Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PRIS > Adaptive Immune Response > Flashcards

Adaptive Immune Response Flashcards

1
Q

What is the adaptive immune system important in?

A
  • important in memory immune responses or later in novel infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How long can it take the adaptive immune system to respond to a new pathogen?

A
  • > 96
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What do B lymphocytes do?

A
  • Secrete antibodies (immunoglobulins)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the two major T lymphocytes

A
  • CD4+ T lymphocytes = Helper T lymphocytes
  • CD8+ T lymphocytes = Cytotoxic T lymphocytes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What do B cell receptors interact with?

A
  • interact directly with antigen
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

How many BCR receptors does a B cell have on its surface?

A
  • Each B cell has 200-500,000 identical BCRs on its surface
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Where can B cell receptors be shed?

A
  • can shed into the blood and tissue fluid as antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are antibodies?

A
  • Antibodies are simply soluble BCRs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What do antibody monomers consist of?

A
  • 2 heavy and 2 light polypeptide chains
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How much do heavy chains weight on an antibody?

A
  • 50 kDa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How much do light chains weight on an antibody?

A
  • 25 kDa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What type of bonds link heavy and light chains together in an antibodies structure?

A
  • Disulphide bonds which are formed between two cysteine acids
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe antibody formation?

A
  • initially each pre-B cell has the same light chain and heavy chain genes (bases are the options they can choose at random)
  • theses genes have multiple options
  • this creates cast diversity - 100 billion
  • leads to different shapes of binding site at top of antibodies
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What crates the diversity within antibody formation?

A
  • it is the gene rearrangement of these V, D and J segments in pre-B cells that creates the diversity
  • this means each B cell has a different receptor for the heavy chain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe how DNA is involved in antibody formation:

A
  1. DNA is cut by recombinase = RAG1 and RAG2 (these cause issue in animals producing B and T cells)
  2. removes non-selected segments
  3. when re-joining, a few additional nucleotides added randomly to heavy chain gene
    - base deletion is also possible
    - introduces more diversity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What do T cell receptors interact with?

A
  • Antigenic peptides in major histocompatibility complex (MHC) molecules
  • they will always recognise antigen if its showing MHC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How do T -cells work (e.g., can they shed like B cell receptors)?

A
  • TCRs cannot shed
  • function by recognising antigens close to it
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

There are two types of MHC molecule - MHC1 and MHC2
What does MHC1 do?

A
  • presents mostly intracellular antigens (present in every nucleated cell)
  • helps detect and kill infected cell (e.g., viral or intracellular infection)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does MHC2 do and where are they found?

A
  • found on antigen presenting cells
  • presents mostly extracellular antigens
  • helps respond to extracellular and intracellular infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What do MHC class 1 molecules recognised by?

A
  • Recognised by CD8+ T cells (only interact with MHC class 1)
  • TCR and CD8 are the molecules that interact
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

MHC is presented in nearly all cells - What is the function?

A
  • Function is T cell mediated killing
  • Killing intracellularly infected cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What helps to stabilise the interaction between a Cytotoxic T cells and MHC class 1 and peptide ?

A
  • CD8
22
Q

What molecule only every interacts with MHC class 2?

A
  • CD4+ T cells only interact with MHC class 2
  • TCR and CD4 are the molecules that interact
23
Q

What is MHC class 2 present on?

A
  • dendritic cells
  • macrophages
  • B cells
24
Q

What is MHC class 2 molecules function?

A
  • Function is T-cell mediated help cytokine release activating B cells
25
Q

What helps stabilise the interaction of the helper T cell with MHC class 2?

A
  • CD4
26
Q

What does a T cell receptor resemble?

A
  • resembles a membrane bound antibody FAB fragment
27
Q

What are TCRs composed of?

A
  • composed of 2 transmembrane glycoprotein chains (alpha and beta)
28
Q

How do T cell receptors form?

A
  • in a similar way to the B cell receptor
  • gene rearrangement
29
Q

What are the 4 main ways that antibodies effect pathogens?

A
  1. neutralisation
  2. opsonisation
  3. antibody-dependent cell-mediated cytotoxicity
  4. activation of complement
30
Q

What is neutralisation of pathogen entry?

A
  • High affinity (bind strongly) neutralising antibodies can block viruses and bacteria from bringing the receptor by which they enter the host cell
  • e.g. antibody can block binding of a virus by blocking fusion event
  • can also stop toxins binding to the cell receptors by which they have their effect
31
Q

What is opsonisation?

A
  • coating pathogen surfaces and facilitating recognition and phagocytosis
  • In addition to innate molecules like complement antibodies can also enhance phagocytosis vis Fc receptors (Bind to bottom of Y antibody) on phagocytes cell surface making it up to 100 times more effective
32
Q

Give an example of how opsonisation works:

A
  • macrophages and neutrophils posses surface Fc receptors to bind Ab to activate phagocytosis
33
Q

What is Antibody-dependent cell-mediated cytotoxicity (ADCC)?

A
  • antibodies bind non-self antigens on host cell
  • Fc receptors on immune cells bind to these antibodies
  • cells such as neutrophils, macrophages eosinophils and NK cells
34
Q

In ADCC why are cross-linking of Fc factors important?

A
  • they are key to apoptosis/ release of perforins etc.
35
Q

Activation of complement can be through innate mechanisms - how does it do this and what is another way it can be activated?

A
  • lectin pathways = innate
  • classical pathways = antibodies
36
Q

What does activation of complement lead to?

A
  • leads to same outcomes
  • optimisation, inflammation, MAC formation
37
Q

In the classical pathway of activation of complement what happens?

A
  • C1q interacts with pathogen surface or with antibodies bound to surface
38
Q

What are Cytotoxic T lymphocytes (CTL)?

A
  • major effector cell of adaptive immune system
39
Q

What do cytotoxic T lymphocytes require before they can do their job?

A
  • requires activation first in lymphoid tissues via MHC class 1/TCR interaction
40
Q

Where do CTL migrate to?

A
  • migrate to infection site
41
Q

What do CTL do?

A
  • recognise infected cells showing off infected pepotided via MHC class 1
42
Q

CTL cells can cause two methods of killing - what are these?

A
  1. perforin/granzyme killing
  2. FAS mediated Killing
    - both leas to apoptosis of the target cell
    - Apoptosis by these mechanisms far more rapid than death due to factor withdrawal or other apoptotic stimuli
43
Q

How do CTL cells know what cells to kill and what cells not to kill?

A
  • all the cells in a tissue are susceptible to the induction of apoptosis by the cytotoxins or armed CD8 T cells but only infected cell are killed
  • specific recognition by the T cell receptor identifies which target cell to kill, and the polarised release of cytotoxic granules ensures that neighbouring cells are spared
44
Q

What do T helper cells do?

A
  • main importance in activating other cells
45
Q

T helper cells release cytokines involved in what?

A
  • increasing antibody production
  • increasing phagocyte activity and NK cell activity
  • increase antigen presentation
  • can also release anti-inflammatory cytokines
46
Q

What is memory response critical to?

A
  • critical to most immunity
47
Q

Memory - during an infection activated T and B cells do what?

A
  • divide via mitosis - as you want more of these
48
Q

Memory - what happens after T and B cells have divided?

A
  • cytokine interleukin (IL_-2 released and IL-2 receptor expressed
  • IL-2 drives T-cell proliferation
49
Q

Memory - what happens at the resolution of the immune response?

A
  • vast majority of these specific T and B cells die
  • some cells can remain as memory T cells, memory B cells and plasma cells (secrete Abs continuously)
  • these can survive in an individual for a lifetime
50
Q

Memory - what are plasma cells?

A
  • differentiated B cell
  • constant release of antibodies
51
Q

What are the locations of plasma cells?

A
  • medullary cords of lymph nodes (lymph)
  • bone marrow (blood)
  • MALT (mucosa)
52
Q

Where can memory B and T cells be found?

A
  • some tissue resident, some in circulation
53
Q

Memory B and T cells allow immune response in a 2nd exposure to be what?

A
  • Faster (easier to activate memory cells)
  • Larger (more antibodies)
  • More efficient ( high affinity BCR and TCR)
  • More effective (different antibody sub-classes)

PRIS (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions