immunology Flashcards
state 2 ways pathogens can cause harm/disease?
- bacteria releases toxins that directly damage tissue
- pathoigens replicate inside and destroy host ells
define an antigen
- molecule that stimulates an immune response
- results in the production of a specific antibody
examples of antigens
glycoproteins
glycolipids
retrovirus
virus with single stranded RNA
describe the non specific immune defence mechanism the body may launch against pathogens
phagocytosis
- pathogen is engulfed by the phagocyte
- engulfed pathogen enters cytoplasm in a vesicle (phagosome)
- lysosomes fuse with phagosome, releasing hydrolytic enzymes (lysozymes)
- lysozymes break down/hydrolyse the pathogen
- waste materials ejected via exocytosis
- phagocyte presents antigens on csm
describe how a pjhagocyte destroys a pathogen present in the blood
- engulfs
- forms a vesicle
- lysosome fuses with vesicle
- enzymes hydrolyse
give 2 other types of cells, other than pathigens, that stimulate an immune response
- cells from other organisms
- cancer/abnormal cells
- cells infected by viruses
cellular response
- phagocyte presents antigen on csm
- T helper cell with a specific receptor binds to antigen, activating it
- rapidly divides by mitosis
- produces many T Helper cells with specifically complementary antigens
when a vaccine is given to a person, it leads to the production of antibodies against a disease causing organism. describe how.
- vaccine contains antigen from pathogen
- phagocyte presents antigen on csm
- t helper cell with specifically complementary receptor binds to the antigen
- t cell stimulates the b cell with a complementary antibody on its surface
- b cell divides by mitosis
- produces same antibody
- b cells secrete large amounts of antibody
what is the role of the t helper cell
- binds to APC
- releases cytokines that attract phagocytes to area
- releases cytokines that activate cytotoxic killer T cells (Tc)
- activates specifically complementary b cell
- form memory Th Cells
what is the role of cytotoxic killer t cells
- destroys infected body cells presenting antigen
- binds to APCs
- releases perforin which creates holes in csm, destorying APC
explain how the humoral response leads to immunity
- b cells specific to the antigen reproduce by mitosis
- b cells produce plasma and memory cells
- second infection produces antibodies in a larger quanitity and quicker
antibody
proteins made in response to antigens
- binding sites bind specifically to antigen
- specific antibody produced by a specific plasma cell
antibody structure
- 4 structure, 4 polypeptide chains, Y shaped
- variable region has different primary structure and didfferent 3 structure
describe and explain the role of antibodies in stimulating phagocytosis
- bind to antigen
- cause clumping
how do antibodies assist in the destruction of pathogens?
- aggultination: clump pathogens together after binding to antigens
- opsonisation: mark pathogens so phagocytes recognise and destroy pathogens more easily
- binds to toxins
- prevent pathogens replication
secondary response
- activation of memory cells to produce antibodies
- second is rapid and extensive
“ more antibodies are produced more rapidly”
antigenic variability
antigens mutate or change shape
eg: flu, HIV
- difficult to develop vaccines against it
- not recognised by memory cell, no 2ndary response
describe the difference between active and passive immunity
active vs passive
- memory cells vs no memory cells
- production of antibodies via plasma cells vs passive involves antibody introduced from some outside source
- active long term because antibody produced in response to antigen
- passive short term because antibody broken down
- active takes time vs passive fast acting
state why some antibodies are referred to as monoclonal
- produced from the same plasma cell
- countet the same specific antigen
tests using monoclonal antibodies are specifc. use your knowledge of protein structure to explain why.
- specific primary structure
- specific tertiary structure
- specifically complementary to one antigen
vaccinations
- contain dead, weakened pathogens
- some may cause side effects
herd immunity
if enough people are vaccinated, little chance of disease spreading
- even nonvax will be protected
uses of monoclonal antibodies
- resesarch
- pregnancy tests/ ELISA tests
- targetting drugs
- killing specifc cells
elisa test
monoclonal antibody fixed to surface of test well
- sample binds to antibody due to complementary shape
- second monoclonal antibody (with enzyme attached) added, binds to molecule
- washed so any unbound antibodies with enzyme are washed away
- substrate added, colour change=positive result
describe the role of antibodies in producing a positive test result in an ELISA test
- first antibody complementry to antigen
- second antibody with enzyme attached is added
- second antibody attaches to antigen
- solution added and colour change
describe the structure of the human immunodeficiency virus (HIV)
- RNA as genetic material
- reverse transcriptase
- protein capsid
- phospholipid envelope
- attachment proteins
HIV replication
- protein on HIV binds to protein found on T helper cells
- capsid fuses with csm and releases viral RNA and enzymes into helper T cell
- HIV’s reverse transcriptase converts viral RNA into cDNA using host nucleotides
- viral cDNA inserted into host genome in nucleus.
- person now infected
- transcription of viral DNA into viral RNA which is translated to produce HIV proteins
- reduction in number of Th cells over time
How can AIDS be detected?
checking number of T helper cells
200 Th cells in AIDS and 800-1200 Th uninfected
- compromises immune system so secondary infections more vulnerable to kill
describe how a person infected with HIV will develop AIDS and die of secondary infections
- high viral load leads to increase in destruction of T hekper cells
- less activation of B cells
- Less production of plasma cells/antibodies
- more able to destroy other pathogens
why dont antibiotics work on viruses?
- prevent bacteria making a normal cell wall by targetting 70s ribosomes
- unable to resist osmotic presure, cells burst due to increase cell volume of water by osmosis
- viruses have capsid
- spend time in host cell so out of reach
