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Infection & Immunity > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

What are the two main characteristics of the acquired immune system?

A

Specificty and memory

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2
Q

What is specificty of the immune system?

A

That distinct antigens elicit responses that target those antigens

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3
Q

What is memory of the immune sytem?

A

Rapid and enhanced response to repeated exposures of the same antigen

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4
Q

What is an epitope?

A

Part of an antigen recognized by the immune systems antibodies, T-cells, B-cells

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5
Q

Why can conformation epitopes be recognized by B-cells and not by T-cells?

A

Conformation epitopes are recognized by B-cells because they can detect the full viral antigen, while for T-cells it needs to be presented on the MHC and the linear epitopes cannot be joined together on the MHC, so conformation epitopes cannot be recognized by T-cells

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6
Q

What are the differences between B-cell antigens and T-cell antigens?

A

T-cell antigens are limited to proteins (and their peptide cuts) and sometimes lipids. All the others do not fit into MHC, while they can be recognized by B-cells

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7
Q

What is the difference between an antibody and an immunoglobulin?

A

Immunoglobulins are the biochemical characteristics, and for antibodies, it is required there is a known antigen

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8
Q

What are linear and conformation epitopes?

A

Linear epitopes are a stretch of continous amino acids, while conformational epitopes are amino acid residues brought together by protein folding

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9
Q

What is the differnce betwen T-cell and B-cell antigens?

A

B-cell antigens can be proteins, lipids, carbs, nulcleic acids and small chemical groups; T-cell antigens are small proteins

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10
Q

What is the difference between antibodies and immunoglobulins?

A

Immunoglobulins are the biochemical characteristics of the molecule, while antibodies have a known antigen

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11
Q

How are heavy- and light-chains held together?

A

With sulfur bridges

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12
Q

Explain the structure of an antibody

A

There is an antigen binding part (Fab) and there is a constant part, the Fc. The antibodies can also be divided into the heavy chain and the light chain.

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13
Q

What are the complementarity-determining regions of antibodies?

A

They are the variable regions of the BCR and TCR that participate in binding of epitopes

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14
Q

What four things can an antibody activate?

A
  • complement
  • phagocytes/for phagocytosis
  • ADCC (antibody-dependent cellular cytotoxicity
  • Mast cells and basophils
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15
Q

How can the immune system activate complement?

A

IgM antibodies can bind C1q, which initiates the classical complement pathway

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16
Q

What is the difference between affinity and avidity?

A

affinity is the goodness of fit between antigen and antibody; avidity is the totally of binding strength to an antigen

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17
Q

Explain the relationship between antigen and antibody dependening on low or high affinity

A

If there is high affinity, there is a long on, short off between antigen & antibody
If there is low affinity short on, long off between antigen & antibody

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18
Q

Why is there a wide repetoire of immunoglobulins and B-lymphocytes?

A

Because lymphocytes have only one specificity, so there are many lymphocytes to ensure there are many different specifities

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19
Q

What is clonal selection and how does it work?

A

The antigen will bind with a B-cell or the antigen fragment + MHC bind to a T-cell, causing cloning of the bound lymphocyte. This one will respond to it once it has been recongized. The clonal cells will become effectors cells and memory cells

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20
Q

What happens to lymphocytes specific for self molecules?

A

They are deleted in lymphoid development, to prevent auto-immunity

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21
Q

Will all lymphocyte specifities be in the body in high numbers?

A

No, when the antigen binds there is cloncal expansion, otherwise, lymphocyte specifities only exist in low numbers

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22
Q

Which Ig is associated with primary response to an pathogen?

A

IgM is associated with the primary response. Later, this becomes IgG.

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23
Q

what is the main difference between the primary response and the secondary response?

A

THe primary response is weak and short, but produce memory cells. The secondary response allows for T and B memory cells to react much faster, there is stronger protection and higher affinity, faster kinetics and higher antibody titers

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24
Q

Which two factors ensure life-long protection?

A

The persistence of memory cells
The persistence of protective antibodies and cytotoxic T-cells

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25
Q

Which three responses can somatic hypermutation cause?

A

The affinity goes down, there is no impact on the affinity, and there is higher affinity to the antigen

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26
Q

What is affinity maturation?

A

The process by which antibodies gain affinity, avidity, and anti-pathogen activity from somatic hypermutation

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27
Q

Can immunological memory be transfered in humans?

A

If it is from purified stem cells, then no, there is no memory transfer, but if not, then there is slight transfer of membranes

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28
Q

What will happen to an infected cell when detected by a T-cell?

A

There is infection of the cell, leading to presentation of the infectious peptide on the MHC. This is recognized by the TCR, which induces release of IFNy and perforin and granzyme, which induces apoptosis, killing the infected cell in a controlled manner.

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29
Q

What are the steps required for T-cell recognition of antigens?

A

Proteins are cut into short proteins, which are shown to the antigen receptor on the T-lymphocyte. The peptide-presentation occurs using an MHC molecule. The T-cell thus recognizes antigen-derived peptide + MHC

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30
Q

How can circulating antibodies attach to cells?

A

They attach to the Fc-receptors, or get transported to mucosal surfaces

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31
Q

Binding of a B-cell to an antigen leads to

A
  • a triggering signal turns them into plasma cells or memory cells
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32
Q

What causes antigen specificity in B and T-cells?

A
  • ability to distinguish antigens with recognition-sites (B-cells)
  • receptor-specificity for a peptide (T-cells)
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33
Q

How does vaccination work for immune response and creating immunological memory?

A

Vaccination relies on a non-pathogenic form of the infectious organism/toxin with antigens to create the memory cells, as they do have the antigen but this won’t cause infection. This leads to protective immunity

34
Q

Which T-cell type is associated with which MHC?

A

Cytotoxic T-cells recognize peptides from MHC-class-I
Helper /regulatory T-cells recognze MHC-class-II

35
Q

What activates naïve T-cells and what happens once they are primed?

A

The naïve T-cells must be shown peptide antigen+ MHC by the dendritic cell. After priming, the T-cells is activated by peptide + MHC on macrophages and B-cells

36
Q

What is ADCC?

A

antibodies will bring NK-cells close to the target by bridge-forming. The NK cells then gets activated and kills the virally infected cells

37
Q

What are the advantages of the memory response?

A
  • Higher frequency of antigenic-specific precursors
  • higher antibody titers
  • faster kinetics
38
Q

How does a T-cell kill a virus infected cell?

A

Viral peptide is recognizd by the TCR, the T-cel becomes activated. The T-cell contains vesicles with granzyme and perforin. Perforin penetrates the cell wall, while granzyme enters the cell and activates caspases, which induce apoptosis. Apoptosis is preferred because otherwise it causes inappropriate inflammation

39
Q

What are the 5 steps of gene rearrangement for a B-lymphocyte?

A

Step 1. RAG-1 and RAG-2 enzymes bind to the signal sequences on D & J areas
Step 2. The complementary signal sequences form a double-stranded stretch with all intervening DNA
Step 3. Ku70 & ku80 cut the DNAs and lead to hairpin formation at the break. There is a double-stranded cut and the intervening sequence is cut off.
Step 4. there is non-homologous end-joining
- the hairpins are cleaved, there is deletion of nucleotides from the coding ends by exonucleases, TdT can be added to the coding ends, btoh strands are then joined together with DNA ligase.
Step 5. there is DJ joining, and an excision circle is seperated from the DNA

40
Q

What happens with the excision circle during replication?

A

The excision circle ends up in one of two daughter cells as it does not replicate

41
Q

What happens if you are RAG-1 or RAG-2 deficient?

A

If you are deficient you cannot do rearrangement so no B- and T-cell synthesis, resulting in SCID

42
Q

What happens if gene rearrangement of the antibody shifts the reading frame?

A

It depends, if it makes the protein sequence end, it can be catastrophic, but since there are two chromosome versions, you have two tries

43
Q

What are the steps of joining V and DJ together?

A

There is rearrangement of the V segment to DJ
There is transcription of the VDJ sgment, the interfering sequence between J and the constant are removed,
There is translation into porotein, and only the first constant segment is used.

44
Q

Why is the newly arranged heavy chain expressed with a fake light chain?

A

It is done to see if the heavy chain is expressed properly

45
Q

What are the steps of class switching from IgM to IgG?

A
  1. AID (activation induced deaminase) causes double stranded DNA breaks
  2. UNG (uracil-N-glycosylase) enzyme repairs the DNA breaks,
  3. there is splitting off of a excesion loop
46
Q

Does switching occur in the heavy or the light chain?

A

The heavy chain

47
Q

Name three things you know about IgM

A

It is associated into a pentamer,
is there in the primary antibody response
is always intravascular

48
Q

Name four things you know about IgG

A

It has four subclasses
Is the highest Ig concentration in serum
Occurs in the secondary antibody response
is transplacental

49
Q

Name four things you know about IgA

A

Has Two subclasses
associates into a dimer
Is the highest concentration in mucosa
Is in breast milk

50
Q

Name three things you know about IgE

A

It has the shortest half life,
Binds to eosinophils and mast cells
Visible in allergy

51
Q

Name two things you know about IgD

A

It has no known antibody activity
Is a BCR on naive B cells

52
Q

What transduces the T-cell receptor antigen recognition signal?

A

The CD3 complex in the membrane

53
Q

How is a B-cell inhibited or co-stimulatory?

A

When the pathogen is bound by the transmembrane IgG, membrane IgG will associate with ITIM, leading to PTPase, which inhibits the ITAM. OR, lyn which stimulates ITAM and leads to B-cell activation

54
Q

How are antibodies transferred from mother to foetus?

A

The maternal blood containing IgG is endocytosed. The FcRn binds IgG in an endosome. There is sorting of FcRn-IgG complexes, in the late endosome, the IgG is exocytosed and IgG dissociates into the fetal blood

55
Q

What does CD in CD3/CD2/etc stand for?

A

Cluster of differentiation

56
Q

Name five characteristics of alpha-beta T-cells

A

It recognizes MHC+peptide
It is expressed on CD4/CD8
MHC is restricted
It helps lymphocyte and macrophage activation
involved in cytotoxic killing

57
Q

How many possible regions of antigen receptor molecules can there be?

A

If only V, D, and J recombination, 40 x 30 x 6 leads to 7200 different combination. If you account for other possibilities, it can be 1.1*10^6, or if you consider junctional diversity, reading frames and N region insertion, it could be 1.3 *10^9

58
Q

What does the MHC do?

A

The MHC is the major histocompatibility complex, which is the molecule that aids in antigen presentation on T-cells

59
Q

Name what you know about Class 1-MHC

A

alpha-chain noncovalently linked to B2-microglobulin, which is necessary for expression of MHC1. The a-chain has an indentation ‘cleft’, that the peptide fits inside

60
Q

Name what you know about Class-2 MHC

A

It has an alpha and beta chain and a cleft. The cleft is open, allowing longer peptides to fit in

61
Q

What fits MHC?

A

Small peptide sections

62
Q

How does a peptide get into a class-2-MHC?

A

An extracellular antigen is endocytosed
In the early endosome, the cell produces MHC2 molecules. The groove is closed by CLIP. The MHC2 goes from the golgi with a vesicle. The MHC2 and antigen vesicles fuse. CLIP gets off, and the protein gets in the groove. There is protein degradation, and the protein is put inside the MHC. The MHC-peptide complex is then exocytosed and expressed on the membrane

63
Q

How does a peptide get into class-1-MHC?

A

A viruses gets endocytosed into the cell. In the nucleus there is viral mrna and then translation of that into viral protein. The proteasome degrades the viral protein into peptide bits. The peptide parts are taken up into the ER via TAP. There is assembly of the MHC+peptide, which is transferred to the golgi, and then vesicle from the golgi. The vesicle is exocytosed and the MHC-1 is presented on the cell surface

64
Q

What will fit in class-1-MHC?

A

Most peptide bits, but the ones with a higher binding strength will fit better and stronger. Those peptides will often be presented on MHC, while the others won’t. Only those segments are necessary to be presented on MHC for antigen-detection

65
Q

Antigens are recognized by which two things?

A

Antibodies (transmembrane or secreted)
T-cell receptors (transmembrane)

66
Q

Why is it advantageous to have a different MHC in a partner?

A

There is broader immunoprotection, and there is maintaince of maximum diversity
Gives survival advantage, because if a certain antigen doesn’t fit well, it causes death in the population

67
Q

What is antigenicity and immunogenicity?

A

Antigenicity is the ability to be recognized by an antibody, while immunogenicity is the ability to elicit an immune response/antibodies

68
Q

What are four characteristics of an immunogen?

A

It is foreign
Requires a certain molecular size, often bigger is better
There is chemical heterogeneity
it is susceptible for antigen-presentation

69
Q

What are immunodominant epitopes?

A

The epitopes that antibodies mainly bind to, e.g. the head of influenze hemagglutinin

70
Q

What types of epitopes would a vaccine target?

A

It would target epitopes of a antigen that is not favourable to mutate, so it is a more constant region, like the stalk in hemagglutinin

71
Q

What are the thermodynamics of antibody-antigen binding?

A

Ab+Ag <-> Ab-Ag complex
the binding constant is Ka = [Ab-Agcomplex] / [Ab]*[Ag]

72
Q

What happens if the association constant is high?

A

That means the antibody has a high-affinity. So the Ab-agcomplex is more likely to be formed than the seperate ab and antigen remain

73
Q

What happens if the dissociation constant is high?

A

Then, the antibody has low affinity. The seperate ab and ag are more likely than the complex

74
Q

What is multivalency?

A

Multivalency is when a antigen has severel epitopes that can be bound simultaneously, which increases affinity

75
Q

How do the groove configuration of mhc class1 and class2 differ?

A

class 1 has a closed groove. while class2 has an open-ended groove. the advatange of an open-ended groove is that the peptides binding can be bigger

76
Q

What is the impact of the anchoring pockets in MHC?

A

The peptides have to fit in the anchoring pockets to be presented, so goodness of fit determines the strength of binding to the MHC.

77
Q

What type of antibody-antigen interactions are there and how do they change?

A

Antibody excess, equivalence, antigen excess. These interactions are dynamic, as overtime the antibody is unbound and then the antigen is bound and then there is antibody excess

78
Q

which cells are antigen-presenting cells?

A

Dendritic cells, macrophages and B-cells, also fibroblasts, glia, beta cellsin pnacreas, vascular endothelial cells

79
Q

Where are class-1-MHC and class-2-MHC on?

A

Class-1-MHC are on all cells in the body and present peptides to CD8+ cytotoxic t-cells
Class-2-MHC are associated with B-cells, dendritic cells, macrophages presenting to CD4+ helper T cells

80
Q

How do haptens elicit an immune response?

A

When they are bound to a protein-carrier, antibodies are elicited

81
Q

How can superantigens activate lymphocytes?

A

They stimulate the same variable region evenwithout antigen specifity, cross-linking MHC-class-2 and TCR Vb

Infection & Immunity (6 decks)

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