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1 REVISION Bismillah > 1. Immunology - Ian Todd > Flashcards

1. Immunology - Ian Todd Flashcards

1
Q
  1. Lymphocytes are made from stem cells found where?
  2. Where are the 2 places where lymphocytes can mature? And what are the 2 categories of lymphocytes known as?
  3. Where do the mature lymphocytes go?
  4. The mature lymphocytes can also go to secondary lymphoid tissues. Name 5 of these…
A
  1. Bone marrow
  2. Bone marrow = B lymphocytes
    Thymus = T lymphocytes
  3. Into the circulation
  4. Tonsils and adenoids, lymph nodes, spleen, peyers patches and bronchus associated lymphoid tissue
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2
Q

Name 5 infectious agents…

A

Viruses, bacteria, fungi, Protozoa and worms

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3
Q
  1. What are the 2 types of T lymphocytes?
  2. When monocytes move out into the blood, what is their new name?
  3. Name the 4 PMN/ granulocyte cells…
  4. Name the 5 mononuclear cells…
A
  1. CD8+ Tc lymphocytes
    CD4+ Th lymphocytes
  2. Macrophages
  3. Neutrophils, eosinophils, basophils and mast cells
  4. Monocytes (macrophages), dendritic cells, NK cells, T lymphocytes and B lymphocytes
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4
Q

What are the 2 types of secreted mediators of immunity?

A

Anti microbial and regulatory/inflammatory

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5
Q
  1. Which 7 leukocytes are involved in the innate response?
  2. Which 2 leukocytes are involved in the adaptive response?
  3. Immunological memory is associated with which response?
A
  1. Neutrophils, eosinophils, basophils, mast cells, monocytes (macrophages), dendritic cells and NK cells
  2. T lymphocytes and B lymphocytes
  3. Adaptive immunity
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6
Q

Innate immunity

  1. Activation speed?
  2. Same/different on repeated exposure to the same microbe? If different then how?
  3. Efficiency high/moderate/low?
  4. Recognition of what on the pathogen?
  5. Recognition by what on the leukocytes?
A
  1. Fast
  2. Same
  3. Moderate
  4. PAMP- pathogen associated molecular patterns
  5. PRR- pathogen recognition receptors
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7
Q

Adaptive (acquired) immunity

  1. Activation speed?
  2. Same/different on repeated exposure to the same microbe? If different then how?
  3. Efficiency high/moderate/low?
  4. Response is general/broad or specific/tailored?
  5. Recognition of what on the microbe?
  6. Recognition by what on the lymphocytes?
A
  1. More slowly
  2. Different - it improves
  3. High
  4. Specific tailored
  5. Antigens
  6. Antigen-specific receptors
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8
Q

Stages of a primary immune response

  1. What are the 4 stages called?
  2. What 2 cells does stage 2 involve?
  3. In stage 3, what is released? What 2 cells does this attract?
  4. In stage 4 what is the antigen carried by? Where is it carried to? What 2 cells does this activate? What else is produced? What happens next?
A
  1. Epithelial barrier, immediate local response (innate), early induced response (innate/inflammatory) and later adaptive response
  2. Complement proteins and macrophages
  3. Inflammatory mediators
    Leucocytes and serum proteins (more complement)
  4. Dendritic cells
    Lymphoid tissue
    T and B lymphocytes
    Antibody production
    Recirculation to site of infection
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9
Q

Following a primary infection, what can happen on second exposure to the same infection?

A

Memory T and B cells give a faster and bigger response

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10
Q
  1. What are the 3 different broad categories of infections?

2. Name the cells involved in each category…

A
  1. Extra cellular infection, intra cellular vesicular infection and intra cellular cytosolic infection
  2. Extra cellular: complement proteins, phagocytes and antibodies
    Intra cellular vesicular: Helper T cells
    Intra cellular cytosolic: interferon proteins, NK cells and Cytotoxic T cells
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11
Q

What are the 5 types of immunopathology?

A

Immunodeficiency, allergy, autoimmunity, transplant rejection and lymphoprofilerative diseases

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12
Q

Give an example of 2 pattern recognition molecules that express receptors that can recognise PAMP’s…

A

Macrophages and Toll-like receptors

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13
Q

When B cells interact with antigens and are activated, they produce a secreted soluble form of their antigen recognition receptors.

  1. What are these also known as? What is their other name?
  2. Where are they released?
A
  1. Antibodies/immunoglobulin

2. Surrounding environment

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14
Q

What are antibodies?

A

Secreted soluble form of antigen recognition receptors on B cells

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15
Q

Antigen:antibody interaction

  1. What can an antigen be? Give an example.
  2. What shape is a normal antibody?
  3. Is each antibody specific for/general to each antigen?
  4. What is at the end of each arm on an antibody? Are they different/identical in terms of which antigen they can bind to?
  5. What is the precise region on the antigen called where the antigen binds to the arm? What is this also known as?
A
  1. Any constituent of the microbe e.g. Surface protein
  2. Y-shaped
  3. Specific for
  4. Antigen combining sites
    Identical
  5. Antigenic determinant
    Epitope
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16
Q
  1. What are the 3 types of interactions between epitope on the antigen and combining site on the antibody?
  2. What type of interactions are these? Do these only work on very short/long distances?
  3. What kind of affinity do each 3 have?
A
  1. Specific interaction, cross reaction and no specificity
  2. Non-covalent
    Very short distances
  3. Specific interaction - high affinity
    Cross reaction - moderate affinity
    No specificity - negligible affinity
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17
Q
  1. Are the surface receptors on B lymphocytes inside the cell or membrane bound?
  2. What is another name for these? (as only the secreted forms are known as antibodies)
  3. The surface immunoglobulins on a particular B cell will have different/identical antigen combining sites?
  4. After the antigen combines with the surface B cell, what happens to the B cell?
  5. The B cell will then differentiate into what type of cell? At this point will it express surface immunoglobulins?
  6. What will the B cell (now activated and differentiated) spend its energy on now?
A
  1. Membrane bound
  2. Surface immunoglobulins
  3. Identical
  4. It becomes activated
  5. Plasma cell
    Will not express surface immunoglobulins
  6. Expressing a secreted form of the surface immunoglobulins which are now called antibodies
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18
Q
  1. What is the first thing that happens when a B cell binds to an antigen?
  2. What advantage does this have?
  3. What happens to the B cells that are activated but don’t differentiate into plasma cells? When would these cells become reactivated?
A
  1. B cell proliferates and makes copies of itself
  2. Expands the pool/clone of lymphocytes specific for that antigen
  3. They become memory cells with epitope a specific for that antigen
    Reactivated on repeat exposure to same antigen
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19
Q
  1. A secondary response to an antigen is efficient in which 2 ways?
  2. Is this a key feature of innate or adaptive immunity?
A
  1. Bigger response
    Faster response
  2. Adaptive immunity
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20
Q
  1. What form of a toxin is used in a vaccination?
  2. What cells does a vaccination aim to produce?
  3. The response is which 2 things?
A
  1. Toxoid
  2. Memory B cells
  3. Bigger and faster
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21
Q

Immunoglobulins structure (antibody structure)

  1. What shape is it?
  2. What is at the end of each arm?
  3. How many polypeptide chains is it made out of? What two groups can they be divided into?
  4. Are the chains within each group identical/different to one another in the group?
  5. Each chain is made of building blocks called what?
A
  1. Y-shaped
  2. Antigen combining site
  3. 4 chains
    2 light chains and 2 heavy chains
  4. Identical
  5. Immunoglobulins domains
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22
Q

Immunoglobulin structure

  1. What is the terminal domain on the heavy chain called?
  2. What is the terminal domain on the light chain called?
  3. What does the first letter stand for?
  4. How is this word related to its structure?
  5. Molecularly, what is different in this region?
  6. Where is there the most difference in this region?
A
  1. VH domain (v heavy domain)
  2. VL domain (v light domain)
  3. Variable
  4. The Vh and Vl domains make up the antigen combining site. They are variable so different antibodies can recognise different epitope.
  5. Amino acid sequence
  6. Hyper variable region
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23
Q

Immunoglobulin structure

  1. About from the variable domains, what other domains are there?
  2. What are these regions not involved in?
  3. What kind of bonds are there between the heavy and the light chains?
  4. What is the flexible part of the heavy chain called? What does this allow?
A
  1. C domains = constant domain
  2. Antigen recognition
  3. Disulphide covalent bonds
  4. Hinge region
    This allows the arms to move
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24
Q

Immunoglobulin structure

  1. What is the part above the hinge region also known as? What does this stand for?
  2. How many of these are there?
  3. What is the part below the hinge region (the stem) also known as? What does this stand for?
A 
1. Fab region
Fragment antigen binding 
2. 2 Fab regions 
3. Fc region 
Fragment crystallisable
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25
Q
  1. How many classes/isotopes of immunoglobulins are there?
  2. Name the classes…
  3. What distinguishes one class from another?
  4. Name the Greek equivalents of the chains mentioned on your answer to question 3.
  5. What type of surface immunoglobulin are all B cells initially programmed to make?
A
  1. 9
  2. IgM, IgG (1,2,3,4), IgA (1,2), IgE and IgD
  3. The precise structure of the constant domains in the heavy chain
  4. Miu, gamma, alpha, epsilon and delta
  5. IgM
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26
Q
  1. When a B cell binds to an antigen, is activated and proliferates, what do some of the IgM antibodies undergo?
  2. Does this happen before or after secretion?
  3. What difference does this change make?
  4. What remains the same?
A
  1. Class switching
  2. Before secretion
  3. The antibody will use a different gene to encode the heavy chains in the constant domains
  4. The antigenic specificity
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27
Q
  1. What is the hinge region like on IgG 1,2 and 4?
  2. What is the neck like on IgG3?
  3. What additional thing does IgE have?
  4. IgA can form what shape? How many antigen combining sites does it therefore have? What holds it together?
  5. What shape is IgM secreted as? How many antigen combining sites does it therefore have? What holds it together?
A
  1. Short
  2. Long and rigid
  3. Constant domain
  4. Dimer
    4 antigen combining sites
    Polypeptide called the J chain (joining chain)
  5. Pentamer
    10 antigen combining sites
    J chain
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28
Q

Name the tissue distribution of the following antibody isotypes:

  1. IgM? (x1)
  2. IgG? (x3)
  3. IgA? (x3)
  4. IgE? (x1) bound to which type of cell?
  5. IgD? (x1)
A
  1. Blood
  2. Blood, tissues and placental transfer
  3. Blood/tissues, mucosal secretions and milk
  4. Tissues (bound to mast cells)
  5. Mucosa of upper aerodigestive tract
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29
Q

Which antibody isotypes interact with the following defence components:

  1. Complement activation (x2)
  2. Phagocyte binding (x2)
  3. Mast cell binding (x1)
  4. NK cell binding (x1)
A
  1. IgM and IgG
  2. IgG and IgA
  3. IgE
  4. IgG
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30
Q
  1. Does Fab or Fc region bind to the microbe?

2. Does the Fab or Fc region stick out? What does this allow it to do?

A
  1. Fab region
  2. Fc region
    It can interact with other immune defence components
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31
Q
  1. What can phagocytes do to microbes in order to get rid of them?
  2. What 2 cell types are phagocytes?
A
  1. Engulf microbes by taking them into their cytoplasms and then digesting them.
  2. Macrophages and neutrophils
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32
Q
  1. What is complement a collection of?
  2. Which 2 places is it found?
  3. What does it complement the effects of?
  4. Various complement proteins can act as what 3 things?
  5. What 2 things activate complement proteins?
  6. Complement proteins in what kind of a pattern (with amplification)?
  7. What is the central event of complement activation?
A
  1. Proteins
  2. Circulation and tissue fluids
  3. Antibodies
  4. Activation enzymes, immune defence molecules and control proteins
  5. Infection and immune activation
  6. Cascade
  7. Conversion of C3 into C3a and C3b
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33
Q
  1. How many C3 convertases are there?
  2. How many pathways can create C3 convertase? What are the names of the pathways?
  3. Describe the first step of each pathway…
A
  1. 2
  2. 3 pathways
    MB-lectin pathway, classical pathway and alternative pathway
  3. MB-lectin pathway: MBL binds to microbial mannose

Classical pathway: (antigen+IgM or IgG) interact with complement proteins [C1q]

Alternative pathway: C3b binds to microbial surface plus Bb plus P

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34
Q

Complement
Classical pathway
1. Which complement protein interacts with an antibody bound to an antigen?
2. Which 2 antibodies can this be?
3. Which 2 complement proteins does this then activate?
4. What 2 complements does this split?
5. Fragments of this combine to form what? What is this also known as?

A
  1. C1q
  2. IgM or IgG
  3. C1rs or C1s
  4. C2 and C4
  5. C4b2a
    C3 convertase
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35
Q

Complement
MB-lectin pathway
1. What does MBL stand for?
2. What does it bind to?
3. What does this trigger the activation of?
4. What does this then breakdown to? This will reassemble to form what?
5. What is this known as?

A
  1. Mannon binding lectin
  2. Microbial mannose
  3. MASP-1 and MASP-2
  4. C4 and C2
    C4b2a
  5. C3 convertase
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36
Q

Complement
Alternative pathway
1. C3b will have what kind of bond with any surface it comes in contact with?
2. What does C3b bind to in this pathway?
3. What does that do to the C3b?
4. What other fragment of what complement protein does it then bind to?
5. What is the third complement protein that binds to the two?
6. What is this complex also known as?

A
  1. Covalent
  2. Microbial surface
  3. Stabilises it
  4. Factor B fragment b
  5. Properdin
  6. C3 convertase
37
Q

Complement
C3 convertase
1. C3 convertase converts C3 into what two fragments?
2. What does each fragment do?
3. What is tick over pathway?
4. C3 convertase can join with what to split C5 (by forming c5 convertase)?
5. What are the 2 fragments that C5 is split into and what does each fragment do?

A
  1. C3a and C3b
  2. C3a: mast cell activation and neutrophil recruitment
    C3b: opsonisation
  3. Tiny amounts of C3b are constantly being made
  4. C3b
  5. C5a: mast cell activation and neutrophil recruitment
    C5b: membrane attack pathway (membrane lysis)
38
Q

Complement
Membrane attack pathway
1. Which complement fragment activates this pathway?
2. Which compliment (in a poly form) forms a highly organised structure causing a hole in the microbes lipid membrane?
3. What 3 complements first join onto the original complement fragment?

A
  1. C5b
  2. C9
  3. C6, C7 and C8
39
Q

Phagocytes

  1. Macrophages are already present where?
  2. Where are macrophages recruited from?
  3. Where are neutrophils recruited from?
  4. What 3 receptors do these phagocytes possess?
  5. PRR on macrophage binds to PAMP of microbe: what does this trigger the activation of? What does this trigger the secretion of?
  6. This interaction also triggers which process?
A
  1. Tissues
  2. Blood monocytes
  3. Blood
  4. Innate receptors for microbes, Fc receptors (FcR) and complement receptors (CR)
  5. Macrophage
    A range of inflammatory mediators
  6. Phagocytosis
40
Q

Phagocytosis

  1. The vesicle with the microbe inside once it has been engulfed is also known as a what?
  2. What fuses with the membrane of the phagosome? What is this joint vesicle called?
  3. What does that release onto the surface of the microbe?
  4. What does this do to the microbe?
  5. By which process is the rubbish chucked out?
A
  1. Phagosome
  2. Lysosome
    Phagolysosome
  3. Enzymes
  4. Digests it
  5. Exocytosis
41
Q

Phagocytosis

  1. What can it be enhanced by?
  2. In particular, the ones made by which organ during times of inflammation?
  3. Give 2 examples of them? What are they referred to as?
  4. What are they referred to as when they bind to the surface of the microbe, facilitating phagocytosis?
  5. What do they also activate?
A
  1. Pattern recognition molecules
  2. Liver
  3. Mannan binding lectin and C-reactive protein
    Acute phase proteins
  4. Opsonins
  5. Complement
42
Q
  1. What is opsonisation?

2. What is an opsonin?

A
  1. Coating of microbes by molecules of the immune system
  2. Any molecule that can stick to the surface of a microbe, which then helps to facilitate the destruction of that microbe
43
Q

Some microbes are too large to be engulfed by phagocytes.

  1. This means that they cannot be digested intracellularly or extracellulary?
  2. What is therefore the main attacking cell that can do the digestion required?
  3. What kind of receptors do they have?
  4. Where are the digestive proteins released?
  5. What 2 antibody classes can these cells bind to when activated due to the type of Fc receptors they have?
  6. Once the digestive enzymes have chewed the outside/inside (?), they can then digest the outside/inside (?)
A
  1. Intracellularly
  2. Eosinophil
  3. Fc receptors and complement receptors (CR)
  4. Onto the surface of the microbe
    5.IgG and IgE
  5. Outside
    Inside
44
Q
  1. What do Fc receptors bind to on the surface of the microbe?
  2. What do Complement receptors bind to on the surface of the microbe?
A
  1. Antibodies

2. C3b

45
Q
  1. IgE antibodies bind to surface of which type of immune cell?
  2. Where are these cells found?
  3. What kind of Fc receptors do these cells express a lot of?
  4. This cell plus the IgE antibody allows the cell to identify what?
  5. How many antibodies much each of these bind to?
  6. Following this, What does the cell trigger once it is activated? What is released? Give a key example…
  7. Give 3 examples of what is newly generated…
A
  1. Mast cell
  2. In tissues
  3. Fc epsilon
  4. Antigens specific for that IgE
  5. 2 or more
  6. De granulation of the mast cell
    Preformed inflammatory mediators
    Histamine
  7. Arachidonic acid, leukotrienes, prostaglandin
46
Q

What are 2 ways a mast cell can become activated and trigger de granulation?

A
  1. Fc epsilon receptor on the mast cell + IgE + antigen cross link
  2. C3a and C5a complement
47
Q

What is the main purpose of inflammation?

A

To draw large numbers of immune components to a site of infection so we can get rid of the infection

48
Q
  1. What are the 6 inducers of inflammation that amplify events?
  2. What 3 things happen to the blood vessel wall in inflammation?
  3. Give the purpose and benefits of each…
  4. What is it called when white blood cells move to the site of infection?
  5. What are the 3 steps of leucocytes moving into the tissues?
  6. What 2 cells facilitate this?
A
  1. C3a, C5a, mast cell products, prostaglandins, cytokines and chemokines
  2. Vasodilatation, vascular permeability and leucocyte adhesion
  3. Vasodilation - more blood and blood moves slowly so more interaction
    Leucocyte adhesion - white blood cells can stick to the wall
    Vascular permeability - leaky junctions so white blood cells and plasma can move
  4. Chemotaxis of of leucocytes
  5. Capture and rolling, activation and flattening, and extravasation
  6. Selectins and integrins
49
Q

The acute phase response

  1. Which 3 cytokines circulate around the body in an acute phase response?
  2. What effect do they have on your temperature?
  3. What affect do they have on your bone marrow?
  4. What affect do they have on your liver?
A
  1. Interleukin 1 (IL-1), interleukin 6 (IL-6) and tumour necrosis factor (TNF)
  2. Raised temperature (fever)
  3. Increased leucocyte release (especially neutrophils)
  4. Acute phase protein release
50
Q

T cell antigen receptor

  1. Where is it expressed?
  2. Is there a secreted form of the antigen receptor (like with B cells)?
  3. How many polypeptide chains is it made of? What are the chains called?
  4. What 2 domains do both chains have?
  5. What makes up the combining site?
  6. What does this allow for?
A
  1. On the surface of a T cell
  2. No
  3. 2 polypeptide chains
    Alpha and beta chain
  4. Variable domain and constant domain
  5. Variable alpha and variable beta domains
  6. Antigenic specificity
51
Q

What are the 2 main types of T cells?

A

Th cells - T helper cells

Tc cells - T cytotoxic cells

52
Q
  1. What is the main function of T helper cells?
  2. What are the 2 main cells that Th cells will help to activate?
  3. What is the result of these 2 cells being activated?
  4. What is the main function of T cytotoxic cells?
A
  1. Helping to activate other cells of the immune system
  2. B cells and macrophages
  3. B cells - produce antibodies
    Macrophages - phagocytose and kill
  4. Killing infected cells
53
Q

T cell recognition of antigen

  1. What molecule must the antigen be?
  2. T cells cannot directly bind to a microbial protein. Where is the microbial protein therefore taken?
  3. What happens to it there?
  4. What is therefore generated that can be recognised by T cells? How can the T cell detect it?
  5. What can the cell be called due to its function in this process?
A
  1. Protein
  2. Inside another cell
  3. Antigen processing (it’s broken down)
  4. Peptides
    Put back on the surface membrane
  5. Antigen presenting cell (APC)
54
Q

T cell recognition of an antigen

  1. When a Th cell is bound to an antigen, what will happen?
  2. When a Tc cell is bound to an antigen, what will happen?
A
  1. It will produce activating signals that activate the antigen presenting cell
  2. It will produce chemicals which kill the antigen presenting cell
55
Q
  1. What is another name for HLA proteins? What is the general name for these in all species (not just humans)?
  2. How many major types of HLA proteins are there and what are their names?
  3. Can an APC express only one HLA protein or can it express all of them?
A 
1. Peptide binding proteins 
MHC - major histocompatibility complex
2. 2 major types
HLA class 1 and HLA class 2 proteins 
3. It can express both HLA proteins (class 1 and class 2)
56
Q

HLA class 1 protein structure

  1. How many polypeptide chains is it made of?
  2. Which chain is anchored in the plasma membrane of the APC? How many domains is this chain made of? Which domain is anchored in the APC?
  3. What is non-covalently bonded to this chain?
  4. Which 2 domains are immunoglobulin-like domains?
  5. Which 2 domains make up the peptide binding cleft? What is held here?
  6. HLA class 1 presents peptides that are recognised by which type of T cell?
A
  1. 2 polypeptide chains
  2. Alpha chain
    3 domains
    Alpha 3
  3. Beta 2 Microglobulin (B2M)
  4. Alpha 3 and Beta 2M
  5. Alpha 1 and alpha 2
    Antigen peptide
  6. Tc cells
57
Q

HLA class 2 protein structure

  1. How many polypeptide chains is it made of? What are the chains called?
  2. Which chains are anchored into the plasma membrane of the APC?
  3. Which 2 domains are immunoglobulin-like?
  4. Which 2 domains make up the peptide binding cleft?
  5. HLA class 2 presents peptides that are recognised by which type of T cell?
A 
1. 2 polypeptide chains 
Alpha and beta chains 
2. Both chains - alpha and beta 
3. Alpha 2 and beta 2
4. Alpha 1 and beta 1
5. Th cells
58
Q

HLA class 1 and Tc cells

  1. What other protein is expressed?
  2. How many polypeptides is it made up of?
  3. What utensils does it look like?
  4. The globular domain is also known as what? What does that interact with on HLA class 1?
  5. Will it bind to HLA class 2?
A
  1. CD8+
  2. 2 polypeptides
  3. 2 wooden spoons
  4. Immunoglobulin-like domain
    Interacts with alpha 3 domain
  5. No
59
Q

HLA class 2 and Th cells

  1. What other protein is expressed?
  2. How many polypeptide chains is it made of?
  3. How many immunoglobulin-like domains does it have?
  4. Which domain of the protein binds with which domain of HLA class 2?
A
  1. CD4+
  2. 1 polypeptide
  3. 4 immunoglobulin like domains
  4. Terminal domain of the chain binds with beta 2 on HLA class 2
60
Q

Antigen processing for HLA class 1

  1. What is the starting antigen?
  2. What takes up the antigen in the cytosol? What does it do to the antigen? What does this produce?
  3. What part of the cell is synthesising new HLA class 1 proteins?
  4. How is what the antigen becomes transported to the HLA protein?
  5. Where does the complex go once formed?
A
  1. Endogenous antigen
  2. Proteasome
    Chews up the antigen
    Producing peptides
  3. Endoplasmic reticulum
  4. Through peptide transporters
  5. To the surface of the cell
61
Q

Antigen processing for HLA class 2

  1. What is the starting antigen?
  2. How is taken into the cell?
  3. The antigen is now inside the cell in a what? What is the name for this?
  4. What is pumped into here? What do they do?
  5. What part of the cell is synthesising HLA class 2 protein? What additional polypeptide chain does it have?
  6. What does the chain block?
  7. Where does the HLA class 2 protein go? What happens to the extra chain here? What does this mean? Where does the new complex go?
A
  1. Exogenous antigen
  2. Endocytosis
  3. Membrane bound vesicle
    Endosome
  4. Proteolytic enzymes
    They chew up the antigen into peptides
  5. Endoplasmic reticulum
    The invariant chain
  6. Peptide binding cleft
  7. Into the endosome
    The proteolytic enzymes degrade the chain
    The HLA class 2 can bind to the antigen peptide
    The complex goes to the surface of the cell
62
Q

What is the main cell type that activates T cells?

A

Dendritic cells

63
Q

Cytokines

  1. What are they?
  2. What do they regulated?
  3. What are they produced by?
  4. What do they bind to?
  5. What does this trigger?
  6. Give an example of 3 cytokines…
A
  1. Secreted proteins
  2. Cellular activity
  3. Many cell types including T cells
  4. Cell surface receptors
  5. Intracellular signalling pathways
  6. Interleukins, tumour necrosis factors and interferons
64
Q
  1. Th cells express which CD? And which HLA class do they interact with?
  2. What are the 2 main cytokines that Th1 cells produce? What does this lead to?
  3. What are the 2 main cytokines that Th2 cells produce? What does this lead to?
  4. Both Th1 and Th2 cells can lead to the production of antibodies by class switching in B cells. What antibodies do Th1 and Th2 make?
  5. Are Th1 and Th2 cytokines mutually amplified/inhibitory?
  6. Where are T helper cells originally generated? What are they known as here?
  7. The polarisation of original T cells depends on what? What polarises them into Th1 cells? What polarises them into Th2 cells?
A 
1. CD4
HLA class 2
2. IL-2 and IFN gamma
Cell-mediated immunity
3. IL-4 and IL-10
Antibody production 
4. Th1: IgG 1-3
Th2: IgG 1-4, IgE and IgA
5. Inhibitory 
6. Thymus
Th 0 cells 
7. The cytokines they are exposed to 
Th1: IL-12
Th2: IL-4
65
Q

What type of cell makes a lot of the cytokine IL-12?

A

Dendritic cells

66
Q
  1. Where do the lymphocytes and the antigen come together?
  2. How do they get there from the site of infection?
  3. What kind of a cell can transport the antigen? Give one important example of a particular cell…
A
  1. In the lymph node
  2. Afferent lymphatics
  3. Antigen presenting cell
    Dendritic cell
67
Q

Lymph node

  1. What part of the lymph node activates specific T and B cells?
  2. What cells activate the antigen-specific T cells?
  3. What cells activate the antigen-specific B cells?
  4. What part of the lymph node is where B cells mature?
  5. Where does the T cell-B cell interaction take place?
  6. Where do the activated B cells go after this? What’s the first thing they do? What is the area now called?
  7. What are the next 2 steps? Which 2 cells can this lead to the formation of?
A
  1. Paracortex
  2. Dendritic cells
  3. T cells
  4. Follicle
  5. Margin between paracortex and follicle
  6. Back into follicle tissue
    Proliferate a lot
    Germinal centre
  7. Antigenic selection and class switching
    Plasma cells or memory cells (not both)
68
Q

Th2 cells

  1. What activates them?
  2. Which cytokine do they make a lot of?
  3. What cell activation does this trigger? Class switching leads to which antibody in particular?
  4. Which cell will this antibody bind to in particular in the tissues?
  5. Th2 cells also make IL-5, which is good at activating which type of cell? Does this cell digest things intracellularly or extracellulary?
A
  1. Antigen presenting dendritic cells
  2. IL-4
  3. B cell activation
    IgE
  4. Mast cells
  5. Eosinophils
    Extracellularly
69
Q

Th2 cells can promote which type of allergy’s?

A

Atopic allergies

70
Q

Which type of T cell can activate macrophages?

A

Th cells

71
Q

Th1 cells can promote what type of inflammation?

A

Granulomatous inflammation

72
Q
  1. What is a free virus particle called?
  2. What are the next 5 steps called?
  3. The next step is release. What are the 2 ways it can be released? What is the difference between the 2?
  4. What happens next?
A
  1. Virion
  2. Attachment, penetration, uncoating, replication and assembly
  3. Cytolysis (no envelope)
    Budding (forming envelope)
  4. The cycle can start again
73
Q

Anti-viral effects of antibodies

  1. What is the effect of the antibody alone?
  2. What are the 2 effects of antibody + complement?
  3. What is the effect of the antibody bound to the infective cells?
A
  1. Blocks binding and entry to cells
  2. Damage to enveloped viruses and opsonisation for phagocytosis
  3. Antibody dependent cellular toxicity
74
Q

Influenza virus

  1. What are the 2 surface proteins called?
  2. What is antigenic drift in terms of changes in the structure? How does this happen?
  3. What is antigenic shift in terms of changes in the structure? How does this happen?
A
  1. Haemagglutinin and neuraminidase
  2. Slow gradual change by mutations during replication
  3. Sudden and large change (a new strain). 2 different strains are simultaneously infecting an individual, so they exchange antigenic material (recombination)
75
Q

Timeline of viral infection

  1. What 4 cytokines are produced first? What is this response known as?
  2. Which cell starts killing infected cells next?
  3. Which cell kills infected cells after a few days?
A
  1. IFN-alpha, IFN-beta, TNF-alpha and IL-12
    Innate response
  2. NK-cells
  3. T-cells
76
Q

Anti-viral action of Interferon alpha and beta

  1. What triggers the infected cell to produce and secrete these 2 interferons?
  2. What do the interferons bind to? What state does this trigger and in which cell?
  3. What does it mean for a cell to be in this state?
  4. It does this via the activation of enzymes which allow what 2 things to occur?
  5. These interferons also enhance the expression of which cell? What cell does it also activate?
A
  1. The presence of the virus in the cell
  2. Interferon receptors on neighbouring cells
    Anti-viral state in neighbouring cell
  3. The cell is resistant to virus replication within it
  4. Degradation of viral mRNA and inhibition of protein synthesis
  5. HLA class 1 proteins
    NK cells
77
Q

Tc cells

  1. Which CD do they express?
  2. Which HLA class are they associated with?
  3. Does it use endogenous or exogenous antigens?
  4. What is the HLA distribution of this HLA class?
A
  1. CD8
  2. HLA class 1
  3. Endogenous
  4. It’s in most cells
78
Q

Natural killer cells - recognition of infected cells
1. Describe the antibody related method of NK cells recognising infected cells…include which antibody in particular…
What does the antibody bind to?
2. Describe the other method of NK cells recognising infected cells…
What is the inhibitory receptor? What is the dominant signal in an abnormal cell?
3. Which HLA class expression is inhibited by many viruses?

A
  1. NK cells express Fc receptors which can bind to the Fc regions of antibodies.
    IgG antibodies
    Whole virus antigens on surface of infected cell
  2. The NK cell can detect abnormal cells when it interacts with it. This is via receptors on the surface of the cell. Normally there is a “kill” and “don’t kill” signal sent to the NK cells. HLA class 1 is the inhibitory receptor, so if the cell does not have it, and it is classed as “abnormal” by the NK cells because “kill” will be the dominant signal.
  3. HLA class 1
79
Q

Target cell killing by NK cells/Tc cells

  1. What is another name for programmed cell death?
  2. What 2 proteins are released from the granules in the killer cells? What do each of them do?
  3. What protein can the killers cells express for another way to kill the target cell? How does this work?
A
  1. Apoptosis
  2. Perforins - perforate the surface membrane of the target cell allowing granzymes and water leading to osmotic lysis
    Granzymes - go into cytoplasm activating the target cells caspases and endonucleases causing apoptosis
  3. Fas ligand - binds to Fas, activating caspases in the target cell, causing apoptosis
80
Q
  1. If a material is recognised as foreign, and the material damaged is foreign, what is the result?
  2. If a material is recognised as foreign, and the material damaged is self, what is the result?
  3. If a material is recognised as self, and the material damaged is self, what is the result?
A
  1. Immunity
  2. Allergy/hypersensitivity
  3. Autoimmunity
81
Q

What are the 2 types of self tolerance?

A

Central tolerance and peripheral tolerance

82
Q

Self tolerance: central tolerance

  1. Where is it generated?
  2. Where does it occur for B cells? Where does it occur for T cells?
  3. For immature lymphocytes , strong interaction with an antigen within this area induces what?
  4. This leads to what kind of deletion of the immature auto reactive lymphocytes that interact with auto antigens in this area?
  5. Central tolerance by itself is not totally effective because what kind of T and B cells are we not taking into consideration that are potentially auto reactive in everybody?
A
  1. Primary lymphoid organs
  2. B cells: bone marrow
    T cells: Thymus
  3. Apoptosis
  4. Clinal deletion
  5. Mature T and B cells
83
Q

Self tolerance: peripheral tolerance
There are a range of these. We will look at 3 only.
1. What is ignorance?
2. What leads to the inactivation of autoreactive T cells?
3. What can inhibit auto reactive T cells?

A
  1. Tissue antigens are not exposed to/in too little amounts so they can’t activate lymphocytes
  2. Auto reactive T cells are inactivated because there is a lack of co-stimulatory signals
  3. Auto reactive T cells are inhibited by regulatory T cells.
84
Q

Susceptibility to autoimmune diseases:

  1. Few factors/complex interplay of factors?
  2. What are 2 key intrinsic factors?
A
  1. Complex interplay of factors

2. Environmental and genetic

85
Q

HLA

  1. How many genes encode HLA class 1 proteins?
  2. How many genes encode HLA class 2 proteins?
  3. How many alleles are there for each of these genes?
A
  1. 3 genes (HLA A, B and C)
  2. 3 genes (HLA DP, DQ and DR)
  3. Hundreds
86
Q

Rheumatoid factor

  1. What does this autoantibody bind to?
  2. Is it sensitive?
  3. Is it specific?
A
  1. Other antibodies (it’s own - IgG)
  2. Yes
  3. No
87
Q

Rheumatoid arithiritis

  1. What does ACPA antibodies stand for?
  2. Is it sensitive?
  3. Is it specific?
A
  1. Anti-citrullinated Protein Antigen antibodies
  2. Yes
  3. Yes
88
Q
  1. How many types of hypersensitivity are there?
  2. What are they called?
  3. Which one is specific to allergies?
A
  1. 4
  2. Type 1, type 2, type 3 and type 4
  3. Type 1
89
Q
  1. In Graves’ disease, autoantibodies stimulate which receptors?
A
  1. TSH receptors

1 REVISION Bismillah (13 decks)

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