ESE Study questions - chiara section Flashcards
Which of these is NOT associated with adjuvants?
1. forms an antigen depot
2. provides non-specific T cell stimulation
3. activates antigen-presenting cells
4. activates complement cascade
- activates the complement cascade
* adjuvants are in vaccinations, and release the antigen slowly and activating antigen presenting cells/antigen depots and providing T cell stimulation
* doesn’t have ability to activate any 3 of the complement cascade
which of the following Ig is involved in mediating allergic reactions?
1. IgG
2. IgM
3. IgE
4. IgA
- IgE
*IgE is involved in allergic reactions - also type I hypersensitivity
*IgE will bind to mast cells
which of the following types of hypersensitivity reactions is antibody mediates?
1. type I
2. Type II
3. Type III
4. All of these
- All of these are antibody mediated
*Type I = IgE
*Type II = IgG and IgM
*Type III is antibody as well
*Type IV is NOT antibody mediated
antigens normally expressed only on embryonic cells but also sometimes found on tumours are known as:
1. oncofoetal antigens
2. maternal
3. neonatal
4. cryptic
- oncofoetal antigens
- present in tumours (onco) and also embryonic cells (foetal)
extracellular bacteria are killed by
1. secreting exotoxins
2. phagocytosis and complement
3. toxin neutralisation
4. C-reactive protein
- phagocytosis and complement system kills extracellular bacteria
which of the following is NOT considered first line of defence against microbial infections at the mucosal surfaces?
1. Defensins
2. mucociliary action of the respiratory tract
3. T and B lymphocytes
4. Tight junctions between epithelial cells
- T and B lymphocytes
- T and B lymphocytes are apart of adaptive immunity, whereas we are talking about mucosal surfaces so what is fighting the infection first
- tight junctions between epithelial cells try to prevent microbes from getting through the tight junctions
- defensins: protein
bacteria growing within macrophags are killed by:
1. complement
2. reactive oxygen and nitrogen intermediates
3. antibody
4. cytotoxic T cells
- reactive oxygen and nitrogen intermediates
some viruses escapethe immune system by antigen shift. this involves:
1. structural reorganisation of existing antigens
2. masking of antigen epitopes
3. point mutations in single genes
4. interchange of genetic materal with other viruses
- point mutations in single genes
* major changes that cause epidemics
mechanisms controlling autoreactive cells that escape to the periphery do NOT include
1. suppression by regulatory T cells
2. anergy
3. antigen sequestration
4. upregulation of costimulatory molecules on APCs
- upregulation of costimulatory molecules on APCs
it is absent not upregulation
anaphylaxis can be triggered by cross-linking of IgE receptors on:
1. monocytes
2. mast cells
3. eosinophils
4. B-cells
- mast cells
List 4 strategies used by infectious organisms to avoid elimination by the immune system?
- changing antigen structure
- masking antigens on surface of the cell
- direct killing of phagocytic cells
- they cause necrosis of inflammatory cells - resistance to antibacterial proteins
- blocking phagocytosis
List 4 strategies used by infectious organisms to avoid elimination by the immune system?
- changing antigen structure
- masking antigens on surface of the cell
- direct killing of phagocytic cells
- they cause necrosis of inflammatory cells - resistance to antibacterial proteins
- blocking phagocytosis
Infectious agents may trigger autoimmunity through different mechanisms. List and briefly explain 2 of those mechanisms:
anergy
- we do not have the additional co-stimulatory molecules in the peripheral cells, so no activation occurs
suppression of autoreactive lymphocytes by treg cells
- inhibit immune response by keeping lymphocytes quiet
antigen sequenstration
- antigens not expressed in the thymus or cryptic in nautre > cells never exposed to self antigens
activation-induced cell death
- through lymphocytes or T cells recognising self antigens =apoptosis
List and briefly explain 5 mechanisms used by tumour cells to escape to evade the immune system in immunocompetent hosts
- clonal selection of antigen-negative variants
- antigen masking
- loss or reduced MHC1 expression - but NKC can still reognise these as they do not need MHC1
- production of immunosuppressive molecules
- immunoregulation (downregulation of co-stimulatory molecules on APCs)
- no co-stimulatory molecules = no activation of T cells
Why would an animal be normal at birth, but then at 5 weeks start showing respiratory clinical signs, with no lymphocytes and reduced antibodies?
- Normal at birth but at 5 weeks of age = respiratory clinical signs
○ Due to maternal antibodies**
○ Exposed to pathogens due to progressive decline in serum Igs
○ No issues in transferring maternal antibodies
Absence of lymphocytes and reduced antibodies (IgG and IgM)*
- Why should we be worried about these*
○ No effective adaptive immune response –> no antibodies being produced
○ Deficient in both B and T lymphocytes
§ Need B lymphocytes to produce antibodies
Why has this animal have IgG still? –> from maternal antibodies left, but is unable to produce their own IgG**
What are 4 causes of anaemia /pale mucous membranes in an animal?
○ Decreased RBCs production
○ Increased RBCs destruction
○ Loss due to haemorrhage
- Chronic infectious or inflammatory conditions
Explain pros between polyclonal and monoclonal antibody production *
- Polyclonal = inexpensive to produce, high affinity, recognise multiple epitopes, higher tolerance for differences in antigen
multiclonal = constant and renewable source
- consistency between lots
- specificity of monoclonal antibodies make them extremely efficient for binding of antigen within mixture of related molecules
Difference between direct and indirect ELISA
- direct = indicator enzyme is on primary AB
- indirect = indicator enzyme is on secondary AB
Neonatal immunity: 4 reasons why we would get failure of passive transfer (immunity) to the young from the mother (colostrum)?
- mother might not be producing antibodies/low
- premature birth
- premature lactation
- low quality colostrum
- ingestion failure (multiple births = competition for colostrum, newborn weakness, poor suckling ability)
- failure of young to absorb the colostrum
There are 5 different mechanisms that infectious agents my trigger an autoimmune response: list 3
1) Up-regulation of costimulatory molecules on APCs -> Antigen presenting cells
2) Modification of the cell antigenic pattern a. Expression of microbial antigen on cell surface or modification of antigenic structure 3) Formation of antigen-antibody complexes (type 3 hypersensitivity reaction > tissue damage) 4) Inflammation > damage to self tissue > structural modification of self-antigens, release of hidden antigens
5) Molecular mimicry: microbial antigens and self antigens sharing the same epitopes
Summary of the adaptive immunity: what are the 2 types of cells in adaptive immunity, and the actions/components of antibodies (list)
1) Antibodies
1. Classical pathway
2. Neutralisation of toxins
3. Opsonisation
4. Inhibition of absorption of viruses
5. ADCC (antibody dependent cellular cytotoxicity)
T lymphocytes
Compare/contrast live and killed vaccinations (3 points on each)
Live:
- Harder to store
- Risk of reversion
- Longer-lasting protection
- Fewer doses of the vaccination needed
- Stimulate humoral and cell mediated response in system
- Greater safety
Adjuvants unnecessary
Killed:
- Easier to store
- Unlikely to cause disease through residual virulence
- Do not replicate in recipient (dead)
- Stable on storage
- Will not spread to animals
- Unlikely to contain live contaminating organisms
Adjuvants required –> adjuvants help body produce immune response strong enough to protect person from disease
