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Fall 2024 > Immunology Exam 3 > Flashcards

Immunology Exam 3 Flashcards

1
Q

What happens when B cells are activated?

A

They proliferate, expansion of antigen specific clones and differentiation into plasma cells

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2
Q

Do plasma cells secrete antibodies?

A

YES

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3
Q

Do memory cells secrete antibodies?

A

NO

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4
Q

Heavy chain/isotope switching

A

When during differentiation B cells produce antibodies of different heavy chain classes that mediate different effector functions and combat different types of microbes

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5
Q

Affinity maturation

A

Affinity of antibodies specific for microbial proteins increases during the response to microbes
Have an increase in antibodies with the improved capacity to bind to and neutralize microbes and their toxins

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6
Q

Why can T cells only help B cell responses to protein antigens?

A

T cells can only recognize peptides derived from proteins and displayed by MHC molecules

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7
Q

T-dependent antigens

A

Most protein antigens show no or weak antibody response
Therefore the B cells need T helper cell help

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8
Q

T-independent antigens

A

Polysaccharides, NA, lipids, and other multivalent antigens can stimulate antibody production without helper T cells
Responses are short lived and require direct activation of B cells by antigens as well as signals via the innate immune system without the role of helper T cells

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9
Q

What happens to antibodies made from helper T cells and protein antigens?

A

Have class switching and affinity maturation because helper T cells stimulate these processes
Generate plasma cells and memory B cells
Most specialized and long lived responses are from protein antigens with helper T cells

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10
Q

Follicular B cells

A

Majority of B cells
Reside in and recirculate through follicles of the lymphoid organs
Are majority of T dependent B cells with class switching and plasma cell creation and high affinity antibody responses

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11
Q

Marginal-zone B cells

A

Peripheral region of splenic white pulp and in outer rim of follicles of lymph nodes
Respond to polysaccharide and lipid antigens mostly
Express antigen receptors of limited diversity and make T independent IgM responses

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12
Q

B-1 cells

A

Mucosal tissues and peritoneum
Respond to multivalent polysaccharide and lipid antigens
Express antigen receptors of limited diversity and make T independent IgM responses
IgM can be produced spontaneously without immunization

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13
Q

Natural antibodies

A

IgM can be produced spontaneously without immunization via B-1 cells
Help clear dead cells that underwent apoptosis and provide protection against some bacterial pathogens

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14
Q

Secondary response

A

Increased heavy class chain switching and affinity maturation
Repeated stimulation by protein antigen leads to an increase in the number and activity of antigen-specific helper T cells

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15
Q

B cell antigen receptor mediated signaling requires…

A

Crosslinking of two or more Ig molecules
Two or more antigen molecules in an aggregate, or repeating epitopes of one antigen molecule, bind to adjacent membrane Ig molecules of a B cell
After the crosslinking, signals are transduced by receptor-associated proteins

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16
Q

IgM and IgD on naive B lymphs

A

Highly variable antigen-binding regions
These membrane receptors have short cytoplasmic tails so they do NOT transduce signals themselves
The proteins associated with them (Ig-alpha and Ig-beta) transduce signals to form BCR complex

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17
Q

Ig-alpha and Ig-beta

A

Part of BCR which have ITAMs (immunoreceptor tyrosine motifs)
When two or more antigen receptors of B cell are brought together by crosslinking, the tyrosine’s on the ITAMs are P’ed by tyrosine kinases
SYK tyrosine kinase is recruited and P’s tyrosine residues on adaptor proteins
Adaptor proteins activate downstream molecules (like enzymes) to activate signaling cascades
Txn. factors are activated and then there is expression of genes responsible for B cell proliferation and differentiation

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18
Q

The complement system

A

A collection of plasma proteins that are activated by microbes and by antibodies attached to microbes and function as effector mechanisms of host defense

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19
Q

What happens when the complement system is activated by the innate immune system?

A

The microbe is coated with the proteolytic fragments of C3. One of the fragments is C3d. B lymphocytes have a receptor for C3d (CR2, or CD21)

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20
Q

What happens when CR2 is engaged on B cells

A

C3d has been bound and the antigen dependent B cell activation is enhanced via activating ITAMs

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21
Q

How do microbial products directly activate B cells

A

Engage in innate pattern recognition receptors
Pathogen-associated molecular patterns of microbes bind to TLRs on PM or endosomes of B cells which causes signaling pathways that work with signals from the antigen receptor
These two signals causes B cell proliferation, Ig secretion, and differentiation

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22
Q

What do protein antigens do to B cells then?

A

They do not stimulate high levels of B cell proliferation, they induce changes in B cells that enhance their ability to interact with helper T lymphocytes

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23
Q

What happens when protein antigen finds B cell?

A

It binds to BCR and the antigen is endocytosed then it is degraded and displayed by class II MHC to helper T cells
Therefore response to cytokines is enhanced
Migration from follicle of the secondary lymphoid organ to T-cell zone

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24
Q

Interactions of helper T cells and B lymphocytes in antibody responses to T-dependent protein antigens

A

Recognition of different epitopes of the same protein antigen by the two cell types
1. CD4 cells are activated by presentation of antigen by class II MHC by dendritic cells and then CD4 cells differentiate into cytokine producing, CD40 ligand having helper T cells
2. Naive B cells are activated in the follicle by exposed epitope on the same protein
3. The activated B and T cells migrate to one another and interact at edges of the follicles where initial antibody response develops
4. Some B and T cells go back into the follicles and form germinal centers where more specialized antibody responses are induced

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25
Q

How do B cells present antigens to helper T cells?

A

Bind protein antigens by their Ig and endocytose the antigens, process them in endosomal vesicles and then display them on class II MHC

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26
Q

Why do B cells present multiple peptides?

A

So helper T cells can recognize multiple epitopes of the same protein antigen later

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27
Q

What ensures B cell and T cell interactions are antigen specific?

A

B cells internalize the antigen they have receptors for and then helper T cells recognize peptides derived from the same antigen

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28
Q

Can B cells activate previously differentiated effector T cells?

A

Yes
They cannot initiate a response from naive T cells tho

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29
Q

Hapten-carrier conjugates

A

B cell binds hapten portion, ingests the conjugate and then displays the peptides to helper T cells
Antibody response is specific to the epitope recognized
The peptides derived from the carrier protein bring the T cell into this situation

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30
Q

B cell epitopes

A

Recognizes one epitope of an antigen and then displays different epitopes of the antigen for helper T cells

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31
Q

What is a hapten?

A

Small chemical recognized by B cells and stimulates strong antibody responses if it is attached to a carrier protein

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32
Q

Conjugate vaccine

A

Way to get antibody response against microbial polysaccharides
Polysaccharide is coupled to a protein. Then the B cells recognizes the polysaccharide and ingests it, displays it for T cells
This stimulates polysaccharide specific B cells
High affinity T dependent antibody responses are induced against the polysaccharide because helper T cells specific for the carrier are engaged

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33
Q

What is induced in a response to polysaccharides?

A

Isotope switching, affinity maturation, long lived plasma cells and memory cells

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34
Q

Results of conjugate vaccines

A

T cells recognize peptides from the attached protein
B cells recognize polysaccharide
Antibody response is specific for the polysaccharide
Is much stronger than T independent responses because helper T cells are able to participate

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35
Q

What do conjugate vaccines protect against?

A

Bacteria
Haemophilus influenzae, meningococci, pneumococci, and typhoid

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36
Q

How do helper T cells activate antigen-specific B cells?

A

When the helper T cells are activated by recognizing an antigen from B cells, they use CD40 ligand and secreted cytokines to activate antigen-specific B cells

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37
Q

Two ways helper T cells activate B cells

A
  1. CD40L ligand from T cells bind to CD40 on B cells
  2. Cytokines secreted by T cells bind to cytokine receptors on B cells

Both of these induce B cell proliferation and differentiation

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38
Q

Cells made from initial T-B cell interactions

A

Low levels of antibodies with switched isotopes and short-lived plasma cells that secrete antibodies for a few weeks

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39
Q

Where do fully developed antibody responses occur?

A

Germinal centers formed by lymphoid follicles and require helper T cells
Some helper T cells express chemokine receptor CXCR5 which pulls the cells into adjacent follicles

40
Q

Follicular helper T cells (Tfh)

A

CD4+ cells that migrate into B cell rich follicles
Generation and function of them depend on the receptor of CD28 family called inducible costimulator which binds to its ligand on B cells

41
Q

What do Tfh cells are their precursors secrete?

A

Cytokines such as IL-4 and IL-13
They determine which antibody isotope is produced by class switching

42
Q

Germinal center

A

Few activated B cells and Tfh cells migrate to the lymphoid follicle to divide rapidly in response to Tfh signals
B cells undergo further class switching and somatic mutations of Ig genes

43
Q

B cells made in early germinal center

A

B cells of moderate affinity develop into memory cells and exit germinal layer

44
Q

B cells made in later germinal center

A

High affinity B cells are produced by repeated Ig mutation and selection
Eventually differentiate into long-lived plasma cells and memory cells

45
Q

Where are proliferating B cells in germinal center?

A

Dark zone

46
Q

Where does selection of B cells occur in germinal center?

A

Less dense light zone

47
Q

How the immune system protects the body from bacteria and viruses

A

They coat (opsonize) them with antibodies so then they can by phagocytosed by macrophages and neutrophils
Best done by IgG molecules

48
Q

What do IgG molecules do to antigen

A

Bind high affinity phagocyte Fc receptors for specific Fc portion of the gamma heavy chains

49
Q

What stimulates the production of IgE antibodies?

A

Helminths
IgE binds and activates mast cells (have high affinity Fc receptors for epsilon heavy chain

50
Q

IgA

A

mucosal immunity

51
Q

How do IgG antibodies have a longer half life than IgM?

A

IgG is able to bind to a specialized Fc receptor (neonatal Fc receptor (FcRn))

52
Q

FcRn

A

Expressed on the placenta and mediates the transfer of maternal IgG to the fetus
When it is expressed on endothelial cells and phagocytes it plays a role in protecting IgG from intracellular catabolism

53
Q

What induces heavy chain class switching?

A

A combination of CD40L mediated signals and cytokines

54
Q

What happens when CD40 or CD40L is absent?

A

B cells only secrete IgM
and fail to switch to other isotopes

55
Q

Switch recombination

A

molecular mechanics of class switching
Taking former VDJ exon encoding the V domain and of an Ig micro heavy chain and moving it adjacent to a different C region downstream of the Ig heavy chain

56
Q

Cytokines produced by Tfh cells do what?

A

Determine which heavy chain isotope is produced

57
Q

Switching to IgE heavy class

A

Stimulated by IL-4 and IL-13 made by Tfh cells
Associated with helminth infections
Induce Th2 cells and related Tfh responses

58
Q

Affinity maturation

A

The affinity of antibodies produced in response to a protein antigen increases with prolonged or repeated exposure to that antigen

59
Q

Where does affinity maturation occur?

A

Happens in the germinal centers of lymphoid follicles and is the result of somatic hypermutation of Ig genes in dividing B cells, followed by the selection of high-affinity B cells by antigen

60
Q

What happens in dark zones of germinal centers?

A

Where B cells are proliferating
Numerous point mutations are introduced into Ig genes

61
Q

What does enzyme AID do?

A

In dark zone
Is required for class switching
Converts cytosines to uracil
The C to T mutations are either removed or repaired by mechanisms that lead to the addition of new nucleotides in the vicinity of the original mutated cytosine

62
Q

Role of FDCs in antigen-antibody complexes

A

Displays the complexes
Are found only in lymphoid follicles
Most antigen in germinal centers carriers attached antibody or complement proteins which bind receptors on FDCs and are therefore displayed by FDCs

63
Q

Antigen-antibody complexes

A

When residual antigen from original infection binds antigen
Activates complement
Complexes are displayed by FDCs

64
Q

B cells interacting with FDCs

A

They recognize the antigen, internalize it, process it and then present it to Tfh cells which provide survival signals

Therefore high affinity B cells are more effective when it comes to competing for an antigen than a low affinity B cell.
More likely to bind to antigen and survive

65
Q

What happens with B cells that have been selected?

A

They return to the dark zone and the process starts all over again

66
Q

Properties of selected B cells

A

Must be able to bind antigen at increasingly lower concentrations and therefore are cells whose antigen receptors are of a higher affinity
Ex. Vaccine boosters

67
Q

What can activated B cells in the germinal centers turn into?

A

Memory B cells: DO NOT SECRETE ANTIBODIES!!! Are in tissues and secondary lymph organs
survive months to years and cycle around waiting to see the antigen again

Plasma cells: SECRETE ANTIBODIES!!!!
Go to circulation and migrate to bone marrow and mucosal tissues

68
Q

T-independent protein antigens

A

Differ from responses to proteins
Most of these differences come from the role of helper T cells in antibody responses to proteins

Engage TLRs providing activating signals to the B cells that enhance B cell activation in the absence of T help

Polysaccharides activate complement system

Crosslinking of BCRs by multivalent antigens may activate B cells strong enough in order to stimulate their proliferation and differentiation without T cell help

69
Q

What can elicit antibody responses without the help of helper T cells?

A

Polysaccharides, lipids and other nonprotein antigens
These non-protein antigens cannot bind to MHC molecules and therefore cannot be seen by T cells

70
Q

How are bacteria killed?

A

They contain polysaccharide rich capsules which can be bound by antibodies which target the bacteria for phagocytosis

71
Q

What are B cell responses regulated by?

A

Products of B cells: antibodies, cell-intrinsic mechanisms (inhibitory receptors and signaling pathways)

72
Q

What happens to activated B cells that do not differentiate into plasma cells or memory cells?

A

Apoptosis

73
Q

Antibody feedback

A

When antibody bound to antigen inhibits further antibody production
Terminates further B cell activation

74
Q

Mechanism of antibody feedback

A

IgG that circulates through blood binds antigen to forming immune complexes

B cells specific for an antigen may bind antigen part of the immune complex by their Ig receptors

Fc tail of attached IgG antibody may be recognized by Fc receptor Fc-gamma-RIIB which is an inhibitory receptor that contains immunoreceptor tyrosine-based inhibitory motif (ITIM) which is P’ed by LYN tyrosine kinase and phosphatase is recruited to ITIM
The phosphatase shuts off antigen receptor-induced kinase-dependent signals. Terminating B cell responses

Terminates further B cell activation once enough IgG are produced

75
Q

Other inhibitory receptors to shut off B cell activation other than Fc-gamma-RIIB?

A

CD22 and CD72 which have ITIMs that are P’ed after the BCR is engaged
P’ed ITIMs recruit tyrosine phosphatase SHP-1 which dampens signaling

76
Q

IgG

A

Neutralization of microbes and toxins

Opsonization of antigens for phagocytosis by macrophages and neutrophils

Activation of the classical pathway of complement

Antibody-dependent cellular cytotoxicity mediated by NK cells

Neonatal immunity: transfer of maternal antibody across placenta and gut

Feedback inhibition of B cell activation

77
Q

IgM

A

Activation of the classical pathway of complement

78
Q

IgA

A

Mucosal immunity: secretion of IgA into lumens of gastrointestinal and respiratory tracts, neutralization of microbes and toxins

79
Q

IgE

A

Mast cell activation

Defense against helminths

80
Q

Antibody Fab (antigen-binding) and Fc regions role

A

Fab region bind to and block harmful affects of microbes and toxins
Fc (made up of heavy chain constant regions) regions are used to activate diverse effector mechanisms that eliminate the microbes and toxins

81
Q

Binding of Fc region

A

Fc region contains binding sites for Fc receptors on phagocytes and for complement proteins
Binding of Fc receptors and complement proteins happens only after Ig molecules recognize and become attached to a microbe or a microbial antigen
Therefore Fc dependent functions require antigen recognition by Fab regions

82
Q

What is affinity maturation induced by?

A

Repeated stimulation with protein antigens
Leads to production of antibodies with a higher and higher affinities for an antigen

83
Q

Benefits of switching to IgG

A

It prolongs the protective functions of the humoral immune response
IgG isotopes survive longer duration in the blood than IgM and other isotopes
IgG has a half-life of three to four weeks because of neonatal Fc receptor (FcRn)

84
Q

Where is FcRn expressed?

A

Expressed in the placenta, endothelium, phagocytes and a few other cell types
Transports antibodies from the mothers circulation to the fetus
FcRn also protects IgG antibodies from intracellular catabolism

85
Q

FcRn and IgG mechanism

A

Way to recycle IgG. Proteins attached to IgG are degraded in the lysosomes and the IgG are taken out of the endosomes
FcRn binds to IgG that is in the cells in the endosome and it recirculates it back into blood or tissue fluids to avoid lysosomal degradation
The IgG-FcRn complexes are sorted to recycling endosomes to be released from the cell
This is why IgG half-life is unusually long

86
Q

What antibodies do at epithelial barrier?

A

Antibody blocks penetration of microbe through epithelial barrier by binding microbe
Without antibody the microbe would enter through epithelial barrier

87
Q

What antibodies do when microbe tries to infect cell?

A

Antibody blocks binding of microbe and infection of cell by binding to microbe
Without antibodies the cell is infected by the microbe

88
Q

What antibodies do when a toxin tries to bind to cell surface receptor?

A

Antibody blocks binding of toxin (caused by endotoxins or exotoxins) to cellular receptor by binding to toxin
Without antibody the toxin binds to cell surface receptor and there is a pathologic effect of the toxin

89
Q

Fc-gamma-RI (CD64) and Fc region of IgG

A

When a microbe is bound by IgG, Fc regions face away from microbe allowing the Fc region to bind to high affinity receptor of Fc regions called Fc-gamma-RI (CD64)
Fc-gamma-RI is expressed on neutrophils and macrophages
Phagocyte extends its PM to endocytose microbe into a phagosome which fuses with lysosomes
Binding of Fc-gamma-RI also activates phagocytes because it contains a signaling chain that triggers biochemical pathways in the phagocytes
Signals lead to creation of ROS, NO, and proteolytic enzymes in the lysosomes of activated neutrophils and macrophages

90
Q

What does the spleen do to encapsulated bacteria?

A

The spleen has large amounts of macrophages and is a major site for phagocytic clearance of opsonized bacteria

91
Q

Fc-gamma-RII

A

Does not mediate effector functions
Shuts down antibody production
Reduces inflammation
Feedback inhibition of B cell activation
Inhibits activation of dendritic cells and are therefore anti-inflammatory

92
Q

Intravenous immune globulin (IVIG)

A

Pooled IgG from healthy donors is given to the sick to treat inflammatory diseases
Is effective because it binds to Fc receptor Fc-gamma-RII

93
Q

Can natural killer cells bind to opsonized cells and kill them?

A

Yes
They express Fc-gamma receptor called Fc-gamma-RIII (CD16) which is an activating receptor for NK cells
Fc-gamma-RIII (CD16) binds an array of IgG antibodies
Signals made by the binding of Fc cause NK cells to release their granule proteins which kill antibody coated cell

94
Q

Antibody-dependent cellular cytotoxicity

A

Process by which Fc-gamma receptor on NK cells is activated by signals produced by receptor which Fc-gamma binds to cell that has been opsonized

Cells with an enveloped virus can express viral glycoproteins on their surface which can be recognized by antibodies which can cause ADCC-mediated destruction of the infected cell

ADCC is one of the ways therapeutic antibodies can be used to treat cancers to eliminate tumor cells

95
Q
A

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