Immunology Flashcards
What is an antigen
foreign molecules on the surface that trigger an immune response.
Describe phagocytosis
*Pathogen engulfed by the phagocyte.
* pathogen enters the cytoplasm in a vesicle (phagosome)
*Lysosomes fuse with phagosome releasing hydrolytic digestive enzymes.
*Lysosome enzymes hydrolyse the pathogen.
* Waste materials are released from the cell by exocytosis
*antigens presented on the cell surface membrane and the phagocyte becomes an antigen presenting cell (APC)
Why is there constantly new vaccines for diseases?
*pathogens DNA can mutate regularly cause a change in their genes which therefore cuases a change i n shape due to different tertiary structure.
*lymphocytes/ memory cells are then not able to bind to the antigen.
This is antigen variabilty
What is an antibody?
Quaternary structure proteins (4 polypeptide chains)
● Secreted by B lymphocytes eg. plasma cells in response to specific antigens
● Bind specifically to antigens forming antigen-antibody complexes
What is agglutination
*when an antibody is able to bind to multiple same pathogens at the same time, leading them to form a big clump
Explain B cell activation
*antibody binds to antigen
*B cell takes in antigen thru endocytosis
*B cell binds with T helper cell receptor and activates it for clonal selection.
*they then undergo mitosis to produce plasma/ B memory cells
What are the roles of plasma and memory cells?
*plasma- produce antibodies
*memory- divide very rapidly into plasma cells and produce antibodies
What is an antigen presenting cell
- one of the host’s cells invaded by a pathogen and is displaying the antigen on its cell surface membrane
What do T-helper cells do?
*release cytokines
*trigger the maturation of B-lymphocytes into plasma cells
* activation of cytotoxic T cells
Role of cytotoxin T cells
*attach to the foreign antigens of infected cells and
*secrete toxic substances that destroy he infected body cells, and pathogen inside
Describe the response of T lymphocytes to a foreign antigen (the cellular
response)
Specific T helper cells with complementary receptors bind to antigen on antigen-presenting cell → activated and divide by mitosis to form clones which stimulate:
● Cytotoxic T cells → kill infected cells / tumour cells (by producing perforin)
● Specific B cells
● Phagocytes → engulf pathogens by phagocytosis
Describe the response of B lymphocytes to a foreign antigen (the humoral
response)
- Clonal selection:
● Specific B lymphocyte with complem recep binds to antigen
● This is then stimulated by helper T cells (which releases cytokines)
● divides (rapidly) by mitosis to form clones - Some differentiate into B plasma cells → secrete large amounts of (monoclonal) antibody
- Some differentiate into B memory cells → remain in blood for secondary immune response
Explain how antibodies lead to the destruction of pathogens
● Antibod bind to antigens on pathogens form an antigen-antibody complex
○ Specific tertiary structure variable region binds to complementary antigen
● Each antibody binds to 2 pathogens at a time causing agglutination (clumping) of pathogens
● Antibodies attract phagocytes
● Phagocytes bind to the antibodies and phagocytose many pathogens at once
What is a vaccine?
● Injection of antigens from (dead or weakened) pathogens
● Stimulating formation of memory cells
Explain how vaccines provide protection to individuals against disease
- Specific B lymphocyte with complementary receptor binds to antigen
- Specific T helper cell binds to antigen-presenting cell and stimulates B cell
- B lymphocyte divides by mitosis to form clones
- differentiate into B plasma cells which release antibodies
- Some into B memory cells
- On secondary exposure to antigen, B memory cells rapidly divide by mitosis to produce B plasma cells
- These release antibodies faster and at a higher concentration
Explain how vaccines provide protections for populations against disease
● Herd immunity - large proportion of population vaccinated, reducing spread of pathogen
○ Large proportion of population immune so do not become ill from infection
○ Fewer infected people to pass pathogen on / unvaccinated people less likely to come in contact
with someone with disease
differences between active and passive immunity
Active:
*initial response to pathogen
*slower as takes longer to create pathogens
*long term
*B memory cells involved
*antibodies secreted by B plasma
Passive:
*antibodies from other organism like mother
*faster
*shorter term immunity because antibody hydrolysed
*no exposure to pathogen
*no B memory cells
Explain the effect of antigen variability on disease and disease prevention
Antigens on pathogens change shape / tertiary due to gene mutations (creating new strains)
*So no longer immune (from vaccine or prior infection)
*B memory cell receptors cannot bind to / recognise changed antigen on secondary exposure
*Specific antibodies not complementary to changed antigen
Describe the structure of a HIV particle
*lipid envelope
*RNA and reverse transcriptase
*capsid
*attachment proteins
Describe the replication of HIV in helper T cells
*HIV attachment proteins attach to receptors on helper T cell
2. Lipid envelope fuses with cell-surface membrane, releasing capsid into cell
3. Capsid uncoats, releasing RNA and reverse transcriptase
4. Reverse transcriptase converts viral RNA to DNA
5. Viral DNA inserted into helper T cell DNA
6. Viral protein enzymes are produced
a. DNA transcribed into HIV mRNA
b. HIV mRNA translated into new HIV proteins
7. Virus particles assembled and released from cell
Explain how HIV causes the symptoms of acquired immune deficiency
syndrome (AIDS)
*HIV infects cell and kills Th cells
*Th cells not able to stimulate B lymphocytes, Tc cells, phagocytes
* B lymphocyte can’t divide into B plasma and B memory
*B plasma can’t produce antibodies for agglutination and destruction of patho
*immune system deterioraties- more prone ro pathogens
*pathogens reproduce, release toxins in cell and damage it
Explain how HIV causes the symptoms of acquired immune deficiency
syndrome (AIDS)
*HIV infects cell and kills Th cells
*Th cells not able to stimulate B lymphocytes, Tc cells, phagocytes
* B lymphocyte can’t divide into B plasma and B memory
*B plasma can’t produce antibodies for agglutination and destruction of patho
*immune system deterioraties- more prone ro pathogens
*pathogens reproduce, release toxins in cell and damage it
Explain why antibiotics are ineffective against viruses
Antibiotics inhibit cell wall synthesis, protein synthesis, DNA replication/transcription
*viruses r acellular and have no organelles so can’t be inhibited
What’s a monoclonal antibody
*antibody created by genetically identical cells
*same tertiary structure
Explain how monoclonal antibodies can be used in medical treatments
● Monoclonal antibody has a specific binding site complementary to antigen found only on a specific cell type
● drug attached to antibody
● Antibody binds to specific cell, forming antigen-antibody complex, delivering drug
Explain how monoclonal antibodies can be used in medical diagnosis
● Monoclonal antibody has a specific binding site to com antigen associated for diagnosis
● Dye attached to antibody
● Antibody binds to antigen, forming antigen-antibody complex
Explain how monoclonal antibodies can be used in medical diagnosis
● Monoclonal antibody has a specific binding site to com antigen associated for diagnosis
● Dye attached to antibody
● Antibody binds to antigen, forming antigen-antibody complex
Explain Direct Elisa
*potential antigen attached to well
*complementary Monoclonal antibodies added in w enzymes attached
*wash to get rid of any unbound antibodies (false positives)
*add substrate- enzyme will create products that release colour
Explain Direct Elisa
*potential antigen attached to well
*complementary Monoclonal antibodies added in w enzymes attached
*wash to get rid of any unbound antibodies (false positives)
*add substrate- enzyme will create products that release colour
Explain Sandwich Elisa
*attach SPECIFIC monoclonal antibodies attach to well
*add sample w potential antigens
*add enzyme bound monoclonal antibodies- if antigen present it attaches
*wash to remove unbound antibodies
*add substrate- enzyme creates products that release colour
Explain Sandwich Elisa
*attach SPECIFIC monoclonal antibodies attach to well
*add sample w potential antigens
*add enzyme bound monoclonal antibodies- if antigen present it attaches
*wash to remove unbound antibodies
*add substrate- enzyme creates products that release colour
Indirect ELISA
- Attach specific antigens to well
- Add sample with potential antibodies, wash well
- Add complementary monoclonal antibodies with enzymes attached → bind to antibodies if present
- Wash well → remove unbound antibodies
- Add substrate → enzymes create products that cause a colour change (positive result)
Indirect ELISA
- Attach specific antigens to well
- Add sample with potential antibodies, wash well
- Add complementary monoclonal antibodies with enzymes attached → bind to antibodies if present
- Wash well → remove unbound antibodies
- Add substrate → enzymes create products that cause a colour change (positive result)
Suggest the purpose of a control well in the ELISA test
● Compare to test to show only enzyme causes colour change
● Compare to test to show all unbound antibodies have been washed away
Discuss some general ethical issues associated with the use of vaccines and monoclonal antibodies
● Pre-clinical testing on animals - potential stress
*but animals not killed & helps produce new drugs to reduce human suffering
● Clinical trials on humans- side-effects
● Vaccines - may continue high risk activities and still pass on antigen
*drug- potential side effects
Suggest some points to consider when evaluating methodology relating to use of Vaccines and antibodies
● Was sample size large enough to be representative?
● Were participants diverse( age, sex, ethnicity and health status)
● control groups used for comparison?
● Was duration of the study long enough to show long-term effects?
● Was the trial double-blind (neither doctor / patient knew who was given drug or placebo) to reduce bias?
Suggest some points to consider when evaluating EVIDENCE and DATA
relating to the use of vaccines and monoclonal antibodies
● What side effects were observed, and how frequently did they occur?
● Was a statistical test used to see if there was a sig diff between start & final results?
● Was the standard deviation of final results large, showing some people did not benefit?
● Did standard deviations of start & final results overlap, showing there may not be a significant difference?
● What dosage was optimum? Does increasing dose increase effectiveness enough to justify extra cost?
● Was the cost of production & distribution low enough?
