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
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
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.
Positive selection. T cell selected to survive on ability to recognise self
Negative selection. T cell deleted if T cell receptor binds self peptide with high affinity
(1 mark for each)
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)
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
‘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).
into inflamed tissue.
(1/2 mark for each)
(1 mark for each)
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).
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)
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).
The gene reaches its maximum expression 12h post LPS addition, whereas
IL6 and TNF peak at 6h post stimulation (1 mark).
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).
|Cytokine||Control macrophages||Gene X depleted macrophages|
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).
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
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).
vIRF is likely to upregulate Gene X (which is antiinflammatory) to promote immune escape (1 mark).
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)
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.
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)
CD4 T cell subtype that induces B cells to produce IgG2a antibodies. (1 mark)
T helper 1
IFNgamma; sandwiche ELISA (1/2 mark for each).
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.
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)
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
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
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.
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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