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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

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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

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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

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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

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43
Q

B cells made in early germinal center

A

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

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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

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45
Q

Where are proliferating B cells in germinal center?

A

Dark zone

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46
Q

Where does selection of B cells occur in germinal center?

A

Less dense light zone

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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

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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

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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

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50
Q

IgA

A

mucosal immunity

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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))

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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

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53
Q

What induces heavy chain class switching?

A

A combination of CD40L mediated signals and cytokines

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54
Q

What happens when CD40 or CD40L is absent?

A

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

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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

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56
Q

Cytokines produced by Tfh cells do what?

A

Determine which heavy chain isotope is produced

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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

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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

What are heminthic parasites dominated by?

A

T helper 2 (Th2) cell activation, IgE antibody production, eosinophilia

96
Q

How are eosinophils activated?

A

Fc-epsilon-RI is not expressed at high levels and lacks its signaling chain in eosinophils so IgE does not activate eosinophils

The cells are recruited by chemokines to sites of infection
May bind to IgG coated parasites by Fc-gamma-RI
They can also be activated by Th2 cytokine IL-5 independent of antibody and release their granule contents which destroys the thick integuments of helminths

97
Q

How complement stimulates inflammatory responses?

A

C3a and C5a both bind to receptor of leukocytes (neutrophils and other leukocytes) and cause inflammatory reactions which can lead to destruction of microbes by leukocytes

98
Q

How complement phagocytose microbes

A

Opsonization of microbe with C3b/C4b
C3b is recognized by phagocytes CR1 receptor
Leads to phagocytosis and killing of microbe

99
Q

Fc-gamma-RI (CD64)

A

High affinity for Ig, binds to IgG
Are on macrophages, neutrophils
Causes to activation of phagocytosis

100
Q

Fc-gamma-RIIB (CD32)

A

Low affinity for Ig
Are on B cells, DCs, mast cells, neutrophils, macrophages
Cause feedback inhibition of B cells
Attenuation of inflammation

101
Q

Fc-gamma-RIIIA (CD16)

A

Low affinity for Ig
On NK cells
Antibody-dependet cellular cytotoxicity (ADCC)

102
Q

Fc-epsilon-RI

A

High affinity for Ig, binds IgE
On mast cells and basophils
Activation (degranulation) of mast cells and basophils

103
Q

Way complement system promotes antibody production

A

breakdown product C3d from C3 is recognized by complement receptor 2 (CR2) on B cells
Enhances B cells response against microbes
With this antigen-antibody complex DCs can recognize these complexes and antigens can then be displayed for more B cell activation

104
Q

Ways complement system is regulated

A

Regulatory proteins which prevent complement-mediated damage to host cells

105
Q

decay accelerating factor (DAF)

A

Hydrolyze C3b and inactivate it
Microbe cell membranes lack DAF
Prevents the binding of Bb in the alternative pathway and C2a in the classical pathway

106
Q

membrane cofactor protein (MCP)

A

Hydrolyzes C3b and inactivates it
Microbe cell membrane lacks MCP

107
Q

C1 inhibitor (C1 INH)

A

Prevents assembly of C1 complex
Therefore blocks initiation of classical pathway

108
Q

Complement receptor (CR1)

A

Interferes with formation of C3 convertase by blocking the binding of Bb in the alternative pathway and C2a in the classical pathway

109
Q

Factor I

A

Cleaves C3b into inactive fragments

110
Q

Why is complement activated for microbes and not host cells?

A

Complement regulatory proteins are made by vertebrae cells but not by microbes
Microbes therefore lack the regulatory proteins

111
Q

Mucosal immunity

A

IgA binds and neutralizes toxins in the lumens of the mucosa-lined organs
Also called secretory immunity
IgA is produced in plasma cells in mucosal tissues and then are transported across epithelia to the lumens of mucosa-lined organs

112
Q

Why is IgA for mucosal immunity?

A

The cytokines that induce switching to this isotope are present in the B cells there
Includes transforming growth factor beta (TGF-beta)

113
Q

How is IgA transported across epithelia to lumen?

A

With special Fc receptor (poly-Ig receptor) which is expressed on basal surface of epithelial cells
Binds IgA, endocytoses into vesicles, transports it to luminal surface
Receptor is cleaved by a protease and then IgA is released into lumen

114
Q

What protects IgA from degradation by proteases in the gut?

A

After the poly-Ig receptor is cleaves by a protease, some of the bound receptor (secretory component) protects the antibody from degradation

115
Q

What antibody is in breast milk?

A

IgA
They are secreted across mammary gland epithelia via poly-Ig receptor

116
Q

How long is baby protected with mom’s antibodies?

A

Six months for IgG since it has a long half-life
At that time the baby will begin to make its own antibodies

117
Q

How do bacteria and viruses evade humoral immunity?

A

Mutate their surface molecules that are needed for entry into host cells so they can no longer be recognized by antibodies

118
Q

Why are gp120 vaccines not affective?

A

There are many variant forms of the gp120 glycoprotein for HIV that one subtype may not protect against other virus subtypes that appear in infected individuals

119
Q

How has COVID-19 evaded vaccine-induced immunity?

A

Causative agent is a spike protein that gain entry into host cells
Variants of spike protein exist which allows proteins to evade the vaccine

120
Q

Ways antigens can evade immune system

A

Antigenic variation (many viruses (influenza, HIV, SARS-CoV-2), some bacteria, Protozoa) Inhibition of complement activation, and blocking phagocytosis (many bacteria) by hyaluronic acid capsule (Strep)

121
Q

Live attenuated viruses

A

Lack of pathogenicity while retaining their infectivity and antigenicity
Production of neutralizing antibodies
Killed viruses such as hepatitis A, polio and rabies

122
Q

Subunit vaccines

A

Composed of microbial proteins and polysaccharides
Can also be produced using recombinant DNA technology like in hepatitis B and human papilloma virus vaccines

123
Q

Conjugate vaccines

A

Microbial polysaccharides that are unable to stimulate T cells are coupled with proteins so T cells are activated and high-affinity antibodies are produced
T cell-B cell interactions
Inactivated microbial toxins with microbial proteins
Stimulates antibodies to bind to and neutralize native toxins and the microbes

124
Q

Nucleic acids as vaccines

A

Advantage is that microbial proteins may be produced in host cells and secreted which would cause a humoral and cell-mediated responses
Nucleic acids engage TLRs and therefore have adjuvant activity
Plasmid DNA vaccines have not been successful

125
Q

Issues with mRNA vaccines

A

Extracellular RNA is unstable
When RNA enters cytosol, innate immune system recognizes it and causes type I interferon response that can cause harmful inflammation
Therefore putting RNA in lipid nanoparticles has helped these issues
Vaccine was successful for COVID-19

126
Q

Hybrid viral vaccines

A

Now used for SASRS-CoV-2 and have been approved for the Ebola virus
When the DNA encoding a microbial antigen can be incorporated into the genome of a replication defective viral vector
Virus is harmless for humans
When it enters the host cell the microbial proteins are produced.

127
Q

Immunologic tolerance

A

Unresponsiveness to self antigens

Lack of response to antigens that is induced by exposure of lymphocytes to these antigens

128
Q

autoimmunity

A

The immune system attacks the individuals own cells

129
Q

Immunogenic antigens

A

lymphocytes are activated to proliferate and to differentiate into effector and memory cells
aka…affective immune response
Microbes are immunogenic antigens normally

130
Q

Tolerogenic antigens

A

When lymphocytes may be functionally inactivated or killed, resulting in tolerance
Self antigens are tolerogenic normally

131
Q

Immunologic tolerance to different self antigens

A

Induced when developing lymphocytes encounter these antigens in the generative (central) lymphoid organs called central tolerance

132
Q

Primary mechanism of central tolerance in T cells

A

Death of immature T cells that recognize self antigens in the thymus

133
Q

Peripheral tolerance

A

Mature lymphocytes that recognize self antigens may be suppressed by Tregs, inactivated (anergy) or deleted (apoptosis)

134
Q

Medullary thymic epithelial cells (MTECs)

A

Transcribe and express genes encoding antigens that are otherwise only expressed by the cells in one or another peripheral tissue type
Expression is induced by AIRE expression

135
Q

Autoimmune regulator (AIRE)

A

Protein that promotes expression of antigens characteristic of the various tissue cell types

136
Q

What happens when there are mutations in the AIRE gene?

A

Autoimmune polyglandular syndrome

Tissue antigens are not expressed in MTECs from lack of AIRE protein
Antigens are expressed normally in peripheral tissues
Immature T cells specific for these antigens are not eliminated and do not develop into to Tregs. They mature into functioning T cells
Enter periphery and attack tissues. The T cells promote production of autoantibodies by B cells since the B cells recognize the T cell cytokines

137
Q

FOXP3

A

required for development and function of T regs
Depends on IL-2
Factor beta (TGF-beta) plays a role in expression of FOXP3

138
Q

IL-2

A

Promotes immune responses by stimulating T cell proliferation
Inhibits immune responses by maintaining functional T regs

139
Q

CTLA-4

A

Inhibitory receptor expressed by Tregs that blocks B7 costimulators from APCs and blocks T cell activation

140
Q

Central B lymphocyte tolerance

A

Occurs in bone marrow
Receptor editing: Change receptor specificity by re-expressing genes to express a new Ig light chain
Deletion: When editing fails, cells receive death signals and die by apoptosis

141
Q

Peripheral B cell tolerance

A

Mature B lymphs that encounter self antigen in peripheral tissues (become functionally unresponsive (anergic))

Transitional B cells (just left bone marrow) that are triggered by self antigen are eliminated by apoptosis

142
Q

Immune privilege

A

Occurs in central nervous system, brain, eyes, testes
Immune responses do not occur in these regions due to suppressive factors released by various cells

143
Q

Infections and Environmental triggers of autoimmunity

A

Molecular mimicry
Tissue injury releases self antigens not normally seen by immune system

Fall 2024 (13 decks)

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