Immune Response Flashcards
1
Q
What is immunity ?
A
- is the ability of organisms to resist diseases due to defence mechanisms that destroy pathogens before they can cause harm.
2
Q
Features of no specific response
A
- immediate response = happens all the time
- same process of all pathogens
- 1st line defence mechanism
E.g. physical barrier - skin, eyelashes, tears, sweat
Phagocytosis
3
Q
Features of specific response
A
- slower but specific to each pathogen
- 3rd line defence
E.g. cell mediated response - T cells
Humoral response - B cells
4
Q
How does cells recognise other cells ?
A
- each specific protein in each cell gives recognition - it has large variety and highly specific 3D tertiary structure
- allow immune system to identify pathogens, non self cells, toxins and abnormal body cells
5
Q
What is the 2nd line of defence include ?
A
- phagocytosis
- inflammation + fever
- anti microbial substance
6
Q
What is lymphocytes ?
A
- are whittle blood cells involved in specific immune response
7
Q
Features of T lymphocytes
A
- made in bone marrow, mature in thymus gland
- for cell mediated response
- respond to non self materials inside body cells - virus and own cells altered by cancer / transplanted
8
Q
Process of phagocytosis
A
- pathogens release cytokines as an attractant to cause phagocytes to move towards itself
- phagocytes have receptors on CSM that recognise and attach to chemicals on the surface of pathogens
- phagocytes engulf pathogens - form phagosome around
- lysosome of phagocytes move into and fuse phagosome= phagolysosome
- lysozymes hydrolyse p’s cell wall to destroy it
- soluble products from hydrolysis will be absorbed in cytoplasm of phagocytes
9
Q
How does phagocytes become an APC after phagocytosis ?
A
- it display non self antigens on its surface membrane = become APC to alert immune system cells to the presence of non self antigen
10
Q
What is antigens ?
A
- part of organisms that is recognised as non self by immune system and which triggers immune response
- proteins that are part of CSM of non self cells
- can triggers production of antibodies
11
Q
Features of B lymphocyte
A
- respond to humoral immunity
- made and mature in bone marrow
- involving antibodies that present in body fluids e.g. blood
12
Q
What does APC do ?
A
- triggers cell mediated response by T cells by displaying non self antigens on their CSM
13
Q
4 Examples of cells that display NS antigens
A
- infected body cells with viral antigens on CSM
- a phagocyte with destroyed pathogens
- transplanted cells - form different shapes antigens than own cell antigens
- cancer cells have abnormal shaped self antigens
14
Q
Process of cell mediated response
A
- Once pathogen’s antigens present on phagocytes = APC
- helper T cells have complementary receptors that attach to antigens of APC
- it activates Th and starts cloning by mitosis to make large amount of clones
- cloned Th differentiate into other types of cells
15
Q
4 cells that Th differentiate into :
A
- remains Th cells + activate B lymphocytes
- stimulate phagocyte into phagocytosis
- become memory cells for specific shaped antigens
- become cytotoxic T cells
16
Q
Function of cytotoxic T cells
A
- destroy abnormal or infected cells
17
Q
How does cytotoxic T cells destroy infected cells ?
A
- release perforin which embeds into CSM of our body cells to make a hole so allow substance in / out of the cell
- body cells are sacrificed to prevent viral replication
18
Q
Purpose of inflammation
A
- a result of the release of histamines = causes dilation of blood vessels SO more blood flow to infected area and deliver more phagocytes to destroy pathogens
19
Q
Where does B lymphocytes produce and mature ?
A
Bone marrow
20
Q
Role of B cells
A
- humoral response involving antibodies and cells
21
Q
1st Process of B cells defend response
A
- each B cells produce antibodies that have specific complementary shape to specific NS antigens that enters the blood or tissue fluids
- they attach to each other and A is taken into B cells by endocytosis = become APC
22
Q
2nd step of B cells DR
A
- then that B cell will collide with helper T cells = it activates B cells to go through clinal expansion by mitosis to make large amount of clones
- then differentiate into plasma cells or memory B cells
23
Q
Role of plasma cells
A
- make antibodies for primary immune response
- for immediate defence of body
24
Q
Role of antibodies
A
- it attached to NS antigens of pathogens and destruct it
25
Role of memory B cells
- for secondary immune response
- long lived and fast response than plasma cells
26
What is secondary immune response ?
- Bm divide again through clonal expansion by mitosis to make more plasma cells and so more antibodies that can attach to antigens = destruction for existed met antigens
- long lasting effect
- fast response
27
Why does secondary response need to be quick ?
- so more antibodies can be produce to destruct antigens as well as pathogens before it causes any harm and symptoms appear = active immunity
28
E.g. how is the specificity of antibodies depends on its variable regions ? (2)
- the primary sequence of proteins are specific
- complementary shapes enables attachment to specific antigens
29
Why does antibodies in fetus that are from the mother only provide short term immunity? (2)
- the from of antibodies as proteins not indefinite in fetus
- only B memory cells provide LT immunity
- they will be destroyed by feral lymphocytes
30
How does the ends of antibodies rotate to one another can help in the role in agglutination ? (1)
- allow antibody to bind to or easily make contact to antigens quickly
31
How does new born infant maybe protected naturally against pathogens ? (2)
- antibodies was transferred from mother
- from breast milk or across placenta
32
E.g. How does specific drug only target to kill cancer cells ? (3)
- antibody only binds / recognise cancer cells
- due to antibody -antigen complex
- enzyme activates thee drug at cancer cells only
33
How antigenic variability has caused some people to become infected more than once with certain virus ? (2)
- memory B cells don’t recognise new NS antigens
- previous antibodies aren’t effective but takes time to produce effective antibodies
34
Passive immunity
- antibodies produced into individuals from an outside source, no memory cells formed, not long lasting immunity
E.g. from mother’s placenta or breast milk to placenta and anti venom
35
Active immunity
Antibodies produced by its own immune system - long lasting immunity
= natural and artificial active immunity
36
How vaccines work ?
- inject an attenuated pathogen in your body which then activates 1st immune response
37
Factors affect success of vaccines
- economically available in sufficient quantities
- side effects can discourage pop.
- producing, storing, and transporting
- train staff to administrate vaccines
- herd immunity needed to break transmission
38
What causes unsuccessful vaccine ?
- can’t induce immunity to everyone
- antigenic variability
- pathogens mutation
- some hide inside organs or cells e.g. cholera in intestines
- objection due to ethics or beliefs
39
Ethics of vaccine
- animal use in testing
- side effects
- trials in developing countries to test effectiveness
- compulsory
- expense
- benefits to population
40
What is HIV ?
= human immune deficiency virus
- A virus that affects immune system leads to AIDS (acquired immune deficiency syndrome ) when immune system deteriorates and fails that exposed to further serious infection
41
How does HIV destroy immune system function ?
- HIV kill helper T cells means no longer ale to activates cytotoxic T cells, B cells and phagocytes that kill pathogens
42
Structure of HIV
- GP120 attachment proteins
- capsid, made of proteins
- lipid envelope - made from CSM of previous host cell
- matrix
- RNA
- reverse transcriptase enzyme
43
How does HIV replicate ?
1) attach to CSM of host helper t using attachment proteins and fuse with it
2) capsid replaced into Th and RNA released into Th cytoplasm
3) reverse transcriptase used to make DNA from its RNA template
4) insert that DNA into human DNA
5) use Th enzyme to make viral proteins
6) viral proteins joined with new viruses = burst to infect other cells
44
What serious infection that can easily kill patients with HIV ?
- candidiasis of respiratory system
- parasite infection
45
Why does antibiotics not work on HIV ?
- A.b works by interfering bacteria’s metabolic reactions by targeting its enzymes and ribosomes
- but viruses live in host cells that uses normal cells enzymes and ribosomes so can’t be targeted
46
What drug used to treat HIV ?
- antiviral drug = reverse transcriptase inhibitors
- slows down progression of HIV and AIDS by targeting reverse transcriptase of HIV
47
Why use micro-titre plates ?
- can perform multiple samples at one time
- can be treated with dilution
48
Where is ELISA test used ?
- detecting drugs in blood samples
- detecting antibodies from another antigens
- allergy testing
49
How does HIV replicate? (6)
1) attachment proteins attach to receptors on helper T cells surface
2) virus fuses with CSM of Th to allow viral RNA enters the cell
3) reverse transcriptase converts RNA into DNA
4) DNA inserted into Th cell DNA in the nucleus
5) DNA then transcribed and viral proteins produced
6) viruses assembled and released from cell causes Th to burst
50
Vaccines protect people against disease. Explain how (5)
M1 vaccines injected with attenuated form of pathogen in your body .
M2 memory cells will be produced
M3 second exposure, memory cells produce antibodies by plasma cells by recognition of same pathogen
M4 rapidly produce more antibodies .
M5 antibodies cause agglutination and trigger other repose to destroy pathogen
51
Diffences of primary and secondary response (3)
M1 primary takes time for antigen presentation and clonal selection and expansion, takes time for B cells to differentiate into plasma cells WHEREAS secondary have no clonal selection needed as Bm already circulate inside the blood
M2 primary produce less antibodies but secondary produce more
M3 primary produce antibodies slower due to clonal expansion and differentiation but secondary do quicker as Bm existed in bloodstream so can differentiate into antibodies by plasma cells much quicker
