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a path 3 > IMMUNO: Immune response to infection > Flashcards

IMMUNO: Immune response to infection Flashcards

1
Q

What are the constitutive barriers to infection?

A
  1. Skin
  2. Mucosal surface barrier
  3. Commensal bacteria barrier
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2
Q

How does the skin act as a barrier to infection?

A
  • Tightly packed keratinised cells
  • Physiological factors
    • Low pH
    • Low O2 tension
  • Sebaceous glands
    • Hydrophobic oils repel water/microorganisms
    • Lysozyme destroys cell walls
    • Ammonia/defensins have anti-bacterial properties
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3
Q

How does the mucosal surface act as a barrier to infection?

A
  • Secreted mucous
    • Physical barrier
    • Secretory IgA (prevent entry/attachment into epithelia)
    • Lysozyme
    • Lactoferrin starves bacteria of iron
  • Cilia – trap and remove pathogens
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4
Q

How does the commensal bacterial act as a barrier to infection?

A
  • 100tn bacteria
    • Compete for resources (scarce)
    • Produce fatty acids & bactericidins to inhibit growth
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5
Q

List the cellular components of the innate immune system?

A
  • Cells
    • Polymorphonuclear cells (neutrophils, eosinophils, basophils)
    • Monocytes and macrophages
    • Natural killer cells
    • Dendritic cells
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6
Q

List 4 soluble components of the innate immune system.

A

Soluble components

  • Complement
  • Acute phase proteins
  • Cytokines and chemokines
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7
Q

Do innate cells differ between individuals?

A

No they are identical in all

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8
Q

List 3 types of polymorphonuclear cells.

A
  • neutrophils
  • eosinophils
  • basophils/mast cells
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9
Q

Polymorphonuclear cells:

  1. where are they produced?
  2. how do they migrate?
  3. how do they detect pathogens?
  4. how do they detect immune complexes?
  5. what can they release?
A
    • bone marrow
    • follow cytokines and chemokines
    • PRR (pattern recognition receptors)
    • Fc receptors
    • enzymes, histamine, lipid mediators, cytokines, chemokines
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10
Q

Name 3 types of mononuclear cells of the innate immune system.

A
  • Monocytes
  • Lymphocytes
  • Macrophages
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11
Q

What is the link between monocyte and macrophage?

A

Macrophages are monocytes which have differentiated in tissue

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12
Q

Name 5 properties of macrophages. How do they differ from neutrophils?

A
  1. Present within tissue
  2. Express receptors for cytokines and chemokines (to detect inflammation)
  3. Express pattern recognition receptors –to detect pathogens
  4. Express Fc receptors for Ig (to detect immune complexes)
  5. Capable of phagocytosis / oxidative and non-oxidative killing
  6. Secrete cytokines and chemokines to regulate inflammation
  • Capable of presenting processed antigen to T cells (they are different to neutrophils in this way)
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13
Q

What are macrophages called in (1) Liver, (2) Kidney, (3) bone, (4)spleen, (5) lung?

A
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14
Q

Where are macrophages called (1)macrophage-like synoviocytes, (2) histocytes, (3) microglia, (4) langerhans cells?

A
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15
Q

Describe phagocyte recruitment.

A
  • Cellular damage and bacterial products –> local production of cytokines and chemokines
  • Cytokines –> activate vascular endothelium –> enhanced vascular permeability
  • Chemokines attract phagocytes (not macrophages as they are already present)
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16
Q

Name 3 PRRs for recognition of micro-organisms on macrophages.

A
  • Pattern-recognition receptors (PRR) – e.g. Toll-like Receptors (TLRs), Mannose Receptors, Fc receptors
    • Recognise generic motifs (Pathogen-Associated Molecular Patterns – PAMPs)
    • PAMPs = bacterial sugars, DNA, RNA
    • Fc receptors bind to the Fc portion of Ig to allow for recognition
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17
Q

Once recognised by PRRs what process occurs and how?​

A
  • Opsonisation & endocytosis (phagolysosome = phagosome & lysosome fusion)
    • Endocytosis is facilitated by opsonisation
    • Opsonins act as a bridge between the pathogen. And the phagocyte receptors
      • Antibodies/complement bind Fc receptors;
      • Complement/ complement receptors e.g. CR1 bind APPs (i.e. CRP)
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18
Q

How does a phagolysosome form?

A
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19
Q

What are the 2 types of microbial killing mechanisms (carried out by all phagocytes)?

A
  • Oxidative killing
  • Non-oxidative killing
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20
Q

Describe how hydrochlorus acid is formed for oxidative killing.

A

Oxidative killing (HOCl acts as an oxidant and anti-microbial)

  1. (1) NADPH oxidase complex converts O2 –> O· (ROS)
  2. (2) Superoxide dismutase converts O· –> H2O2
  3. (3) Myeloperoxidase converts H2O2 (+ Cl-) –> hydrochlorus acid (HOCl)(Requires H2O2 and chloride )

HOCl is a highly oxidative killing mechanism

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21
Q

Describe the main 2 components of non-oxidative killing.

A

Non-oxidative killing

  • Release of lysozyme and lactoferrin into phagolysosome
  • Enzymes present in distinct specific granules which can provide coverage against many bacteria and fungi
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22
Q

How can phagocytosis lead to abscess formation? Which cells are involved?

A
  • Neutrophil’s role
    • The phagocytosis depletes neutrophil’s glycogen reserves and is followed by neutrophil death
    • As the cell dies, residual enzymes release and liquify local tissues
    • Accumulation of dead/dying neutrophils in tissues –> pus formation
    • Extensive pus formation causes abscess formation
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23
Q

Describe the function of phagocytes in infection using this diagram.

A

Diagram 1: Stars show infective organisms. Cytokines and chemokines are released in response. Phagocytes and neutrophils come from the bone marrow into the bloodstream. These adhere to vessel wall and migrate into tissues to phagocytose. Macrophages survive and go on to signal to T cells but neutrophils die and cause pus formation.

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24
Q
A
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25
Q

What is the main function of Natural Killer Cells?

A
  1. Present within blood and migrate to inflamed tissues (kills ‘altered self’ or virus-infected)
  2. Express inhibitory receptors for self-HLA molecules to prevent mal-activation by normal-self
  3. Express a range of activator receptors (i.e. natural cytotoxicity receptors to recognise heparan sulphate proteoglycans)
  4. Integrate signals from inhibitory and activator receptors HLA (inhibitory signals are dominant but if downregulated when something goes wrong they can kill more)
  5. Secrete cytokines to regulate inflammation (promote dendritic cell function)
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26
Q

What is the role of Dendritic cells (reside in peripheral tissues)?

A

Represent the INNATE-ADAPTIVE transition. They mainly process antigens and present it at the cell surface as peptides.

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27
Q

What receptors do dendritic cells express?

A
  • Cytokine-Rs and chemokine-R -detect inflammation
  • PRRs -detect pathogens
  • Fc receptors for Ig -detect immune complexes
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28
Q

Which chemokine mediates dendritic cell migration to the lymph nodes via lymphatics? What causes dendritic cells to mature?

A

Dendritic cells mature after phagocytosis. They then (1) upregulate HLA, (2) express co-stim molecules (3)migrate to lymph nodes.

CCR7 mediates their migration via lymphatics to lymph nodes.

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29
Q

How do dendritic cells prime the adaptive immune response?

A

Present processed antigen to T cells in lymph nodes to prime the adaptive immune response

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30
Q

How do lymphocytes enter lymph nodes?

A

Antigens from sites of infection enter the thoracic duct which drains into the blood. From the blood the lymphocytes enter lymph nodes.

31
Q
A
32
Q

What are the components of the adaptive immune system?

A
  • ‘Humoral’ immunity (means soluble)– B lymphocytes, antibodies
  • ‘Cellular’ immunity – T lymphocytes (CD4 T-cells, CD8 T-cells)
  • Soluble components – cytokines, chemokines

*Cellular and humoral are old terms. Think of it as B cells, T cells and soluble components.

33
Q

What are the characteristics of the adaptive immune response?

  • Is receptor repertoire entirely genetically encoded?
  • What is the specficity like?
  • What happens to cells which are adequately specific at first encounter?
  • What happens in re-encounter of an antigen?
A
  • Wide repertoire of antigen receptors
    • Receptor repertoire is not entirely genetically encoded
    • Genes for segments of receptors are rearranged and nucleic acids deleted/added at the sites of rearrangement almost randomly (potential to create 1011 to 1012 receptors)
    • Autoreactive cells are likely to be generated (mechanisms delete/tolerate these must work)
  • Exquisite specificity – detects small differences in molecular structure
  • Clonal expansion – cells with appropriate specificity will proliferate during infection
  • Immunological memory – pool of memory cells for the next response
34
Q

What are primary lymphoid organs? Where do B and T cells originate and mature? ​

A
  • They are organs involved in lymphocyte development
    • Bone marrow – T and B cells derived from haematopoietic stem cells here, only B cells mature here
    • Thymus – T cells mature here, most active in foetal/neonatal -→ involutes after puberty
35
Q

What are secondary lymphoid organs? What is their function?

A
  • They are where the immune response occurs i.e. sites of interaction between naïve cells and microorganisms
    • Spleen (NOT PRIMARY, no S cells?)
    • Lymph nodes
    • Mucosal Associated Lymphoid Tissue (MALT)
36
Q

Describe T cell maturation process.

A
37
Q

What is the difference between CD4 and CD8 positive cells?

A
38
Q

Aer low/intermediate/high affinity T cells negatively selected? Does the maturation for CD8/CD4 development begin before or after?

A

Maturation to CD4/CD8 happens after this affinity selection. When this occurs, cells with intermediate affinity for HLA II differentiate as CD4 T cells; cells with intermediate affinity for HLA I differentiate as CD8 T cells.

39
Q

Which cells have HLA I/II?

A

Every cell has MHC I (HLA A, B, C)

Only APCs have MHC II (HLA DP/DQ/DR)

40
Q

What are the main 2 functions of CD4+ “helper” cells?

A
  • Recognise peptides (from extracellular proteins)
    • Presented on HLA Class II molecules (HLA-DR, HLA-DP, HLA-DQ)
  • Immunoregulatory functions via cell-cell interactions and expression of cytokines
    • Provide help for developing full B-cell response
    • Provide help for developing some CD8+ T-cell responses
41
Q

Which cells express perforin and granzyme? What are three other functions of these cells?

A
  1. Kill cells directly – they are specialised cytotoxic cells. Do this by performin and grazymes and expression of the Fas ligand
  2. Recognise HLA 1 associated peptides – HLA-A/B/C
  3. Secrete cytokines IFN-gamma, TNF-alpha
  4. Important in viral and tumour defence
42
Q

Which cells are important in the response against tumours?

A

Cytotoxic CD8+ T cells – good for any disease where there is something wrong with the cell intracellularly

43
Q

Describe T cell memory response.

A
  • T and B cells are both invovled in memory
  • First response wanes quickly but a pool of more reactive T cells remains ready for the next response
44
Q

What cytokines polarize the formation of Th1 cells? What is their main function/what receptors do they express?

A
45
Q

What cytokines polarize the formation of Th17 cells? What is their main function/what cytokines do they express?

A
46
Q

Which cells express FoxP3 and CD25? What cytokines polarize their formation? What other cytokines do they express?

A

(function: negatively regulate the immune response)

47
Q

What is the function of TfH? Which centres are they important in?

A

(germinal centre reaction in development of B cell responses)

48
Q

What do Th2 cells express? What are they AKA? What role do they have in disease?

A
49
Q
A
50
Q

Describe the sequence of B cell maturation into different plasma cells.

A

Originate in bone marrow from haematopoietic stem cells

  • –> lymphoid progenitors
  • –> pro B cells
  • –> pre B cells
  • –> out of the bone marrow into periphery as IgM expressing B cells

2 fates of IgM expressing B cells once they leave the bone marrow:

  1. If antigen engagement –> develop into plasma cells which express IgM
  2. Germinal centre reaction in lymph node –> develop into cells expressing IgG, IgE or IgA
51
Q

What is the germinal centre reaction for B cell maturation dependent on? What is the process?

A

CD4+ T cell interaction CD40L:CD40.

Process:

  1. Dendritic cells prime CD4+ T cells
  2. CD4+ T cells help B cell differentiation (required CD40L:CD40)
  3. B cell proliferation, Somatic hypermutation, isotype switching –>
  4. –> high affinity IgG, IgA, IgE secreting plasma cell and memory cells
52
Q

What immunodeficiency syndrome results from loss of the CD40 ligand?

A

loss of the CD40L – hyper IgM syndrome

53
Q
A
54
Q

What is somatic hypermutation? What is isotype switching? Where do these occur?

A

Somatic hypermutation - editing of the B cell receptor every time it encounters the antigen so that it becomes very high affinity.

Isotype switching - ability to change from IgM to IgA, E or G

Happens in secondary lymphoid organs

55
Q

Which T cell subtype is involving in help with this class switching?

A

TfH cells – CD4+ cells

56
Q

How do low/medium/high affinity B cells get selected?

A

THIS IS NOT THE SAME AS T CELLS – NO INTERMEDIATE OR LOW AFFINITY ALLOWED TO SURVIVE

They undergo central tolerance – any recognition of self means that they are destroyed to prevent autoreactivity

57
Q

Where does central tolerance take place?

A

In the bone marrow

58
Q

What do immunoglobulins consist of?

A
  • Soluble proteins made up of 2 heavy and 2 light chains
    • Heavy chain determines the antibody class (IgM, IgG, IgA, IgE, IgD)
      • Subclasses of IgG and IgA also occur
59
Q

What are the functions of the Fab and Fc regions on antibodies?

A
  • Identify pathogens/toxins (Fab-mediated) – esp. bacteria of all kinds
  • Interact with other components of immune response (Fc-mediated)
    • Complement
    • Phagocytes
    • NK cells
  • Particularly important for extracellular pathogens (i.e. bacteria and toxins)
60
Q

What is the structure of IgA/D/E/G/M in relation to the normal antibody structure?

A

IgA is a dimer

IgM is a pentamer

61
Q

Describe B-Cell memory. What 3 changes occur compared to naïve response?

A
  • In naïve response: there is IgM first; IgG is delayed
  • In memory:
    • lag time between antigen exposure to production of antibody is decreased (to 2-3 days)
    • Titre of antibodies produced is greatly increased
    • Response is dominated by IgG antibodies of high affinity
  • Response may be independent of help from CD4+ T lymphocytes
62
Q
A
63
Q
A
64
Q

When a pathogen binds to a B cell what is the response?

A

Recognise the pathogen by their receptors (which are the same as the antibodies).

They produce IgM early.

Later, if the B cell has been primed by a CD4 cell that has previously recognised the antigen (presented to it by DC) then it can encourage the B cells to undergo proliferation and somatic hypermutation and isotype switching to produce a lot of high affinity antibodies.

65
Q

Where is complement produced? How many proteins does it consist of?

A
  • >20 types of proteins, produced in the liver and present as inactive molecules in circulation
  • When triggered, enzymatically activate each other in a biological cascade
66
Q

What are the 3 complement pathways?

A
  1. Classical
  2. Mannose binding lectin
  3. Alternative
67
Q

How is each complement pathway activated? What is the caveat of the classical pathway? Why can the MBL pathway happen earlier in the immune response? Which PAMPS can activate C3 in the alternative pathway?

A

​Classical pathway (Antibody + C1 –> C2, C4 –> C3)

  • Activated by antibody-antigen immune complexes. There is a conformational change which exposes the binding region for C1. Its binding activates the cascade.
  • BUT the adaptive immune response needs to have been activated – so this will not occur early in the immune response.

Mannose Binding Lectin (MBL –> C2, C4 –> C3)

  • Binding of MBL to microbial cell surface carbohydrates
  • Direct stimulation of classical pathway via C4 and C2 only (not C1)
  • i.e. not dependant on acquired immune response so can happen earlier

Alternative pathway (Involves factors B, I, P )

  • C3 binds to bacterial cell wall components directly via e.g. PAMPS like LPS (gram -ve) or teichoic acid (gram +ve)
  • Not dependant on acquired immune response but requires factors B I P
68
Q
A
69
Q

What does the MAC do to membranes? What is the central complement involved in forming MAC?

A

Central component is C3

MAC is the membrane attack complex (via C5-9) which punches holes in membranes

70
Q

What are the other functions of complement (other than MAC formation)?

A
  1. Increase vascular permeability and cell movement
  2. Opsonisation of immune complexes so soluble
  3. Opsonisation of pathogens to promote phagocytosis
  4. Active phagocytes
  5. Promote mast cell and basophil degranulation
71
Q

What is the function of cytokines?

A
  1. Small protein messengers
  2. Immunomodulatory function
  3. Autocrine or paracrine dependent action

Examples include IL-2, IL-6, IL-10, IL-12, TNF-alpha, TGF-beta

72
Q

What is the function of chemokines?

A
  1. Chemoattractant cytokines
  2. Direct recruitment / homing of leukocytes in an inflammatory response

CCL19 and CCL21 are ligands for CCR7 and important in directing dendritic cells to lymph nodes

Other examples of chemokines include IL-8, RANTES, MIP-1 alpha and beta

73
Q

Which chemokines are important in directing dendritic cells to lymph nodes and which receptor is involved?

A

Receptor: CCR7

Chemokines: CCL19, CCL21

a path 3 (89 decks)

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