immunity Flashcards
antigen
foreign molecule
stimulates immune repsonse - production of antibody
How are cells identified by the immune system?
Each type of cell has specific molecules on its surface that identify it
Often proteins → have a specific tertiary structure (or glycoproteins / glycolipids)
what type of cells can immune system identify
- Pathogens - disease causing microorganisms
- Cells from other organisms of the same species
- Abnormal body cells eg. tumour cells or virus-infected cells
- Toxins (poisons) released by some bacteria
Describe phagocytosis of pathogens
1 Phagocyte attracted by chemicals / recognises (foreign) antigens on pathogen
2 Phagocyte engulfs pathogen by surrounding it with its cell membrane
3 Pathogen contained in vesicle / phagosome in cytoplasm of phagocyte
4 Lysosome fuses with phagosome and releases lysozymes
5 Lysozymes hydrolyse / digest pathogen
what do t lymph recognise
antigen presenting cells
what do t lymph do
Specific helper T 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 (humoral response - see below)
● Phagocytes → engulf pathogens by phagocytosis
Describe the response of B lymphocytes to a foreign antigen
humoral response
- Clonal selection:
○ Specific B lymphocyte with complementary receptor (antibody on cell surface) binds to antigen
○ This is then stimulated by helper T cells (which releases cytokines)
○ So 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
what are antibodies
● 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
describe how antibodies work
● Antibodies bind to antigens on pathogens forming an antigen-antibody complex
○ Specific tertiary structure so binding site / 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
primary response
Primary - first exposure to antigen
○ Antibodies produced slowly & at a lower conc.
○ Takes time for specific B plasma cells to be
stimulated to produce specific antibodies
○ Memory cells produced
secondary response
● Secondary - second exposure to antigen
○ Antibodies produced faster & at a higher conc.
○ B memory cells rapidly undergo mitosis to
produce many plasma cells which produce
specific antibodies
whats a vaccine
● Injection of antigens from attenuated (dead or weakened) pathogens
● Stimulating formation of memory cells
how do vaccines protect 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
- Some differentiate into B plasma cells which release antibodies
- Some differentiate 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
active immunity
initial exposure to antigen
memory cells involved
Antibody produced and secreted
by B plasma cells
slow and takes longer to develop
Long term immunity as antibody can be produced
LT response to a specific antigen again
passive immunity
no exposure to antigen
no memeory cells
antibody introduced from another organism
fast acting
short term
antigen variablity
● Antigens on pathogens change shape / tertiary structure 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 / cannot bind to changed antigen
structure of HIV
lipid envolope
rna sqiggly line
RT mushroom
capsid circles
attachment protein
replication of hiv in t helper cells
- HIV attachment proteins attach to receptors on helper T cell
- Lipid envelope fuses with cell-surface membrane, releasing capsid into cell
- Capsid uncoats, releasing RNA and reverse transcriptase
- Reverse transcriptase converts viral RNA to DNA
- Viral DNA inserted / incorporated into helper T cell DNA (may remain latent)
- Viral protein / capsid / enzymes are produced
a. DNA transcribed into HIV mRNA
b. HIV mRNA translated into new HIV proteins - Virus particles assembled and released from cell (via budding)
why are antibiotic ineffectivr against virus
● Viruses do not have metabolic processes (eg. do not make protein) / ribosomes
● Viruses do not have bacterial enzymes / murein cell wall
What is a monoclonal antibody?
● Antibody produced from genetically identical / cloned B lymphocytes / plasma cells
● So have same tertiary structure
