Cell recognition and immunity Flashcards
What are the key features of your innate immune system
- non-specific
- immediate
- same for all pathogens
What are the key features of the adaptive immune system
-specific
- spefic to each pathogen
- slower
Skin and skin flora (commensal bacteria) as a natural barrier to infection- innate immune system
barrier to opportunistic infection. Vit C maintains strong connective tissue. Flora outcompete pathogenic bacteria.
Blood clotting and inflammation as a natural barrier to infection- innate immune system
Blood clotting seals wounds, inflammation isolates region.
Phagocytosis as a natural barrier to infection- innate immune system
cellular digestion of microbes / infected cells / cellular debris.
Ciliated mucous membranes as a natural barrier to infection- innate immune system
Cilliated mucous membrane trap microbes in inhaled air.
Lysozyme as a natural barrier to infection- innate immune system
Lysosomes are in tears, saliva and stomach.
Hydrochloric acid as a natural barrier to infection- innate immune system
Hydrochloric acid is present in stomach.
Detail the process of phagocytosis.
- Phagocyte e.g. macrophage
- Pathogen e.g. bacteria release toxins
- Phagocyte engages chemotaxis using protein receptors in its cell surface membrane
- Engulfs through Endocytosis on binding with pathogen
- Phagosome (vesicle) containing pathogen
- Lysosomes contain hydrolytic lysozymes (e.g. proteases)
- Fusion forming phagolysosome / phagocytic vacuole
- Digestion by hydrolysis
- Release of contents by exocytosis
Define an Antigen
molecules, which when recognised as non-self (foreign) by the immune system and can stimulate an ‘immune response’ thus producing antibodies
often proteins on the surface of cells / viruses
N.B. proteins have a specific ‘tertiary structure’ / shape which can cause them to be antigens
Antigens are specific so allow the immune system to identify
pathogens (disease causing organisms) e.g. viruses, bacteria, fungi
cells from other organisms of the same species e.g. organ transplant, blood transfusion
pathogens contained in vacuoles / vesicle / phagosomes within phagocytes
toxins released from bacteria
abnormal / cancerous cells
describe the strcuture of an antibody
Proteins produce by B lymphocytes / plasma cells.
2 longer, heavy polypeptide chains bonded to 2 lighter polypeptide chains via disulphide bonds from two cysteine molecules
Constant region
Hinge region- Gives flexibility which allows the antigen- biding site to be placed at different angles when binding to antigens
Highly variable region acting as ‘antigen binding site’
Antigen binding site- Matches the epitodes (The part of the antigen which binds to the the antibody) of antigens Vary between antibodies and they have spefic amino acid sequences unique to the antigen
N.B.
each B cell produces a different antibody
each antibody can bind to one specific antigen shape
Antibody-antigen complex
The variable region of an antibody is complementary to a specific antigen molecule.
Binding creates an antibody-antigen complex.
Opsonisation
marks pathogen / cells for phagocytes
Agglutination
makes phagocytosis easier
Neutralisation
Neutarlise toxins so it cannot enter the host cell and the host cell remains healthy
Cell mediated response:
Phagocytes present antigen to T cells
Matching T cell receptors on T helper and T cytotoxic cells
T helper cells release cytokines
T cytotoxic cells undergo clonal expansion / mitosis
T cytotoxic cells bind to antigen and destroy pathogen / infected cell / cancerous cell by releasing perforin
Humoral / antibody mediated response:
Phagocytes present to B lymphocytes
B cell have antibody receptors in their cell surface membrane
Specific B cell binds to specific antigen
B cell engulfs antigen by endocytosis, hydrolysed and presented on the cell surface membrane
T helper cells bind to the antigen (peptide) on the specific B cell, releasing cytokines
Specific B cell undergoes clonal expansion / mitosis to form many plasma cells
Plasma cells produce and release matching antibodies
Antibodies can form antibody-antigen complexes - agglutination, opsonization, neutralisation, inactivation
Memory B / T cells form…
Explain active immunity
Exposure to antigen either through infection by pathogen or vaccination
Stimulates an immune response
Antibodies are produced
Memory B / T cells produced / long term
Memory cells will recognise antigen / pathogen if exposed in future leading to a rapid immune response
e.g. measles virus
Explain passive immunity
Antibodies only
No exposure to antigen
No immune response
No memory B / T cells
Immediate protection / short term
e.g. tetanus toxin
Primary and secondary immune response
Primary response is an initial exposure to an unknown antigen resulting in an immune response
Primary response will be slower but produces memory B / T cells (active immunity acquired).
Secondary immune response - memory B / T cells recognise the antigen and respond…
More rapidly
More intense / high concentration of antibodies released
Prolonged
Give four different forms of vaccines
- heat treated - active
- attenuated (live but alternated-active)
- fragments - active
- Antibodies only- passive
Define herd immunity
vaccination of a large number of people at the same time, interrupts transmission of the disease, reduces probability of infected coming into contact with non-vaccinated
Features of successful vaccine programme
- economically viable
- enough cover over population in order to obtain herd immunity where possible
- produce, store and transport effectively
- organised administration with trained staff
Why vaccines may not eliminate virus
- pathogens mutate
- variability alters the antigen shapes on the surface of pathogens for example flu
- antigens ‘drift’ gradual alteration (poor immune recognition)
- antigens ‘shift’ significant alteration in shape (no immunity, no recognition)
Why are antibiotics ineffective against viruses?
Viruses are acellular (non-living)
Viruses do not have any metabolism
Antibiotics target bacteria using specific modes of action e.g. affecting murein cell wall production or inhibiting protein synthesis
How does the HIV virus replicate?
Viral gp120 glycoprotein attachment proteins bind to CD4 receptors on T helper cells
On entering the host cell reverse transcriptase synthesises cDNA copy of the viruses RNA genome
Double stranded copy is then produced which integrates into the T helper cell’s chromosomal DNA
This is proviral DNA
Proviral DNA acts as a template for the transcription of viral RNA copies
Translation of viral genes to produce viral proteins e.g. capsid, reverse transcriptase, gp120
HIV viruses are assembled
HIV viruses exit the cell by “budding”, removing some of the cell membrane
This destroys the T helper cell
Explain how HIV causes the symptoms of AIDS.
Destruction of T helper cells results in an inability to fight infection
Fewer T helper cells can bind with specific B cells
Cytokines are not released
No clonal expansion of B cells
No plasma cells, so no antibody production against antigen
No clonal expansion of T cytotoxic cells
No targeting of antigen in body cells e.g. viral infection, cancerous cells etc.
Opportunistic pathogens can cause disease i.e. AIDS (acquired immunodeficiency syndrome)
Describe the use of monoclonal antibodies in targeting medication to specific cells.
Monoclonal antibodies can bind to one very specific antigen.
They are produced in vitro using hybridoma cells (specific B cells fused with mice cancer cells).
Examples:
Monoclonal antibodies are used in therapeutic medicine.
Breast cancer cells have specific protein antigen on the cell surface.
Monoclonal antibodies can target these.
Radioactive or cytotoxic drugs can be attached to the monoclonal antibodies thus killing the cancer cells.
Very specific / targeted with limited side effects.
Monoclonal antibodies are used in medical diagnosis.
Pregnancy test, HIV test, prostate cancer diagnosis (PSA protein in blood)
Describe the use of antibodies in diagnostic ELISA tests.
- HIV antigen / protein attached to well of test plate
- anti-HIV antibodies from infected patient forms antibody-antigen complex with HIV antigen - immobilised
Plate washed to remove any other unbound antibodies…
- Enzyme attached anti-human (mouse) antibodies bind to attached anti-HIV antibodies - immobilised
Plate washed to remove unbound antibodies / “free” enzyme complexes…
- Immobilised enzyme catalyses reaction producing a coloured substrate (HIV +ve)
Describe aseptic technique when inoculating a sterile, agar plate.
Cuts should be covered with waterproof dressing
No eating or drinking
Windows and doors closed to avoid airborne contamination
Wipe down bench with disinfectant before and after working
Report any spillages immediately
Work using aseptic technique
Wear a plastic, disposable apron
Flame inoculating loops until red hot OR sterilise the glass, L-shaped spreader
Tape dishes securely in cross formation after inoculation
Label all plates clearly: name, date, organism
Never remove lid of sealed Petri dish
Never incubate microorganisms above 30oC
Sterilise all media and containers after use in autoclave
Dispose of all cultures in Petri dishes in autoclave bag and autoclaving them
