Basic Immunology In Class Test

Front 1

What are the two branches of the immune system?

Back 1

Innate and Adaptive

Front 2

State two major differences between the innate and adaptive response.

Back 2

The adaptive response is more specific
The adaptive response involves memory of past infections

Front 3

What are the differences between the innate and adaptive response regarding effector cells?

Back 3

Innate: Phagocytes (macrophages and neutrophils), NK cells, eosinophils, mast cells
Adaptive: T cells and B cells

Front 4

What are the differences between the innate and adaptive response regarding effector molecules?

Back 4

Innate: lysozyme, complement proteins, interferons, lactoferrin and defensins
Adaptive: cytokines and antibodies

Front 5

What are mechanical barriers to infection?

Back 5

Tight junctions between epithelial cells
Mucociliary escalator

Front 6

What are chemical barriers to infection?

Back 6

Acidity of the stomach acid
Acidity of vaginal secretions
pH of skin, sweat, tears etc

Front 7

What is meant by 'microbiological' barriers to infection?

Back 7

Bacteria having a symbiotic relationship

Front 8

What is the structure of macrophages, and how do they circulate in the blood?

Back 8

Mononuclear (one nucleus)
Circulate as monocytes (precursor to macrophages, before activation)

Front 9

Where are macrophages found?

Back 9

Within tissues

Front 10

What are 3 properties/characteristics of neutrophils?

Back 10

They have a multi-nucleus (polymorphonuclear) with granules.
They circulate in the blood for 6 hours before being disposed of by the spleen.
They are the most abundant leukocyte.

Front 11

What are the properties/characteristics of eosinophils?

Back 11

Bi-lobed nucleus
Prominent granules
Aid protozoal infection (parasites etc)

Front 12

What are the properties of mast cells?

Back 12

Found alongside blood vessels below epithelial cells
Mononuclear cells with many granules
When activated, they secrete histamine
Involved in allergic response

Front 13

What are the properties of NK cells?

Back 13

Large cytotoxic cells involved in killing cells infected with a virus

Front 14

What are the 4 stages of the innate response?

Back 14

1. Adherence of bacteria to epithelium
2. Penetration of epithelium, e.g cut or burn
3. Local infection of tissues ---> activation of macrophages
4. Macrophages overwhelmed ---> recruitment of neutrophils

Front 15

What are the 3 stages of the adaptive response?

Back 15

1. After around 96 hours the bacteria will enter the lymphatic system, tothe lymph nodes
2. The antigen released from that bacteria will be presented by antigenpresenting cells (APC’s) and then bind to specific T-Cells, causingactivation and release of cytokines
3. Released cytokines from (Th2 cells) activate B-Cells which areconverted into many plasma cells which release soluble antibodieswhich aid the components of the innate immune system in removingthe micro-organisms

Front 16

What are the functions of the two major lymphocytes?

Back 16

- B cells mature into plasma cells which release soluble antibodies
- T cells mature into T helper cells (CD4+) which release cytokines, they mature into cytotoxic T cells (CD8+), and they may also mature into memory T cells (either CD4+ or CD8+).

Front 17

Describe the function of Toll-Like Receptors (TLRs), giving one named example.

Back 17

- TLRs recognise sequences on non-self cells known as pathogen-associated molecular patterns (PAMPs)
- There are approximately 10 TLRs in humans, each recognise different PAMPs
- TLR-4 recognises lipopolysaccharide which is present on gram negative bacteria

Front 18

What is Phagocytosis?

Back 18

1. An activated macrophage recognises a pathogen, such as a bacterium
2. Macrophage begins to engulf bacerium, forming a phagosome
3. The phagosome containing the bacterium fuses with a lysosome within the cell, forming a phagolysosome
4. The lysosome releases lysozymes which breaks down components of the bacterial cell wall, leading to bacterial death

Front 19

What is opsonisation?

Back 19

- The process of altering the surface of a pathogen to facilitate phagocytosis
- This makes phagocytosis quicker and more efficient

Front 20

Describe the process of opsonisation.

Back 20

Hydrolysis of the complement protein C3 into C3a and C3b
C3b + Factor B ---> C3b,B
C3b,b + Factor D ---> C3b,Bb

Front 21

What is C3 convertase?

Back 21

C3b,Bb
Amplifies hydrolysis of C3 into C3a and C3b

Front 22

Which complement proteins make up the membrane attack complex?

Back 22

C5b, C6, C7, C8 and C9

Front 23

What function do C3a and C5a have?

Back 23

Activation of mast cells to produce histamine

Front 24

What is the function of the membrane attack complex?

Back 24

The membrane attack complex is a channel that forms on a microbial cell membrane, which results in cell lysis due to influx of extracellular fluid

Front 25

What are the functions of TNF-α?

Back 25

- Recruitment of IL-8 (a chemoattractant) and E-Selectin (adhesion molecules) during neutrophil recruitment
- Increases localised vascular permeability, which increases access to inflammatory cells and mediators

Front 26

What are functions of IL-1?

Back 26

- Endogenous pyrogen (causes an increase in body temperature to stop bacteria replication)
Causes expression of adhesion molecules (e.g. E-Selectin)
- Recruitment of IL-8 (chemoattractant)
- Increases localised vascular permeability

Front 27

What are the functions of IL-8?

Back 27

- IL-8 is a potent chemoattractant/chemokine involved in many processes, including the recruitment of neutrophils at infection sites

Front 28

What are the functions of IL-6 and IL-12?

Back 28

- Endogenous pyrogen
- Activate T Cells and B Cells (lymphocytes)
- Induces maturation of T Cells and B Cells

- Increases antibody production by B Cells

Front 29

What are the symptoms of inflammation?

Back 29

Rubor, calor, dolor, tumor

Front 30

What is the first stage of neutrophil recruitment?

Back 30

Rolling Adhesion-
TNF-α increases expression of adhesion molecules (E-Selectin)
Neutrophils roll along the surface endothelium, and carbohydrates on their surface adhere to the E Selectin molecules which stalls the movement of the neutrophils

Front 31

What is the second stage of neutrophil recruitment?

Back 31

Tight Adhesion-
IL-8 receptor on the neutrophil binds to a molecule of IL-8 on the surface endothelium
LFA-1 molecules on the neutrophill bind to ICAM-1 molecules on the surface endothelium

Front 32

What is the third stage of neutrophil recruitment?

Back 32

Diapedesis-
The neutrophils respond to high levels of IL-8 (a chemoattractant) and squeezes between endothelial cells where IL-8 is present at higher concentrations.
Diapedesis means 'oozing action'

Front 33

What is the fourth stage of neutrophil recruitment?

Back 33

Migration-
Neutrophils move through the tissue matrix towards the site of infection under the influence of a concentration gradient of IL-8
The neutrophils release proteolytic enzymes which degrade the tissue matrix increasing the rate of migration

Front 34

Which antibody isotype forms pentamers around a J chain in the secreted form?

Back 34

IgM

Front 35

Which antibody isotype is the most abundant in the blood?

Back 35

IgG

Front 36

Which antibody isotype is mostly found in mucosal secretions?

Back 36

IgA

Front 37

Which antibody isotype is mostly associated with the allergic response, and which receptor will it bind to on mast cells?

Back 37

IgE, FcεRI

Front 38

A previously healthy 8-year-old boy is infected with an upper respiratory tract virus for the first time. During the first few hours of infection, what will occur?

Back 38

The innate immune system responds rapidly to the viral infection and keeps the viral infection under control.

Front 39

What is a unique property of the adaptive immune system?

Back 39

Highly diverse repertoire of specificities for antigens

Front 40

A standard treatment of animal bite victims, when there is a possibility that the animal was infected with the rabies virus, is administration of human immunoglobulin preparations containing anti rabies virus antibodies. Which type of immunity would be established by this treatment?

Back 40

Passive humoral immunity (antibody mediated immunity)

Front 41

At 15 months of age, a child received a measles-mumps-rubella vaccine (MMR). At age 22, she is living with a family in Mexico that has not been vaccinated and she is exposed to measles. Despite the exposure, she does not become infected. Which of the following properties of the adaptive immune system is best illustrated by this scenario?

Back 41

Memory

Front 42

A vaccine administered in the autumn of one year may protect against the prevalent strain of influenza virus that originated in Hong Kong that same year, but it will not protect against another strain of influenza virus that originated in Russia. This phenomenon illustrates which property of the adaptive immune system?

Back 42

Specificity

Front 43

In which phagocyte(s) are granules found?

Back 43

Neutrophils and eosinophils

Front 44

Name the substances stored in azurophilic/primary granules.

Back 44

Cathepsin G
Elastase
Proteinase 3
Defensins
etc.

Front 45

Name the substances stores in specific/secondary granules.

Back 45

Lactoferrin
Cathelidicin
Collagenase
Gelatinase

Front 46

Name the substances stored in tertiary granules.

Back 46

Gelatinase

Front 47

Describe the process in which the antimicrobial substance is produced within the neutrophil.

Back 47

1. NADPH Oxidase transfers electrons to molecular oxygen generating superoxide free radicals
2. The superoxide is converted into H2O2 via the enzyme SOD
3. The addition of Cl- to H2O2 generates HClO (hyperchlorous acid) via the enzyme myeloperoxidase which is an antimicrobial agent.

Front 48

Where are T-cells produced, and where do they mature?

Back 48

Produced in bone marrow, mature in thymus

Front 49

Where are B-cells produced, and where do they mature?

Back 49

Produced in bone marrow, mature in bone marrow

Front 50

What do activated B-cells differentiate in to?

Back 50

Memory cells and plasma cells

Front 51

What do activated T-cells differentiate in to?

Back 51

CD4+ helper T cells
CD8+ cytotoxic T cells (to kill viruses)

Front 52

State the postulates of the clonal selection hypothesis.

Back 52

1. Each lymphocyte has a specific receptor which recognises a specific antigen

2. Lymphocytes that have receptors for 'self 'antigens' are deleted at an early stage

3. The interaction between a lymphocyte and an antigen results in activation of the lymphocyte

4. The cells that differentiate from the activated lymphocyte will be identical to the parent cell, and have the identical specificity.

Front 53

Howis the diversity of lymphocyte antigen receptors generated?

Back 53

By rearrangement of gene segments coding for T-cell receptors on T-cells and surface immunoglobulins on B-cells

Front 54

What Fc antibody isotype does the anti-RhD antigen have?

Back 54

IgG

Front 55

How long after sensitisation to an antigen does the effector phase occur?

Back 55

7-10 days

Front 56

Where are MHC I and MHC II found?

Back 56

MHC I is found on all cells (except RBC) and binds to CD8+
MHC II is found on antigen presenting cells (macrophages, dendritic cells, B-cells) and binds to CD4+

Front 57

Describe the process of T-cell activation.

Back 57

- MHC II on the APC will present an antigen to the TCR, which will recognise it as foreign
- There is co-stimulation of CD28 (on the T-cell) to the B7 molecule on the APC
- When the B7 glycoprotein binds to the CD28 molecule on the T cell, it results in IL-2 being released from the T-cell and IL-2 receptor synthesis on the T-cell, causing T-cell proliferation
- There is a CD3/TCR signalling complex required for activation
- CD4 molecule tells MHC II that it is a CD4+ cell

Front 58

What is the structure of the TCR?

Back 58

- There are two distinct chains - alpha and beta
- Constant regions (at the bottom) and variable regions (which make up the antigen recognition site)
- Coded for by the VDJC genes
- Approximately 11.7x10^6 different antigen receptors

Front 59

Describe the process of antigen processing and presentation.

Back 59

1. Lysosomes in macrophages degrades bacteria producing bacterial peptide fragments
2. MHC II within macrophage vesicles finds peptide fragments and binds to one
3. Bound peptides are transported to the macrophage cell surface for presentation to activate T-cells

Front 60

Describe the effect of TNF-α and IFN-γ on activated macrophages.

Back 60

TNF-α and IFN-γ are released from activated CD4+ Th1 helper cells and act on activated macrophages increasing the efficiency of bacterial killing

Front 61

Describe the effect of IL-4, IL-5 and IL-6 on B-cells.

Back 61

IL-4, IL-5 and IL-6 are released from activated CD4+ Th2 cells and act naiive B-cells, causing them to become plasma cells and increase antibody synthesis.

Front 62

Describe how CD8+ cells kill viruses.

Back 62

When MHC I binds to the TCR on CD8+ cytotoxic cells, the CD8+ cell will release perforin and granzymes which induce programmed cell death (apoptosis).

Front 63

Describe how the activation signal in T-cells is turned off.

Back 63

- When T-cells become activated, they begin to express CTLA-4 which has a higher affinity for B7 than CD28
- This delivers inhibitory signals to activated T-cells

Front 64

What are the 3 most important functions of macrophages?

Back 64

1. Phagocytosis of opsonised bacteria
2. Regulation of neutrophil recruitment to a site of infection
3. Presentation of foreign antigens to naiive T-cells in the lymph nodes

Front 65

What are the 3 most important functions of activated T-cells?

Back 65

1. Activation of macrophages by TNF-α and IFN-γby CD4+ Th1 cells
2. Activation of B-cells by IL-4, IL-5 and IL-6 by CD4+ Th2 cells
3. The killing of viruses by activated CD8+ cytotoxic cells

Front 66

Which portions of the antibody make up the variable region?

Back 66

2x Vl light chains
2x Vh heavy chains

Front 67

Which portions of the antibody make up the constant (Fc) region?

Back 67

2x Cl light chains
6x Ch heavy chains

Front 68

What are the 2 halves of the antibody bonded by?

Back 68

Disulfide bonds

Front 69

Describe how activated T-cells help to activate naiive B-cells.

Back 69

- CD4+ Th2 helper cells recognise antigen on B-cell MHC II molecule and synthesise cytokines
- The CD40L molecule on the CD4+ Th2 cell binds to the CD40 molecule on the naiive B-cell
- These processes cause IL-4, IL-5 and IL-6 to be released which stimulate B-cells to proliferate and differentiate

Front 70

Describe how IgA moves across epithelia into external secretions.

Back 70

- IgA movement across epithelial cells is known as transcytosis
- The Poly-Ig receptor (specialised transport protein) binds to the IgA as it enters the cell
- The Poly-Ig - IgA complex undergoes endocytosis inside a vesicle within the epithelial cell.
- Once at the apical end of the epithelial cell, the IgA and extracellular binding component of the Poly-Ig receptor will enter external secretions
- The Poly-Ig receptor is cleaved leaving behind a residual part of the Poly-Ig receptor which is non-functional and will be degraded.

Front 71

State the 3 inhibitory/neutralisation functions of antibodies.

Back 71

1. Inhibition of bacterial cells to host cells
2. Neutralisation of bacterial exotoxins
3. Inhibition of viral infection

Front 72

State the 2 stimulatory functions of antibodies.

Back 72

1. Opsonisation of bacteria for quicker and more efficient phagocytosis
2. Activation of complement C1 to enhance opsonisation with C3b

Front 73

What is the classical pathway of complement activation?

Back 73

- IgG or IgM in the blood bind to pathogens and activate the classicalpathway
- IgM is rapidly producedfollowing infection of the blood and activates complement
- The pentameric structure makes IgM a potentactivator of complement

Front 74

What is the lectin pathway of complement activation?

Back 74

When lectins bind to carbohydrate molecules on bacterial/viral cell surfaces

Front 75

What is the alternate pathway of complement activation?

Back 75

- Spontaneously activated complement bindsto the surface of the pathogen, where it forms a C3 convertase (C3b,Bb) that isstabilised by properdin (factor P) on the pathogen topromote the further formation of C3b
- A lack of regulatory molecules, as foundon host cells, means that pathogens become fully opsonised by C3b

Front 76

Name the functions of complement proteins.

Back 76

- Recruitment of inflammatory cells by C3a and C5a
- Opsonisation of pathogens by C3b and immune complex binding of C3b and removal through CR1 on RBC
- Formation of the membrane attack complex (C5b, C6, C7, C8 and C9)

Front 77

What is antibody-dependent cell-mediated cytotoxicity?

Back 77

- The destruction of antibody coated target cells is called antibody-dependent cell-mediated cytotoxicity and is triggered when antibody bound to the cell surface interacts with Fcγ IgG receptors on the NK cell

- In the absence of MHC I, virally - infected cells express viral proteins on their surface that can be recongised by IgG antibodies
- When bound by IgG antibodies, the cells are recognised by NK cells and are killed
- Cytotoxicattack involves the release of granules containing perforin to perforate thetarget cell, and granzymes which penetrate through the poresand induce cell death by membrane damage and/or apoptosis

Front 78

What is the mechanism of lysozyme?

Back 78

- Lysozyme are glycoside hydrolyses which catalyse the breakdown of bacterial cell walls

Front 79

What is the mechanism of definsins?

Back 79

- Small cationic proteins
- Bind to bacterial cell walls leading to perforation, leading to efflux of ions and other important molecules from the cell causing cell death

Front 80

What is the mechanism of lactoferrin?

Back 80

- Lactoferrin can be found in the secondary granules of neutrophils
- Sequesters free iron, which is required for bacterial cell growth

Front 81

Name the type 1 interferon(s).

Back 81

IFN-α
and
IFN-β

Front 82

Name the type 2 interferon(s).

Back 82

IFN-γ

Front 83

State the names of all 3 chemoattractant molecules

Back 83

- IL-8 (interleukin - 8)
- PAF (platelet activating factor)
- LTB4 (leukotriene B4)

Front 84

In antigen presenting cells (APCs) where is MHC II produced and stored?

Back 84

- Produced in ER (endoplasmic reticulum)
- Stored in vesicles

Front 85

How are eosinophils activated?

Back 85

- Parasites such as tapeworms become covered with specific IgE and IgA antibodies
- The eosinophils have high affinity FcεRI receptors on their surface, and use these to adhere to the tapeworm as IgE and IgA will bind to the receptor
- Clusteringof either IgA or IgEreceptors activates the eosinophil triggering the release of reactive oxygenspecies and highly basic eosinophil granule contents to kill the tapeworm

- 5 molecules of IgA increase killing x1000

Front 86

What happens in the early phase of allergen response?

Back 86

- There is degranulation and release of histamineacting on H1 receptors, which causes vasodilation and increases vascular permeabilityand bronchial smooth muscle contraction (bronchoconstriction)
- Release of proteases (tryptase) from granules
- Release of secondary mediatorssynthesised from arachidonic acid eg leukotriene C4 (LTC4) a potent bronchoconstrictor

Front 87

What happens in the late phase of allergen response?

Back 87

- Mastcells synthesise and release cytokines that stimulate an inflammatory responseby T-cells and eosinophils
- Characterised by the continued synthesis and release ofinflammatory mediators by mast cells, especially vasoactive mediators such asvascular endothelial growth factor (VEGF) which causes vascular leakage andtissue oedema

(8-12 hours)

Front 88

What is type I hypersensitivity?

Back 88

- the 'wheal and flare' response
- IgE meditated mast cell activation, leading to release of Histamine, prostaglandins and other mediators of the inflammatory response

Local Blood Vessels:
Histamine acting on H1 receptors on blood vessel smooth muscle:
Increase in vascular permeability leading to visible oedema (swelling)
There is also plasma exudation and tissue oedema

Nerve Endings:
Blood vessels dilate (vasodilation)

Front 89

What are the symptoms of an allergic reaction?

Back 89

Itch, local swelling, hypotension, wheezing, diarrhoea

Front 90

Anaphylaxis Treatments:

Back 90

- Epipen (adrenaline injection)
- Injectable anti-histamines
- Corticosteroids

Front 91

Which antigen(s) will people with blood type A have on their erythrocytes?

Back 91

Type A

Front 92

Which antigen(s) will people with blood type B have on their erythrocytes?

Back 92

Type B

Front 93

Which antigen(s) will people with blood type AB have on their erythrocytes?

Back 93

Both Type A and Type B

Front 94

Which antigen(s) will people with blood type O have on their erythrocytes?

Back 94

Neither antigen

Front 95

Which antibody/antibodies will people with blood type A contain in their plasma?

Back 95

Anti-B

Front 96

Which antibody/antibodies will people with blood type B contain in their plasma?

Back 96

Anti-A

Front 97

Which antibody/antibodies will people with blood type AB contain in their plasma?

Back 97

Neither antibody

Front 98

Which antibody/antibodies will people with blood type O contain in their plasma?

Back 98

Both Anti-A and Anti-B

Front 99

Which blood group is considered to be the universal donor?

Back 99

Type O

Front 100

Which blood group is considered to be the universal recipient?

Back 100

Type AB

Front 101

What happens if there is transfusion of incompatible blood?

Back 101

- Antibodies to incompatible blood are usually of the IgM isotype andcause agglutination, complement activation and intravascular hemolysis with release of hemoglobin and subsequent kidney damage
- IgM is a potent complement activator and caninduce the formation of the terminal membrane attack complex (MAC) on RBC,overwhelming the complement regulatory proteins, in the presence of sufficientIgM and cause RBC lysis

Front 102

What is haemolytic disease of the newborn?

Back 102

-Peoplewhose RBCs have the RhDantigen are Rh+ and peoplewho lack the RhDantigen are Rh-
- Normally, the blood doesn't contain anti-RhD antibodies
- Mother's who are Rh- have babies who are Rh+, and during childbirth blood from the baby's circulation may come into contact with the mother's circulation
- The mother will then start producing anti-Rh antibodies (sensitisation phase)
- This means with subsequent pregnancies there is an increased risk of the mother's immune system attacking the foetus, causing RBC lysis
- Each new pregnancy results in re-sensitisation

Front 103

How can haemolytic disease of the newborn be treated?

Back 103

-Givingthe Rh- mother preformed anti-RhD antibodies immediately after thebirth of the first child
-These can destroy the foetal RhD+ red blood cells before they sensitisethe mother to produce anti-RhD antibodies.