immunology Flashcards
what is an immune response
body invaded by pathogen, series responses ensure pathogen rapidly identified (as non self) & destroyed before damage organism
what is an antigen
molecule (usually protein) that stimulates immune response that results in production of a specific antibody e.g. glycoproteins, glycolipids
how does the body know a cell is an own cell rather than foreign/pathogen
each cell has specifically shaped antigen on plasma cell surface membrane
what is a phagocyte
- WBC’s that can distinguish between cells that do or do not have correct antigens.
- engulf & destroy cells with non-self antigens (phagocytosis)
- detect chemical signals produced by pathogens
what makes phagocytosis non-specific and why is specific immunity needed
works same way for any cell/pathogen w non-self antigen. take too long destroy all pathogens in infection, could damage tissues so specific immunity needed
Describe the non-specific defence mechanisms the body may launch against pathogens (5 marks)
phagocytosis – No Mark
1. Pathogen is engulfed by the phagocyte.
2. Engulfed pathogen enters the cytoplasm of
the phagocyte in a vesicle;
3. Lysosomes fuse with vesicle releasing
digestive enzymes;
4. Lysosome enzymes break down the pathogen.
5. Waste materials are ejected from the cell by exocytosis;
Describe how a phagocyte destroys a pathogen present in the blood.
- Engulfs;
- Forming vesicle/phagosome and fuses with lysosome;
- Enzymes digest/hydrolyse;
Give two types of cell, other than pathogens, that can stimulate an immune response.
- (Cells from) other organisms/transplants;
- Abnormal/cancer/tumour (cells);
- (Cells) infected by virus;
what do T cells do:
responsible for stage of immune response called cellular response.
1) rather than T helper cells responding to pathogen and its antigens directly they bind to antigen presenting cells, with specifically complementary antigen
2) once TH cell ( w specific receptor molecule) bind to antigen it’s activated & rapidly clones by mitosis
the cloned TH daughter cells differentiate into 3 different types of cell:
1) TH:
- specific Th cell bind to antigen presenting cell
- release cytokines that attract phagocytes to area infection
- release cytokines that activate cytotoxic killer T cell (Tc)
- activates specifically complementary B cell
- form memory TH cells
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;
- Macrophage presents antigen on its surface;
- T (helper) cell with complementary receptor protein binds to antigen;
- T cell stimulates B cell;
- (With) complementary antibody on its surface;
- B cell divides to form clone secreting / producing same antibody;
- B cell secretes large amounts of antibody;
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 larger quantities AND quicker
describe B cell activation
- TH cell w correct receptor binds presented antigen, locates & activates specifically complementary B cell
- TH cell release cytokine chemicals that signal B cell clone by mitosis
- B cell differentiate 2 types cell:
1. plasma cells - produce & secrete specific antibodies into blood plasma
2. memory B cells - stay in body, respond pathogen rapidly if another infection
what is the primary response
process from initial recognition of pathogen as non-self up to producing antibodies
what is an antibody
Protein made in response to foreign antigen – has binding sites which bind specifically to an antigen. specific antibody is produced by specific ‘Plasma cell’.
what is the structure of an antibody?
- quaternary structure made of 4 polypeptide chains
- Y shape
- main part same in all (constant region)
- variable regions(binding sites) have diff primary structure so diff tertiary structure for each antibody
- specific antibodies only complementary 1 antigen
how do antibodies assist in destruction of pathogens
1)AGGLUTINATION: Specific antibodies bind to the antigens on pathogen and clump them together
2) OPSONISATION: marking pathogens so phagocytes recognise and destroy the pathogen more efficiently.
3) LYSIS: Bind to antigens and lead to destruction of the pathogens membrane.
4) ANTI-TOXIN & ANTI-VENOM: Bind to toxins or venom (both usually proteins) to prevent these molecules from binding to their complementary target receptors.
5) Prevent pathogen replication
Describe and explain the role of antibodies in stimulating phagocytosis.
- Bind to antigen OR Are markers;
- (Antibodies) cause clumping/agglutination OR Attract phagocytes;
what is the secondary response
activation of memory cells to produce antibodies
- rapid & extensive
- antigen destroyed before can cause disease (immunity)
- more antibodies produced, more rapidly
what is antigenic variability and why is it a problem
- 2ndary response effective, most pathogens same shape antigens, memory cells recognise
- some pathogens antigens mutate & change shape (e.g flu, HIV)
- difficult develop vaccine
Describe the difference between active and passive immunity
- Active involves memory cells, passive does not;
- Active involves production of antibody by plasma cells/memory cells;
- Passive involves antibody introduced into body from outside/named source;
- Active long term, because antibody produced in response to antigen;
- Passive short term, because antibody (given) is broken down;
- Active (can) take time to develop/work, passive fast acting;
what are vaccines
- contain antigens from dead or weakened pathogens
- stimulate primary response
- memory cells recognise antigen if re-infection
what is herd immunity
If enough individuals in the population are vaccinated (85%), then there is little chance of the disease spreading, therefore even non-vaccinated individuals will be protected.
vaccine ethical issues
- animal testing
- human testing…are they being put at risk?
- accessible to all or only rich?
- side effects vs possible benefit
- should be compulsory?
- loss genetic variability if organism eliminated
