2.4- Cell Recognition & The Immune System Flashcards
What is an antigen?
- Cell-surface molecule which stimulate immune response
- Usually (glyco)proteins, sometimes (glyco)lipids or polysaccharides
- Immune system recognises as “self” or “non-self”= enables identification of cells from other organisms of same species, pathogens, toxins & abnormal body cells
How does phagocytosis destroy pathogens?
- Phagocyte moves towards pathogen via chemotaxis
- Phagocyte engulfs pathogen via endocytosis to form a phagosome
- Phagosome fuses with lysosome (phagolysosome)
- Lysozymes digest pathogen
- Phagocyte absorbs products from pathogen hydrolysis
Explain role of antigen-presenting cells
Macrophage displays antigen from pathogen on its surface (after hydrolysis in phagocytosis)
Enhances recognition by T helper cells which cannot directly interface with pathogens/ antigens in body fluid
Give 2 differences between specific and non-specific immune responses
Nonspecific: (inflammation, phagocytosis)= same for all pathogens
Immediate
Specific: (B and T lymphocytes)= complementary pathogen
Time lag
Name the 2 types of specific immune response
- cell-mediated
- humoral
Outline process of cell-mediated response
- Complementary T helper lymphocytes bind to foreign antigen on APC
- Release cytokines that stimulate:
a) clonal expansion of complementary T helper cells (rapid mitosis): become memory cells or trigger humoral response
b) clonal expansion of cytotoxic T cells: secrete enzyme perforin to destroy infected cells
Outline process of humoral response
- Complementary T helper lymphocytes bind to foreign antigen on antigen-presenting T cell
- Release cytokines that stimulate clonal expansion (rapid mitosis) of complementary B lymphocytes
- B cells differentiate into plasma cells
- Plasma cells secrete antibodies with complementary variable region to the antigen
What is an antibody?
- Proteins secreted by plasma cells
- Quaternary structure: 2 ‘light chains’ held together by disulfide bridges, 2 longer ‘heavy chains’
- Binding sites on variable region of light chains have specific tertiary structure complementary to an antigen
- The rest of the molecule is known as the constant region
How do antibodies lead to destruction of a pathogen?
Formation of antigen-antibody complex results in agglutination, which enhances phagocytosis
What are monoclonal antibodies?
Antibodies produced from a single clone of B cells
What are memory cells?
- Specialised T helper/ B cells produced from primary immune response
- Remain in low levels in the blood
- Can divide very rapidly by mitosis if organism encounters same pathogen again
Contrast primary and secondary immune response
Secondary response:
- Faster rate of antibody production
- Shorter time lag between exposure & antibody production
- Higher concentration of antibodies
- Antibody level remains higher after secondary response
- Pathogen usually destroyed before any symptoms
What causes antigen variability?
- Random genetic mutation changes DNA based on sequence
- Results in different sequence of codons on mRNA
- Different primary structure of antigen= H bonds, ionic bonds & disulfide bridges form in different places of tertiary structure
- Different shape of antigen
Explain how antigen variability affects incidence of disease
- Memory cells no longer complementary to antigen= individual not immune= can catch disease more than once
- Many varieties of a pathogen= difficult to develop vaccines containing all antigen types
Compare passive and active immunity. Give examples of both types.
- both involve antibodies
- can both be natural or artificial
Passive natural: antibodies in breast milk/ across placenta
Passive artificial: anti-venom, needle stick injection
Active natural: humoral response to infection
Active artificial: vaccination
Contrast passive and active immunity
Passive:
- no memory cells & antibodies not replaced when broken down= short-term
- immediate
- antibodies from external source
- direct contact with antigen not necessary
Active:
- memory cells produced= long-term
- time lag
- lymphocytes produce antibodies
- direct contact with antigen necessary
Explain principles of vaccination
- Vaccine contains dead/ inactive form of a pathogen or antigen
- Triggers primary immune response
- Memory cells are produced and remain in bloodstream, so secondary response is rapid & produces higher concentration of antibodies
- Pathogen is destroyed before it causes symptoms
What is herd immunity?
- Vaccinating large proportion of population reduced available carriers of the pathogen
- Protects individuals who have not been vaccinated e.g. those with a weaker immune system
Suggest some ethical issues surrounding use of vaccines
- production may involve use of animals
- potentially dangerous side effects
- clinical tests may be fatal
- compulsory vs opt-out
Describe structure of HIV
- Genetic material (2x RNA) & viral enzymes (integrase & reverse transcriptase) surrounded by capsid
- Surrounded by viral envelope derived from host cell membrane
- GP120 attachment proteins on surface
How does HIV result in symptoms of AIDS?
- Attachment proteins bind to CD4 receptors on T helper cells
- HIV particles replicate inside T helper cells killing or damaging them
- AIDS develops when there are too few T helper cells for immune system to function
- Individuals cannot destroy other pathogens & suffer from secondary diseases/ infection
Why are antibiotics ineffective against viruses?
Antibiotics often work by damaging murein cell walls to cause osmotic lysis. Viruses have no cell wall.
Viruses replicate inside host cells= difficult to destroy them without damaging normal body cells
Suggest clinical applications of monoclonal antibodies
- Pregnancy tests by detecting HCG hormones in urine
- Diagnostic procedures e.g ELISA test
- Targeted treatment by attaching drug to antibody so that it only binds to cells with abnormal antigen e.g. cancer cells due to specificity of tertiary structure of binding site
Explain principle of a direct ELISA test
Detects presence of a specific antigen.
1. Monoclonal antibodies bind to bottom of test plate
2. Antigen molecules in sample bind to antibody. Rinse excess.
3. Mobile antibody with ‘reporter enzyme’ attached binds to antigens that are ‘fixed’ on the monoclonal antibodies. Rinse excess.
4. Add substrate for reporter excess. Positive result: colour change
