Describe what steps are taking place for numbers 1, 2, 3 and 4. (2 marks) rolling activation firm adhesion transmigration

BIO0

  1. a) You have had an injury to the skin that has become infected. Where are the following cells before and after the infection? (4 marks)
    1. B cells: Before: lymph node, After: lymph node (1 mark)
    2. Dendritic cells: Before: skin, After: Lymph node (1 mark)
  • Neutrophils: Before: Blood, After: skin (1 mark)
  1. Macrophages: Before: skin, After: skin (1 mark)
  1. Briefly state the role of lymph node compared to the spleen (1 mark)

Lymph node: Immune response to pathogens and antigens in peripheral tissues

Spleen: Immune responses to blood borne antigens and pathogens Both answers must be correct in order to get the 1 mark

  1. a) Name two differences between IgA and IgG (1 mark)

IgA consists of 2 IgA molecules joined by the J chain , IgG is a dimer. IgA is secreted into mucosal tissues, IgG is found in the serum

  1. Why is IgM better at driving complement mediated lysis of cells than IgG? (2 marks)

Pentameric structure of IgM increases strength of cross­linkage of complement molecules triggering efficient complement activation. IgG is dimeric, requires multiple IgG molecules to come together to enable the same degree of cross­linkage and complement activation.

BIO00002I

  1. a) T cells undergo two types of selection processes during their development. Name the two processes and explain what happens to the T cell during these processes. (2 marks)
  2. i) ii)

Positive selection. T cell selected to survive on ability to recognise self

MHC

Negative selection. T cell deleted if T cell receptor binds self peptide with high affinity

(1 mark for each)

  1. In addition to the above two processes, describe three other changes that occur in T cells to complete their development. (3 marks)
    1. Rearrange T cell receptor (1 mark)
    2. Express CD4 and CD8 co­receptors and T cell receptor on the surface (1 mark)
  • Maturation into single positive CD4 or CD8 expressing T cells (1 mark)

          

  1. a) Outline how natural killer cells destroy viruses and name a mechanism for how this works. (1 mark)

Antibody binds to virus coat protein . The bound antibody can to receptor on NK cell called the Fc receptor triggering release of cytotoxic granule contents that kill virus or virus infected cells. This is termed antibody­dependent cellular cytotoxicity (ADCC)   (abbreviate ADCC accepted)

  1. Briefly describe two different approaches by which viruses impede viral peptide expression on MHC class I molecules. (2 marks) i) ii)

Will accept any two of the following answers (1 mark each):

Blocking peptide entry to endoplasmic reticulum

Retention of MHC Class I in endoplasmic reticulum

Degradation of MHC class I proteins

Directly binds to surface MHC Class I molecules and interferes with functional interactions with the T cell receptor

  1. What does the term ‘capping’ refer to and why is it important in T cell activation? (2 mark)

‘Capping’ is relocation of cell surface molecules involved in T cell activation to a central location on the T cell surface. (1 mark)

Capping is important for forming the immunological synapse; a structure essential for initiating intracellular T cell signalling (1 mark).

BIO00002I

  1. The above diagram documents movement of immune cells from blood vessels

into inflamed tissue.

  1. a) Describe what steps are taking place for numbers 1, 2, 3 and 4. (2 marks)
    • rolling
    • activation
    • firm adhesion
    • transmigration

(1/2 mark for each)

  1. For i, ii and iii in the diagram above, name the family of molecules that govern the steps in migration shown (3 marks).
    1. selectins ii) chemokines

iii)        integrins

(1 mark for each)

  1. Define what the term allergy refers to. Explain the immunological mechanisms contributing to an allergic response. (3 marks)

Allergy is an exaggerated immune response to a harmless antigen/molecule/particle e.g. cat hair, grass pollen. (1 mark)

IgE binds to receptors on mast cells, leads to degranulation of mast cell contents including histamine. Results in increase in mucus production and constriction of airways. (2 marks­ 1 mark for IgE, 1 mark for mast cell degranulation, histamine and associated events).

  1. a) Outline what is meant by passive and active immunisation. (2 marks)

Passive­ transfer of antibodies to a pathogen from one individual to another.

(1 mark) [note\; will accept IgG from mother to foetus].

Active­ innoculation of a harmless form of a pathogen to elicit protective immunity upon re­exposure with pathogenic form of same pathogen (1 mark)

  1. Describe two different approaches to elicit active immunisation and for each approach name a pathogen it immunizes against. (2 marks)

 

  1. i)
  2. ii)

Answers can be from

Live, attenuated­ polio, chicken pox, MMR

Inactivated ­polio, Hepatitis A

Toxoid­ Diptheria, tetanus

Subunit­ Hepatitis B, Influenza, Meningococcal

(1/2 mark for the approach, 1/2 mark for naming a pathogen).

          

 

 

  1. It has been suggested that a new gene (Gene X) is involved in the response of human primary macrophages to bacterial Lipopolysaccharride (LPS). The following graph shows RNA levels of IL6, TNF, and Gene X (arbitrary units –
  2. AU) following treatment of macrophages with 100 ng/ml LPS.

 

  1. Compare and contrast the regulation of Gene X with that of IL6 and TNF. (3 marks)

Differences

The gene reaches its maximum expression 12h post LPS addition, whereas

IL6 and TNF peak at 6h post stimulation (1 mark).

Similarities

Gene X and IL6 and TNF are all induced by LPS within 3h of LPS addition (1 mark) and remain up­regulated at 24h post LPS addition (1 mark).

  1. The following table shows protein levels of IFNb, IL6, and TNF (pg/ml) in control macrophages and macrophages lacking gene X (Gene X depleted) 24h post LPS stimulation. What conclusion can be derived from these data with regards to Gene X function and why? (2 marks)
Cytokine Control macrophages Gene X depleted macrophages
TNF 1254 3000
IL6 3995 5545
IFNb 3.2 15.6

Levels of all tested inflammatory cytokines are higher in macrophages lacking Gene X (1 mark). This indicates that Gene X has an

immunosuppressive/anti­inflammatory (both acceptable) function (1 mark).

  1. Suggest a possible gene product for Gene X and the mechanism employed to mediate its function. (2 marks)

Any one from the four below (1 mark for the gene product and one for the function):

Anti­inflammatory cytokine ­ inhibiting pro­inflammatory signalling

Phosphatase ­ inactivating a pro­inflammatory kinase substrate

Ubiquitin ligase ­ leading to degradation of a pro­inflammatory mediator MicroRNA ­ suppressing expression of a pro­inflammatory mediator

  1. Gene X is a component of the immune response to a non­cytopathic virus that establishes chronic infection independently of Gene X function. Infection with this virus can lead to tissue damage. What would be the most likely outcome of infection with this virus in an individual deficient for Gene X function, with regards to tissue damage and why? (2 marks)

 

Tissue damage during non­cytopathic virus infection is commonly the outcome of the immune response/inflammation (1 mark). Lacking Gene X, an immunosuppressive component of the response, will lead to increased inflammation and therefore enhanced tissue damage in the long­term (1 mark).

  1. A DNA virus encodes a protein called vIRF, which has strong anti­inflammatory functions, and contributes significantly to immune escape by this virus. It has been found that vIRF regulates transcription of Gene X. What is the most likely effect of vIRF on expression of Gene X? (1 mark)

vIRF is likely to up­regulate Gene X (which is anti­inflammatory) to promote immune escape (1 mark).

  1. Patient A and Patient B are infected with the Ebola virus. The ability of each patient to make an effective antibody response to a membrane protein of the Ebola virus was assessed by ELISA. The optical density readout at 405 nm was plotted against serial dilutions of each patient’s serum as shown in the graph.
    1. For both patient A and patient B, identify the serum dilution range corresponding to the linear and saturation points of the respective data. (2 marks)

Patient A 1:400­1:3200 linear points; 1:100­1:400 saturation points

 

Patient B 1:800­1:3200 linear section, 1:100­1:800 saturation points. (½ mark for each section per patient)

  1. Explain why the saturation points must never be used for calculating an antibody response to a given antigen. (1 mark)

Saturation point represents a condition where an excess of antibody for a given antigen is present, the antibody binding sites on the antigen become saturated leaving excess unbound antibody free is solution. Since only antibody bound to antigen can be detected, and free antibody in solution is washed away during washing steps then inaccurate calculations of antibody concentrations would occur.

  1. The total concentration of serum antibodies to the membrane protein of the Ebola virus in the positive control sample was 50 mg/ml. From the graph above, name the patient that exhibited the higher antibody response to the viral protein and, explaining your calculation, determine the total concentration of antibodies to the Ebola virus membrane protein in this patient. (2 marks)

Patient B.

Positive control and Patient B have an equal OD at 1:3200 and 1:1600 dilution, respectively. Concentration of serum antibodies in the positive control at 1:3200 dilution is 0.0156mg/ml. This value equates to a 1:1600 serum dilution from patient B, thus total concentration of antibodies in patient B

serum to Ebola virus is 0.0156 x 1600= 25mg/ml.

(1/2 mark for patient, 1.5 marks for calculations)

  1. On further investigation of the above patients serum, the predominant class of antibody to the Ebola virus membrane protein was IgG2a. Name the

CD4 T cell subtype that induces B cells to produce IgG2a antibodies. (1 mark)

T helper 1

  1. An ELISA was developed to measure the cytokine concentrations made by this CD4 T cell subtype in response to Ebola virus. Name a cytokine secreted from this CD4 T cell subtype and the type of ELISA used to measure its concentration in serum. (1 mark)

IFNgamma; sandwiche ELISA (1/2 mark for each).

  1. The ELISA was performed and the data documented in the graph below was obtained. Which data (negative control, patient sample, or positive control) suggests that the ELISA was inappropriately conducted. Give an explanation for your answer. (1 mark)

Negative control. This is serum that is known to be devoid of the cytokine of interest. The O.D. should be almost zero for all serum dilutions if the experiment worked.

 

  1. On reviewing the protocol steps in the ELISA, it was noted that one was accidentally omitted. Suggest which protocol step was omitted and explain its role in an ELISA assay. (2 marks)

Blocking step (will accept addition of skimmed milk so long as the other answer has the word blocking). Important in blocking any areas of the well that does not have bound antigen thereby preventing non­specific binding of the primary serum which could give a false positive result. (1 mark for blocking/or milk and 1 mark for explanation)

          

EITHER

  1. A) Describe the activation mechanisms and main functions of the complement system.

The Complement is a system of soluble pattern­recognition receptors and effector molecules that detect and destroy microbes

Three main groups of receptors initiate the response:

C1q (classical pathway): Interacts with an antibody coated pathogen surface Mannose­binding lectin (MBL) and ficolins (lectin pathway): Recognise carbohydrates on pathogen surfaces

C3 (alternative pathway): It undergoes spontaneous hydrolysis leading to deposition of C3 convertase on pathogen surface

The amplification cascade:

Circulating proteins react with each other to fight infection

A number of complement proteins are inactive precursor proteases

(zymogens) that are themselves activated by proteolytic cleavage. At sites of infection, the complement system is activated through a triggered­enzyme cascade:

An active complement enzyme generated by cleavage of its zymogen precursor cleaves its substrate (another complement zymogen) to its active enzymatic form.

The activation of a small number of complement proteins at the start of the pathway is hugely amplified resulting in the rapid generation of a

disproportionately large complement response.

Strong regulatory mechanisms to prevent uncontrolled complement activation

Complement function

The complement helps antibodies and phagocytes clear microbes from an organism in three ways:

Opsonisation: enhancing phagocytosis

Chemotaxis: some complement proteins act as chemoattractants to recruit more phagocytes to the site of complement activation

Pathogen lysis: complement components damage certain bacteria by creating pores in the bacterial membrane.

Immune complex clearance by the complement

Antibody­antigen complexes are formed in the circulation

Complement activation leads to deposition of C3b on the immune complex

Complement receptor CR1 on erythrocytes binds immune complexes through C3b

Erythrocytes go to the spleen and liver where phagocytes remove the immune complexes from the surface of erythrocytes

OR

  1. B) Discuss the similarities and differences in the development, activation and function between CD4+ T cells and CD8+ T cells.

Similarities

Develop in thymus.

Undergo positive and negative selection.

Rearrange a receptor on their surface

Respond to peptide fragments of whole proteins

Both restricted recirculation patterns

Require two signals for activation

Function to respond to intracellular pathogens (principally)

Generate memory cells.

Differences

CD4 recognise MHC class II­peptides, CD8 recognise MHC class I­peptides CD4 responds to peptides presented via an exogenous pathway, CD8 respond to peptides generated via an endogenous pathway OR

cross­presentation of exogenous antigens

CD4 can differentiate into different subtypes of T cells; Th1, Th2,TH17, Tregs

CD8 differentiate into cytotoxic killers.

CD4 use cytokines to activate other cells (act as helper cells); IFNgamma, IL­4

CD8 transform into killers that specifically kill target cells; perforin and granzyme B.

(Higher marks if these similarities are discussed/explained fully).

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