CHAPTER 5: IMMUNITY Flashcards
1
Q
what are diseases
A
- a disease is a condition that interferes with the normal functioning of an organism; usually with specific symptoms.
- can be infectious or noninfectious
2
Q
what are pathogens
A
- Most microbes are harmless (non-pathogenic) - only about 1% can cause disease
- Most pathogens are species-specific and tissue-specific
- Pathogens are agents that cause diseases in their hosts
- can be extracellular → pathogen in the body but not in the cells yet (innate response)
- can be intracellular → pathogens in the cells (adaptive response)
3
Q
cellular vs non-cellular pathogens
A
- cellular: made of cells and can reproduce independently
- bacteria, parasites (worms), fungi, protozoa
- non-cellular: not made of cells and cannot reproduce independently → need the cells of the host to reproduce (hijack)
- viruses, prions
4
Q
what are antigens
A
antigens are substances that cause/stimulate an immune response
5
Q
self vs non-self antigens
A
- Self-antigens: antigens on cells that are recognised by self-receptors as being part of the same body
- tolerated by the immune system
- Non-self antigens: antigens that do not belong to the body’s own cells
- attacked by immune system
6
Q
distinguishing self from non-self
A
- plasma membrane of this immune cells carries:
- self-antigens that identify this immune cell as ‘self’
- cell surface receptors for self-antigens so that this cell can identify and not attack other body cells
- cell surface receptors for foreign antigens so that the immune cell can identify foreign material and signal other immune cells to eliminate it
7
Q
MHC I vs MHC II markers
A
- both are located on the outside of cells, anchored to the cell membrane and are specific to individuals.
- MHC-I markers are present on all nucleated cells
(not red blood cells) of the body and present the peptide fragments from inside the cells- they signify if a cell is ‘self’ or ‘non-self’
- if the correct MHC-I marker is not detected, immune cells will cause it to undergo apoptosis.
- MHC-II markers are only found on specific cells in the immune system such as macrophages, dendritic cells, and B lymphocytes
- all involved in antigen presentation → present the antigens from outside the cell.
8
Q
bacteria
A
- prokaryotic microbes and their genetic material is double-stranded DNA
- If bacteria multiply in areas they are not normally found they can cause disease
- Intracellular and extracellular
- Symptoms of bacterial infection are often caused by the toxins the bacterium produces
Bacteria can cause disease in humans if:
1. They can enter a person who can act as a host.
2. They have the capacity to reproduce within the host.
3. They act adversely on tissues in their host (exotoxins, adverse enzyme production)
9
Q
protozoans
A
- single-celled, eukaryotes
- infection by ingestion of cysts by sexual transmission or insect vectors
- able to multiply in humans, enabling them to survive in a human host while causing disease.
- symptoms: blood, gut and lymphatic system
- Eg. Malaria – bites of mosquitos
- Ingesting contaminated food
10
Q
fungi
A
- eukaryotes
- grow from the tips of filaments (hyphae) that make up the bodies of the organisms (mycelia)
- opportunistic pathogens - immune system is weak
- usually external or skin infections
- Eg. Candida albicans - Thrush (oral
candidiasis) - Athletes food – tinea (Trichophyton spp.)
- Eg. Candida albicans - Thrush (oral
11
Q
parasites (worms)
A
- (not microbes) can be seen with the naked eye
- transmitted via soil contaminated with human faeces that contains eggs of those worms
- Eg hookworm, roundworms, whipworms
12
Q
viruses
A
- comprise of nucleic acid (DNA or RNA) surrounded by one or more coats of protein.
- replicate only within host cell
- viruses cause disease by killing body cells
- to make more viruses, a virus takes over a host cell and uses it as a ‘factory’
- release of viral particles from an infected cell may be by budding or by cell lysis
- infected host cell ‘explodes’ as its plasma membrane disintegrates and viral particles are released into the extracellular fluid from where they can infect other cells.
13
Q
what is the immune system
A
the body system that helps resist infections and disease through specialised cells
14
Q
3 levels of the immune system
A
INNATE - present from birth, no immunological memory, not acquired
- the first line of defence
- innate
- non-specific
- skin, stomach acid, etc.
- the second line of defence (hasn’t infected cells yet)
- innate
- non-specific
- macrophages, inflammation, complement proteins
- the non-specific cellular and molecular responses to pathogens that have breached the first line of defence and have entered the body.
- The innate immune response is nonadaptable, and does not change during an individual’s lifetime.
ADAPTIVE - more targeted to a specific pathogen
- third line of defence
- acquired (learns and has memory)
- specific
- B cells, T cells, antibodies
- takes time to develop
15
Q
first line of defence
A
- physical barriers act to prevent the entry of pathogens
- chemical barriers act to inhibit the growth or development of pathogens and/or act to destroy pathogens
- microbiota barriers act to prevent the growth or colonisation of microorganisms that may be pathogenic.
16
Q
first line of defence: physical barriers
A
- intact skin
- skin microbiome
- mucus: traps and prevents entry of pathogens
- earwax
- nostril hair
- acidic environment - digestive, reproductive, and urinary systems
17
Q
first line of defence: chemical barriers
A
- destroys pathogens on the outer body surface, body openings, and on inner body linings
- sweat, mucus, tears, saliva (all have enzyme lysozyme that kills pathogen)
- stomach acid - kills pathogens
18
Q
first line of defence: microbiological barriers
A
- presence of normal flora
- non-pathogenic bacteria in regions of the body
- inhibits the growth of pathogenic microbes
- also called “commensal bacteria”
- gut contains many microbes [mainly bacteria] which exist in a “mutualistic relationship” with the person.
- prevent the growth of colonies of other species of bacteria by outcompeting them for nutrients and adhesion sites, and secreting antimicrobial chemicals
19
Q
first line of defence: plant barriers
A
- plants do not have an immune system comparable to animals, but they have developed structural, chemical and protein-based defences
- cuticle: waxy covering - prevents penetration and virus and bacteria entering
- thick bark
- leaf orientation (horizontal or vertical) - vertical is less susceptible to pathogens
- thorns and spikes
- antimicrobial or antifungal compounds (plants can naturally make this)
- formation of galls
- growing ‘gall’ tissue around the area containing the infective agent to prevent spread to other areas (containing the pathogen)
20
Q
second line of defence
A
if the preventative strategies don’t keep the pathogen out, foreign antigens need to be recognized
21
Q
cells of the immune system
A
- immune system cells are white blood cells → leukocytes (another name for white blood cells) made in bone marrow
- each has a specific role in defending the body from pathogens and infectious disease
- involved in innate immunity
22
Q
dendritic cells (phagocyte)
A
- found in tissues
- reside in and patrol the skin and mucosal surfaces
- can migrate to lymph nodes
- engulf and destroys pathogens by phagocytosis
- antigen-presenting cells that can activate an adaptive immune response
23
Q
what are phagocytes
A
- phagocytes (macrophages, monocytes, neutrophils, dendritic cells)
- do not recognize specific antigens but instead recognize patterns on antigens
24
Q
macrophages (phagocyte)
A
- found in tissues
- identify and eliminate pathogens by phagocytosis
- antigen-presenting cells that can activate the adaptive immune system
25
Q
eosinophils
A
- present in the respiratory, gastrointestinal and urinary tracts
- assist in defending against larger multicellular parasitic agents
- granules with toxic chemicals and induce the degranulation of histamines from mast cells
26
Q
neutrophils (phagocyte)
A
- found in blood
- first cells to arrive at the infection site
- attracted to foreign materials by chemical signals
- engulf and destroy pathogens by phagocytosis
- granules in cytoplasm contain antimicrobial agents or enzymes to assist with destruction
27
Q
process of phagocytosis
A
- the phagocytes recognize the microbe via a receptor
- the phagocyte engulfs the microbe via endocytosis
- the vesicle containing the microbe fuses with a lysosome
- the lysosome (organelle) empties its digestive enzymes into the vesicle → lysosomes have a lot of digestive enzymes
- the enzymes digest the microbe
- the particles are released from the phagocyte
28
Q
natural killer (NK) cells
A
- found in blood/lymph
- kill virus-infected cells
- attack cells lacking self markers - missing/abnormal MHC markers
- have granules filled with potent chemicals
- NATURAL KILLER CELL ACTION: DEGRANULATION
- when an NK cell recognizes an abnormal cell, it releases proteases (enzymes) and perforin
- perforin punches holes in the cell membrane, allowing the proteases to enter
- these trigger apoptosis (destroys it from the inside)
29
Q
mast cells
A
- found in tissue - close to the external environment (eg. surface of the skin)
- mediate inflammatory response
- contains chemicals in granules - cytokines, histamine
- histamines increase permeability - in terms of blood vessels
- cytokines attracts other immune cells
30
Q
humoral innate immunity
A
- immune response in the ‘humors’ → body fluids
- eg. lymph, blood
- complement proteins
- interferons
- (extracellular body fluids)
- soluble/dissolved in fluid eg. blood, lymph
31
Q
complement proteins
A
- inactive enzymes in blood that complement the function of immune cells
- activated when they make direct contact with the molecules on the surface of a pathogen
- complement proteins activate other complement proteins to form a cascade (like a domino effect)
- complement proteins can cause inflammation (acts as chemotaxis), enhance phagocytosis or cause lysis
works against both cellular and non-cellular pathogens
32
Q
opsonisation (action of complement proteins)
A
- makes pathogens more susceptible to elimination by phagocytosis
- coat the surface of pathogen cells and the phagocytes have receptors for the complement proteins (bind to the opsonised microbe)
33
Q
chemotaxis (action of complement proteins)
A
- movement of cells in response to a chemical stimulus
- small complement peptides that diffuse from the pathogen surface act as chemical signals
- attracting immune cells involved in the inflammatory response to the site of the infection
34
Q
lysis (action of complement proteins)
A
- membrane attack complex (MAC) forms on the plasma membrane of the pathogen due to complement proteins
- the MAC inserts into the plasma membrane of the pathogen, producing a pore
- this allows fluid to enter and causes the pathogen cell to swell and burst
35
Q
interferons
A
- a group of cytokines (signalling proteins)
- virally infected cells release interferons to prepare neighbouring cells for a possible ’attack’
- the interferon secreted acts as warning signals to nearby cells
- signal change in plasma membrane making entry of virus more difficult (make PM less fluid)
- signals neighbouring uninfected cells to prepare to destroy RNA to reduce protein synthesis
- signal neighboring infected cells to undergo apoptosis
- activates immune cells such as NK cells
36
Q
inflammation - major weapon of innate immunity
A
- reaction to an infection/injury/damaged tissue/pathogen
- localised to the site
- prevent the spread of antigen, removes the pathogen and dead cells, restores the tissue to normal (healing)
- results in heat, pain, swelling and redness
37
Q
process of inflammation
A
- vascular stage → blood cells
- cellular stage → immune cells
- resolution → normal state restored and inflammation is stopped
38
Q
vascular stage
A
- damaged cells release cytokines → attracts neutrophils
- mast cells release histamines → causes capillaries to become permeable (leaky) and wider (vasodilation)
- vasodilation: increases blood flow to damaged area and the increased blood flow produces heat and redness
- permeable: protein-rich fluid (exudate) can escape from capillaries to the infected region
- the exudate causes swelling and the swelling causes pressure on surrounding tissues, stimulating nerve endings→ cause pain
39
Q
cellular stage of inflammation
A
- phagocytes are attracted to the site by cytokines → phagocytose antigen
- complement proteins opsonise pathogens → phagocytosis can occur
- platelets travel to the site to block wound → important for clotting
- pus indicates that this stage is occurring
- consists of mainly dead phagocytic cells and other immune cells, dead tissue, dead pathogens
40
Q
resolution stage
A
- occurs when the tissue is returned to normal state → infection is under control
- the release of cytokines stop and anti-inflammatory cytokines are released
- resolution occurs when the antigen is removed from the site of infection
- if resolution does not occur, chronic inflammation may occur
41
Q
lymphatic system
A
- transport network
- consists of
- lymph
- lymph vessels
- lymph organs
- production and maturation of immune cells
- allows for the process of antigen recognition by T and B cells
42
Q
roles of components of lymphatic system
A
- thymus: maturation of T cells
- bone marrow: maturation of B cells (B+ T both made in bone marrow but B stays there and T cells move through the lymphatic system to the thymus)
- lymph nodes: meeting, activation and response
- lymph vessels connect lymphoid organs (transport)
-
spleen: filters blood
- contain B, T, dendritic cells and macrophages
- activation of B and T cells
43
Q
primary lymphoid organs
A
- primary tissue where B and T cells are made
- bone marrow
- source of pluripotent stem cells - leukocytes originate (lymphocytes: B and T cells)
- the site of maturation of B cells
- thymus
- thymus is the site where T cells mature after being released from the bone marrow
44
Q
secondary lymphoid organs
A
- mature B and T cells are activated
- where antigens presentation occurs (also filter lymph - the fluid)
- lymphoid organs contain lots of lymphocytes → B and T cells
- spleen
- filters blood → clearing of bacteria and/or viruses and worn-out red blood cells
- contains T and B cells
- contained macrophages and dendritic cells
- lymph nodes
- main site of antigen recognition → leading to the adaptive immune response
45
Q
lymph nodes
A
- small bean-shaped structures
- the site of ANTIGEN RECOGNITION in which T and B lymphocytes come into contact with their specific antigens → adaptive immune response occurs
- swell when infections occur → number of B and T cells in the lymph nodes increase → this produces the so called swollen glands
46
Q
maturation of lymphocytes
A
- activated by meeting their complementary antigens
- antigens presented by macrophages or dendritic cells
- B and T lymphocytes have receptors for only ONE SPECIFIC ANTIGEN
- B cells make antibodies to eliminate pathogens (antibody-mediated)
- T cells eliminate infected or diseased cells (cell-mediated)
47
Q
how is adaptive immune response initiated
A
- pathogen enters (first line of defence breached)
- meet at the entry point by phagocytes that engulf and eliminate’
- some of the digested fragments of the antigen are displayed on the MHC II receptors on the surface of dendritic cells or macrophages
- APCs migrate to the lymph nodes and present the antigen to the T helper cells that carry complementary receptors for the antigen
- T helper cells release cytokines
- initiates the adaptive immune response
- humoral B cells
- cell-mediated T cells
- NEUTROPHIL IS NOT AN ANTIGEN PRESENTING CELL BUT CAN UNDERGO PHAGOCYTOSIS
48
Q
role of helper t cells
A
- only activated by antigen-presenting cells that present antigen on the MHC II marker
- once active, clone and secrete cytokines which
- help activate cytotoxic T cells (Tc)
- help activate B cells into plasma cells
- help activate macrophages to remove antibody-coated pathogens by phagocytosis
49
Q
how does antigen presentation occur
A
- pathogen undergoes phagocytosis
- antigen fragment is presented on the MHC II molecule to helper T cells
- helper t cells have a receptor
50
Q
what is adaptive immunity
A
- adaptive immunity involves a specific response against a specific pathogen → with memory retained for future infections
- this immune response is usually only required if an infection is not cleared by the innate response
- specificity: adaptive immune cells (B and T cells) have unique receptors that recognise specific antigens
- immunological memory: remember antigens after primary infection → to enable a more rapid and stronger response in case of future infections
51
Q
adaptive cell mediated response
A
- intracellular pathogens
- T cells deliver the cell-mediated immune defences that include the direct elimination of the pathogen-infected cells and other abnormal cells such as cancer cells
- are activated by antigen-presenting cells
- stimulated by Th
- memory T cells
- cytotoxic T cells
52
Q
humoral response
A
- extracellular pathogens
- B cells deliver the humoral immune defences by
- secreting antibodies that bind to surface antigens on pathogens and label them for elimination → antibodies also bind to soluble toxins
53
Q
action of cytotoxic T cells
A
- cytotoxic T cells recognise virus-infected cells and can also recognise abnormal proteins
- eg. DNA mutations in cancer cells which often results in abnormal MHC-I markers
- this means cytotoxic T cells can target and eliminate cancer cells.
- once activated, T cells recognise the presence of foreign antigens on the surface of body cells by intracellular pathogens
- can be initiated by APC presents antigen using MHC II
- use T helper cells
- cytotoxic T cells proliferate, producing activated cytotoxic T cells and memory T cells through clonal selection and expansion
- memory T cells retain memory of antigens met previously
- clonal selection: Tc cell binds with its antigen in lymph nodes
- clonal expansion: the activated Tc cells divide into many identical copies (clones) all having identical antigen binding receptors
54
Q
steps in cell-mediated immunity
A
- APCs display foreign antigen on MHC II marker to specific helper T cells usually within lymph node
- helper T cells undergo clonal selection and expansion
- interleukins (type of cytokine) are secreted by helper T cell to stimulate immature T cells
- upon stimulation by cytokines release by Th cells, cytotoxic T cells proliferate and produced activated cytotoxic T cells and memory T cells through clonal selection and expansion
- cytotoxic T cells destroy the cells through apoptosis
55
Q
apoptosis by cytotoxic T cells
A
- if a cytotoxic T cell (has toxic granules) recognises an infected cell it
- releases perforin (a protein that inserts into the plasma membrane and creates pores)
- enzyme (granzyme B) enter via the pore and trigger apoptosis from within the cell
- this ensures that the virus cannot spread
- similar to the action of NK cells but cytotoxic T cells are specific for certain antigens and form memory cells
56
Q
B lymphocytes role in humoral immunity
A
- B lymphocytes (cells) are covered in receptors → known as antibodies
- antibodies are membrane-bound or free
- B cells are ‘selected’ when they find an antigen (extracellular pathogen) complementary to the antibody
- most need to be activated by Th cells
- some become memory B cells
- most become plasma cells
57
Q
clonal selection and expansion in B cells
A
- clonal selection: B cells bind with its specific antigen in lymph nodes
- clonal expansion: the activated B cells divide into many identical copies (clones) all having identical antigen-binding receptors
58
Q
memory cells vs plasma cells
A
- memory cells:
- not active
- ‘lifelong’
- plasma cells:
- active
- short-lived
- secrete antibodies
- each plasma cell can only produce one type of antibody.
59
Q
events of humoral immunity
A
- an antigen gains entry to the body for the first time
- comes into contact w/ many naive B cells in the lymph nodes that don’t recognise it
- eventually, the antigen meets a B cell that can recognise and binds to it
- called clonal selection
- helper T cells that have also bound to the antigen release cytokines to activates the selected b cell- the binding of antigen to T helper cells activate the selected B cell to differentiate and proliferate into B plasma cells and B memory cells.
- results in the production of a large number of B cells w antigen-binding receptor antibodies
- clonal expansion
- plasma cells secrete soluble antibodies against the specific antigen
- memory B cells remain in the lymphoid tissue after the infection has resolved
- initiate immune responses more rapidly and stronger upon re-exposure to the same antigen
- produces large amounts of the specific antibody
60
Q
structure of antibodies/immunoglobulins
A
- they are antigen-binding proteins made by plasma B cells
- made of 4 polypeptide chains → 2 heavy and 2 light chains (quaternary structure) → constant region (doesn’t vary between antibodies of the same class)
- each antibody has 2 identical specific antigen-binding sites on both sides of the antibody
- variable region is the antigen binding site → differs between antibodies
- located at the end of each arm of the Y shaped molecule
- the variable region gives antibody its specificity for binding antigen
- each antibody can only bind to one specific antigen
- there are billions of antibodies each w a different antigen-binding site
61
Q
classes of antibodies
A
- IgG: main antibody in blood
- IgM: first antibody to appear and provides defence until sufficient IgG is formed
- IgA: attaches to the surfaces of mucous membranes
- IgE: stimulates the release of histamine and other chemicals that cause allergies
- IgD: antibody found on B cells
62
Q
action of antibodies
A
- antibodies do not directly eliminate antigens
- they can:
- bind to antigens and form a coating that neutralises pathogens by blocking their receptors so that the pathogens cannot attach to healthy body cells and infect them and stop them from functioning neutralisation (common)
- bind to surface antigens to target them for phagocytosis opsonisation
- bind to surface antigens to target them for lysis by complement proteins
- antibodies bind to surface antigens on pathogens to form antigen-antibody complexes → causing them to clump together and be more visible to the immune system agglutination (common)
- precipitation —antibodies bind to soluble antigens, making them insoluble. This causes them to precipitate out of the solution, creating a solid that is much more visible to the immune system. This occurs due to the cross-linking between antigens and antibodies.
- inflammation —antibodies can trigger the release of histamine, causing inflammation. They also activate a complement cascade.
- PIANO acronym
63
Q
memory B cells
A
- memory B cells remain in the lymphatic tissue to remember the antigen for future infections
- they initiate immune responses more rapidly and strongly upon re-exposure to the same antigen, producing large amounts of the specific antibody.
- antibody levels peak in the primary response at about day 14 and then begin to drop off as the plasma cells begin to die (low and short-lived)
- there are more memory cells than there were naive B cells for the primary response
- so secondary response: more plasma cells are generated and antibody levels are consequently 100-to-1000 fold higher
64
Q
what are allergens
A
- antigens are substances that cause/stimulate an immune response → doesn’t have to be biological (wood splinter)
- pathogens are agents that cause disease in their response
- allergies are caused by an immune response to allergens (antigens)
- allergic reaction is an abnormal overreaction when exposed to an allergen
- usually harmless → some are hypersensitive
- involves the cells of both the innate and adaptive immune system
- not all antigens are pathogens
- allergies are caused by an immune system response to allergens (antigen ) eliciting an allergic response
65
Q
what is an allergic reaction
A
- a reaction to a normally harmless substance
- the substance that causes an allergic response is an allergen (not antigen)
- key players in allergic reaction:
- mast cells
- antibodies → immunoglobulin E (IgE) - overproduction of IgE antibodies causes an allergic response
66
Q
steps in an allergic response
A
first exposure:
- allergen (eg. pollen) enters into the bloodstream (first exposure)
- B cells- specific to the allergen (bc extracellular) differentiate into plasma cells and make antibodies
- IgE antibodies attach to mast cells
- called ‘PRIMED’ → ready to respond to the allergen
secondary exposure:
- mast cell is primed with IgE antibodies specific for that allergen
- the allergen binds to antibodies on mast cells
- cross-links form→ more than one antibody binds with the allergen (activates more than one antibody)
- histamines will only be released when there is a crosslink (when allergen binds to j one antibody, histamines aren’t stimulated - no inflammation)
- histamine is released from the mast cell
- cytokines are released → attracting more immune cells
- an allergic reaction occurs
- increased blood flow
- increased permeability of blood vessels
- sustains and increases reaction (more histamine can be released)
67
Q
how can you be immune from a disease
A
when we have antibodies against an antigen → we won’t develop the disease
68
Q
sources of antibodies
A
-
active: own immune system produces long-term immunological memory (produces own antibodies and makes memory B cells)
- secondary response is more enhanced due to memory
- long-lasting
- more effective
- immunity develops over weeks
- eg. infected, vaccine
-
passive: external source, short term, NO immunological memory (made externally so memory B cells aren’t produced) → quicker response eg. get bitten by snake, antivenom injected
- short lasting
- less effective
- immunity is immediate
- eg. from mother, injected vaccine
69
Q
means of gaining immunity
A
- can be natural or artificial
-
natural immunity:occurs without deliberate intervention
- infection, mother-child
-
artificial immunity: is created by deliberate intervention and exposure
- vaccine, injection of antibodies
70
Q
active immunity
A
- natural
- infection by pathogen-causing agent
- antibodies form with identical antigen binding sites that bind to the antigens
- pathogen destroyed by high amounts of antibodies
- formation of memory cells
- artificial
- deliberate introduction of a disabled pathogen
- eg. injection
- the adaptive immune response is activated to produce the antibodies
71
Q
passive immunity
A
- natural
- receives antibodies from a natural source
- eg. breastfed milk →colostrum via the placenta, IgG
- artificial
- provided by injection of antibodies such as antivenom or antitoxins
- eg. clostridium tetani, rabies virus, antivenom (after pathogen enters the body, these are injected)
72
Q
tonsils
A
- Have specialised cells called microcells that can trap antigens and present them to macrophages or dendritic cells [APCs] which will then engulf them and take them to the lymph nodes 7 present them to the B & T lymphocytes
73
Q
infection vs disease
A
Infection is the invasion and growth of a pathogen in the body
Disease is a condition that impairs the normal functioning of an organ, structure or system of an organism
74
Q
how does a virus hijack a cell
A
- Virus adheres and inject viral nucleic acid or is taken up by cell.
- Viral nucleic acid moves to nucleus where it is transcribed.
- Viral mRNA is then translated (USES CELL’S ORGANELLES TO REPRODUCE)
- Viral protein is then packaged
- cell bursts releasing the viruses
