4.1 Communicable Disease, Disease Prevention And The Immune System Part 2 Flashcards
Define immune response
Specific response to an antigen which involves lymphocytes and antibody production
Give examples of non-specific immune response
- macrophages engulf + digest pathogens in lymph node + present antigens
- neutrophils engulf + digest pathogens in blood + around the body
Explain how macrophages are involvded in cell mediated response
Present antigens on their surface to activate T helper cell to start cell mediated immunity
Give key aspects of T helper cells and how they are involved in cell mediated immunity
- made in bone marrow, mature in thymus gkand
- specic receprots that bind to antigens on APCs
- one activated release interlukins, stimulating T cells to divide by mitosis (develop into T-killer or T memory)
- interlukins cause B-lymphocytes to divide by mitosis + stimulate process of phagocytosis
Give key aspects of T memory cells and how they are involved in cell mediated immunity
- live for a long time
- part of immunological memory
- developed from cloned T cells
Give key aspects of B lymphocytes in humoral response
- activated by T helper cells
- divides by mitosis to form cloned B cells
- makes lots of B memory cells (provide immunological memory)
- makes plasma cells (which make antibodies)
Give key aspects of T killer cells and how they are involved in cell mediated immunity
- specific receptors for antigens
- release toxins (hydrogen peroxide) to kill infected cells + perforin to make holes in cell surface membranes
Give key aspects of T regulator cells
- controls + regulates the immune system
- stops immune system once pathogen is eliminated
- prevents autoimmune disease
Give key aspects of T helper cells in humoral response
- activates B lymphocytes at stat of humoral response
What is identification?
An antigen acts as an ID to tell your cells a pathogen if foreign
What is presentation?
Antigens presented on membranes by macrophages
What are distress signals?
Cells damaged by pathogens, so part of the pathogen is placed on the membrane to tell T lymphocyte to destroy it
What are cytokines?
Chemical messengers released by cells - cell signalling
What are interleukins?
Stimulate other T cells + B lymphocytes to divide rapidly by mitosis + stimulate phagocytosis
What is interferon
Stimulates T killer cells + inhibits virus replication
How does the interleukin cytokine work?
Has a specific shape which binds to complementary shaped receptors on B lymphocyte, which then activates mitosis of B lymphocyte
How do monokines work?
Macrophages release specific shaped monokines, which bind to other complementary receptors on B lymphocytes, activating cell activity (production of antibodies)
Give key aspects of T-lymphocytes
- processed in the thymus
- have receptors on their cell surface membrane
- millions of different shapes with different shaped receptors for binding to different antigens
Explain the process of T-lymphocytes in cell mediated immunity
- Surface of T-helper cell with specific receptors bind to antigens on APC - clonal selection
- T helper cell divides by mitosis - clonal expansion
- Formed clones of activated T helper cells
What do the clones of activated T helper cells do?
Release interleukins that:
- stimulate B cells to divide by mitosis
- stimulate phagocytosis
- stimulate the development of T killer cells
- may develop into T killer cells
- T killer cells release toxins that kill infected cells + release perforin
What is the difference between clonal selection and clonal expansion?
Clonal selection: When receptors of a T or B lymphocyte bind to a specific antigen, selectively stimulating the proliferation of the cell by clonal expansion
Clonal expansion: When selected T or B lymphocytes divide by mitosis to make clones - mass proliferation of T/B lymphocytes
Give key aspects of humoral immunity
- involves B-lymphocytes (processed in bone marrow)
- respond to antigens found outside cells (extracellular pathogens)
- deals with antigens found in humors/body fluids
- produces antibodies
- relies on activated T helper cells made in cell-mediated immunity
Give key aspects of B-lymphocytes
- have antibodies on their cell-surface membrane
- millions of different types of B-lymphocytes - each has a different antibody which binds to a different antigen
- when an antigen on a pathogen enters the body, a B-lymphocyte with a complementary antibody will bind to engulf it
- it then processes the antigen and presents it (has become an APC)
Explain the process of humoral immunity
- T helper lymphocyte becomes activated by APC
- B-lymphocyte presents antigens from pathogens on its surface - forming a B cell APC
- Activated T-helper lymphocyte binds to antigens presented on B-cell APC (clonal selection)
- Interleukins produfced by activated T helper cells to activate B cells
- Activated B lymphocyte divides by mitosis to form a clone of B cells (Clonal expansion)
- Clone differentiates into plasma cells + B memory cells
- Plasma cells produce specific antibodies for specific antigens
- Memory B cells provide immunological memory
What if the same antigen is encountered again?
- the memory B cells will recognise the antigen on the pathogen with their antibody receptor
- the memory cells divide rapidly making clones, which differentiate to form plasma cells - which make antibodies
- memory b cells remain in the body for a long time - however eventually reduce - need for booster vaccines
- secondary immune response
Compare humoral-mediated immunity and cell-mediated immunity
Humoral
- antibody mediated
- B lymphocytes
- mode of action: antibody circulating in serum
- primary defense against extracellular pathogens
Cell-mediated
- cell mediated
- t lymphocytes
- mode of action: direct cell to cell contact or secreted soluble products
- primary defense against intracellular bacterua
Compare secondary and primary response
Primary
- response takes longer
- smaller antibody conc in blood
- because of clonal selection + expansion
Secondary
- response is quicker
- larger antibody conc in blood
- due to immunological memory provided by memory cells
When might a secondary response take place?
- contact with pathogen for 2nd time
- contact with pathogen for 1st time but after relevant vaccination
What is active and passive immunity?
Active: Form own antibodies + memory cells from exposure
Passive: Get antibodies from mother via milk/placenta or injected with antibodies
What is natural and artificial immunity?
Natural: Exposure to pathogens through infection
Artificial: Immune system stimulated by safe form of antigen
Explain differences between active and passive immunity
Active
- exposed to antigen
- takes time to work
- long term protection
- memory cells made
Passive
- no contact with antigen
- immediate
- short term protection
- no memory cells
Define vaccination
Deliberate exposure to harmless antigenic material which activates an immune response to allow production of antibodies + memory cells
What is herd immunity?
When a population has a high % vaccinated so disease can no longer spread - vaccinations in school
What is the difference between a pandemic and epidemic?
Pandemic: Disease spreads rapidly across multiple countries
Epidemic: Disease spreads rapidly at a local or national level
Why are some diseases difficult to eradicate
- difficult to diagnose
- not enough of pop vaccinated
- boosters needed
- migrants can carry diseases
- can mutate frequently
- antivax/concerns about side effects
What is an autoimmune disease?
- immune system fails to recognise antigens as self
- incorreclty identifies as non-self so antibodies made against cells
- phagocytes/T killer cells attack + break down cells
What groups are considered more vulnerable and are given vacinations more regularly?
- elderly
- children
- pregnant women
- compromised immune system
- chronic diseases
- health workers
What can cause auto-immune diseases?
- genetics
- immune system responds to pathogen/microorganism abnormally
- T regulator cells not working properly
Why are new medicines needed?
- new diseases emerge
- some diseases still have no effective treatment
- resistance to antibiotics
- mutation/evolution of microorganism
Where are medicines sourced?
- plants + microorganisms
- animals
- extreme environments
Why may it be difficult to discover new drugs in the future?
- decrease in biodiversity due to habitat destruction
- deforestation, pollution, fishing, industrialisation
What modern methods are scientists using to make drugs?
- computer programmes
- design 3d models of molecules in bodies + antigens of pathogens
- allowing models of potential drug molecules to be built to target particular area of a molecule
Give key aspects of pharmocogenetics
- combining knowledge of drug action with personal genetic material
- doctors look at genome of patients + pathogen to increase chance of treatment working
- personalised medicine
How do antibiotics work?
- disrupt cell wall
- disrupt membranes
- inhibit protein synthesis
- inhibit DNA/RNA processes
- disrupt metabolism
What are multodiscs and why are they used by hospitals?
Discs which contain multiple antibiotics to test their effectiveness
- cheap
- quick to carry out tests
- compare antibiotics under same conditions
- allows early treatment of patient - don’t give patient antibiotic that doesn’t work
- prevent antibiotic resistance occuring
How does antibiotic resistance occur?
- mutation for resistance occurs in bacteria
- these bacteria survive and reproduce ( antibiotic = selection pressure)
- allele passed to offspring
- happens over many generations
Why is antibiotic resistance occurring in society?
- widespread antibiotic use in the past (over prescribing, use of agriculture, used for viral infections)
- people not finishing full course
- natural selection - selection pressure of antibiotic
- plasmids containing the antibiotic resistance genes shared by bacteria
