functions of antibodies?

A
  1. Opsonisation
  2. Neutralisation
  3. Precipitation (immune complex formation)
  4. Complement activation
  5. Direct cell activation by Fc receptors - phagocytes, mast cells
  6. Antibody dependent cell mediated cytotoxicity (NK cell activation)
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17
Q

What is opsonisation?

A

Process by which a pathogen is marked or highlighted for ingestion and removal by a phagocyte

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18
Q

What does opsonisation involve?

A

Binding of an opsonin (eg antibody) to an antigen or pathogen which then attracts phagocytes

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19
Q

What does antibody/Fc receptor binding on phagocytes result in?

A

Facilitates phagocytosis

Activates important components of the complement system such as C3b and C4b (more opsonisation)

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20
Q

What is the name of the process where antibody can block internalisation of toxins/virus by blocking binding to virus receptor?

A

Neutralisation

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21
Q

What is the other way of neutralising viruses?

A

Antibodies can bind to the viral envelope proteins that allow docking and entry into their host cell

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22
Q

What is the name of the complex lattice work o antigen & immunoglobulin?

A

Immune complex

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23
Q

What do immune complexes do to provide protection?

A

Limit diffusion of the antigen molecules

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24
Q

What is precipitation of protein/antibodies?

A

-

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25
Q

What is agglutination?

A

-

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26
Q

Which pathway of complement system is activated by antibodies?

A

Classical pathway

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27
Q

What are the two immunoglobulins that cause complement activation on binding to microbial surfaces?

A

IgM (pentamer)

>2 IgG molecules

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28
Q

How do antibodies cause direct cellular activation?

A

Fc receptors on cells can trigger specific functions

e.g. IgE triggers mast cell activation through the high affinity Fc epsilon receptor 1 (FceR1) in allergic reactions

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29
Q

What does ADCC stand for?

A

Antibody Dependent Cell-mediated Cytotoxicity

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30
Q

Which cells re involved in ADCC?

A

Effector cells of the innate immune system - NK cells, monocytes, macrophages, eosinophils

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31
Q

What is the consequence of ADCC?

A

Lysis of the cell being opsonised by specific antibodies

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32
Q

Which portion of the antibody is recognised by what receptor on the effector cell?

A

Fc portion of the antibody recognised by Fc receptor of an effector cell

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33
Q

What do NK cells release on binding to antibody?

A

Cytokines such as interferon (IFN)

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34
Q

How do cytokines help in the immune response?

A

They attract and activate phagocytes, and cytotoxic granules containing perforin and granzymes

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35
Q

What is anti-helminth immunity an example of?

A

ADCC

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36
Q

Which type of antibody recognises the antigens on the parasites (helminth)?

A

IgE

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37
Q

What receptor of an eosinophil binds the IgE in anti-helminth immunity?

A

Fc receptor (FceR1)

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38
Q

What do polyclonal antibodies recognise?

A

Multiple epitopes on one antigen - inexpensive, low tech

39
Q

What do monoclonal antibodies recognise?

A

Only one epitope on antigen - high tech, expensive

40
Q

What type of antibody does immunoglobulin replacement therapy involve?

A

Polyclonal IgG

41
Q

What is an example of monoclonal antibodies?

A

anti TNFa therapy in rheumatoid arthritis

42
Q

Where are the secondary lymphoid tissues found?

A

Lymph nodes, spleen, lining of the internal body surfaces (gastrointestinal, respiratory & urogenital)

43
Q

What does the spleen filter?

A

Blood - for pathogens

44
Q

What do the lymph nodes filter?

A

the lymphatics that drain peripheral tissues

45
Q

What are the lymphoid tissues in the gut called?

A

Peyer’s patches

46
Q

Where do Peyer’s patches drain from?

A

They drain antigen directly from the gut where most of our pathogens that we face are located into mesenteric lymph nodes

47
Q

Why do lymphocytes recirculate between secondary lymphoid tissue?

A

In order to maximise opportunity to encounter and therefore respond to antigen

48
Q

What percentage of lymphocytes are in the blood, spleen and other secondary lymphoid tissues?

A

5% in blood
20% in spleen
75% in other secondary lymphoid tissues

49
Q

How do lymphocytes enter the spleen? (specialised vessels)

A

Through the walls of the marginal zone blood sinusoids

50
Q

How do lymphocytes enter all other secondary lymphoid tissues?

A

Through high endothelial venules (afferent lymphatics)

51
Q

What molecule co-ordinates the migration of lymphocytes towards secondary lymphoid tissues?

A

Selectins

52
Q

How do lymphocytes leave the spleen?

A

Through the red-pulp blood sinuses

53
Q

How do lymphocytes leave other secondary lymphoid tissues?

A

Via the efferent lymphatics which ultimately drain via the main lymph vessels into the venous system

54
Q

What do T zones do?

A

Provide the microenvironment where T and B cells are recruited into antibody responses

55
Q

What happens to T cells once in the secondary lymphoid tissue?

A

Once through the wall of the high endothelial venule, recirculating T cells are attracted by chemokines produced by dendritic cells to move over their surface.
A peptide expressed by MHC on the cell surface of a DC has the best chance of being quickly recognised by a recirculating T cells and activated

56
Q

What happens to B cells once in the secondary lymphoid tissue?

A

Recirculating B cells migrate from the high endothelial venules, along the walls of the intra-nodal lymphatics into the follicles
In the walls of the lymphatics they have the opportunity of encountering antigen in the lymph. The antigen may be free in the lymph or carried by cells that transport intact antigen.

57
Q

What is T cell priming?

A

Antigen-specific activation of naive recirculating helper T cells at the surface of a DC

58
Q

What does priming require?

A

Encounter with appropriate costimulatory molecules on the surface of DC as well as the interaction of the T cell receptor with an MHC class II/peptide complex it recognises

59
Q

Will the T cell be primed if it encounters an MHC II/peptide complex it recognises, but appropriate co-stimulation is not available?

A

No - the T cell may be induced to kill itself by apoptosis

60
Q

What do regulatory CD4 T cells do?

A

Prevent self-reactive T cells that escape negative selection in the thymus causing autoimmunity

61
Q

How do regulatory CD4 T cells work?

A

Act by intefering with the priming of naive T cells

62
Q

What happens when there are no Treg influences?

A

the process of T cell priming alters the behaviour of helper T cells

63
Q

What are the two physical parts of the spleen?

A 
Lymphocyte rich white pulp area (with T zones + follicles + a capillary blood supply)
Red pulp (consists of blood sinusoids perfusing a macrophage bed)
64
Q

What is the function of the red pulp?

A

Remove debris and pathogens from the blood

65
Q

What is the function of the white pulp?

A

Mount immune responses

66
Q

Where is the primary interface between pathogens and the adaptive immune system in the spleen?

A

Marginal sinus

67
Q

How do lymphocytes enter white pulp areas?

A

Through fenestrated epithelium

68
Q

What is another name for red pulp sinusoids?

A

Cords of Billroth

69
Q

Where does the blood go after passing the cords of Billroth?

A

Drains into venous sinusoids, which in turn drain into the splenic vein

70
Q

How do recirculating T & B cells and newly-produced virgin B cells enter the T zones of the white pulp?

A

By crossing from the marginal zone blood sinusoids

71
Q

What are patients at risk from following splenectomy?

A

System infection from encapsulated bacteria, especially pneumococcus

72
Q

What is hyposplenism?

A

A poorly functioning but not an absent spleen

73
Q

What are some causes of hyposplenism?

A

Coeliac disease, sickle cell anaemia

74
Q

What types of immunoglobulin are natural antibodies?

A

IgM and IgA

75
Q

Do natural antibodies need antigen for production?

A

No

76
Q

What are natural antibodies important in?

A

In providing resistance to common pathogens in the first 48hrs of infection as they are sticky and bind to many different bacteria

77
Q

What are B cells that produce natural antibodies called?

A

B1 cells

78
Q

Where are B1 cells found?

A

In the peritoneal and pleural cavities - do not require secondary lymphoid organs for their maintenance

79
Q

Where are B1 cells produced?

A

In the foetal liver and early in life in the bone marrow. (Ceases after infancy)

80
Q

Why is the repertoire of antigen receptors on B1 cells more restricted than that on recirculating B cells?

A

Because only a proportion of the V segments in immunoglobulin V region genes is used and junctional diversity between D and J segments and V and DJ is not increased by the action of Tdt during heavy chain variable gene rearrangement

81
Q

What is Lipid A? In what type of TI antibody response is it used?

A

The lipid component of the lipopolysaccharide

Type 1 TI antibody response

82
Q

In what type of bacteria is lipid A found?

A

Gram (-)

83
Q

Why is Lipid A an obvious target for the immune system to recognise bacteria?

A

Lipid A is not produced by mammals

84
Q

What are the bacterial cell wall components and the LPs directly recognised by?

A

Pattern recognition family of Toll receptors

85
Q

What type of antibdy is the Type 1 TI antibody response associated with?

A

Mainly IgM but also some IgG

86
Q

Why can’t Type 2 TI antibody responses be evoked in the first 5 years of life?

A

Some bacteria have a thick polysaccharide capsule that hide components of the cell wall that stimulate Toll receptors

87
Q

What type of bacteria cannot be recognised by Toll receptors?

A

Polysaccharide encapsulated bacteria - Streptococcus pneumoniae, Haemophilus influenzae, Neisseria menigitidis

88
Q

What sort of B cells are involved in the Type 2 TI antibody responses?

A

Non-recirculating, pre-activated B cells in the splenic marginal zone

89
Q

What can marginal zone B cells originate from?

A

B1 cells or recirculating B cells

90
Q

What are the properties of marginal zone B cells?

A

They are rapidly recruited into immune responses after re-exposure to the antigen that evoked them

91
Q

What are the two components to T cell dependent responses?

A
  1. Rapid extrafollicular (not dependent on B follicles) antibody responses
  2. Germinal centre dependent B follicular responses
92
Q

What type of antibody are produced by rapid extrafollicular antibody responses?

A

Mainly IgM but some IgG

93
Q

Are the antibodies produced extrafollicularly of high affinity of low affinity?

A

Not particularly high affinity

94
Q

What type of antibody are produced by germinal centre dependent B follicular responses?

A

IgG high affinity antibodies

Immunity, Infection and Haematology (6 decks)

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