Topic 8 Flashcards

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1
Q

immunity

A

resistant to infectious disease

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2
Q

what is essence of immune defence

A

-the ability of immune system to distinguish between body’s own cells and molecules from foreign cells and molecules that carry non-self antigens

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3
Q

human immune system

A

collection organs, tissues, cells and molecules- protect us from various damaging agents around us

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4
Q

where do cells of immune system come from

A

multipotent stem cells in bone marrow

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5
Q

lymphatic system

A
  • consists of thin walled lymphatic vessels that contain lymph
  • reaches all tissues of body and interconnects lymphoid organs
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6
Q

bone marrow

A
  • forms soft tissue in hollow centre of long bones

- source of multipotent stem cells

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7
Q

thymus

A
  • located just behind sternum of ribcage
  • site of T cell development
  • shrinks with age
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8
Q

spleen

A

flattened organ lying in upper left sector of abdomen

  • blood filters through it- removes bacteria and viruses as well as worn out RBC
  • contains B/T cells
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9
Q

lymph

A
  • fluid that circulates throughout lymphatic system

- formed when interstitial fluid is collected through lymph capillaries

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10
Q

lymph vessels

A

lined by endothelial cells and have thin layer of smooth muscles

  • these collect lymph that leaks into tissue and returns back to circulatory system
  • located alongside to blood vessels
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11
Q

primary lymphoids

A

bone marrow and thymus- site of B and T cell maturation

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12
Q

secondary lymphoids

A

lymph nodes and spleen- activation site of B and T cells

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13
Q

lymph nodes

A
  • small bean shaped structures
  • located in lymph vessels
  • located along blood and lymphatic vessels- enables B and T cells to enter and exit lymph nodes
  • site where foreign antigens interact with B/T cells
  • swell when infection occurs
  • traps cancer cells/bacteria
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14
Q

innate immune system features

A
  • non-specific
  • present in animals, plants, fungi and invertebrates
  • response is not antigen specific
  • non specific response to class of pathogens
  • immune response occurs mainly at site of infection
  • reacts only against microbes
  • present at birth
  • activity is always present-immediate and rapid response
  • short lasting defense
  • no memory
  • cellular attack on bacteria and virus-infected cells
  • attack via soluble proteins/inflammation
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15
Q

adaptive immunity

A
  • specific
  • present in only jawed vertebrates
  • antigen specific response
  • specific response to each pathogen
  • response occurs in lymph nodes
  • reacts against microbes and foreign molecules
  • develops after infection/immunisation
  • normally inactive- slower response- maximum response occurs after days or weeks.
  • long lasting defense
  • has memory
  • cellular responses attack infected cell
  • antibodies target extra cellular pathogens
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16
Q

first line of defense

A
  • strategies that have been evolved to stop pathogens entering at body’s surface
  • includes both physical and chemical barrier to prevent pathogen’s entry
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17
Q

types of physical barriers

A

intact skin

  • mucous membranes
  • cilia
  • blood clots
  • ear wax
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18
Q

chemical barrier

A

mucous

  • tears
  • saliva
  • sebum
  • natural micro-flora
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19
Q

intact skin features

A
  • constantly shedding of dead skin cells- stops pathogens from entering
  • skin contains sebaceous glands-secrete sebum- provides protective and antimicrobial film on skin
  • sweat secretes dermcidin- acts as anti-microbial agent against wide range of pathogens
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20
Q

mucous membrane features

A
  • inner spaces of airways, gut and urogenital tract- lined with mucous membranes
  • these consist of epithelial cells- have tight junctions to prevent microbial entry
  • special cell in mucous membranes-secrete thick gelatinous fluid called mucus
  • also contain cilia- hair-like out-foldings found in airways
  • cilia trap pathogens and regularly beat- moves mucus from deep airway to back of throat
  • allows mucus to be swallowed- pathogens then destroyed by stomach acid
  • or expelled through nose and mouth by coughing and sneezing
  • some mucous membranes are washed constantly- mouth washed by saliva- urogenital tract washed by urine
  • washing prevent establishment of pathogens
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21
Q

presence of normal micro-flora

A

non-pathogenic bacteria that are established in parts of the body
-presence of harmless bacteria inhibits growth of pathogenic microbes

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22
Q

plants physical barriers (first line of defence)

A

thick intact cuticle/waxy leaf surface

  • thick bark
  • hairs on leaf surface
  • thorns/spines on leaf surface
  • hairs around stomatal opening
  • gall formation around infected area-stops spread
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23
Q

plants chemical barriers (second line of defence)

A
  • wounds plugged by resin
  • secretion of enzymes and antibiotic like substances- destroy pathogens
  • chemicals with bad smells or tastes-deter most predators
  • molecules that mimic predators hormones- disrupt normal life cycle
  • specialised proteins which bind to and inactivate many pathogens and insects
  • specialised hair like structures on leaves- secrete sticky substance which when touched by insects- trap them and cause them to starve
  • produce gum to seal off infected area
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24
Q

second line of defence

A
  • has number of components- depends on recognition of self from non-self
  • involves action of immune cells and soluble proteins that produce inflammation
  • cells involved- phagocytes and natural killer cells
  • soluble proteins- complement proteins and interferons
25
Q

phagocytes

A

-engulf and destroy microorganisms and other foreign material that enters body via phagocytosis

26
Q

types of phagocytes

A
neutrophils
macrophages
dendritic cells
eosinophils
basophils(mast cells)
27
Q

neutrophils

A
  • located in blood
  • identify and mount phagocytic attacks on microbes
  • kills engulfed microbes by toxic chemicals
  • first to arrive at infection site
28
Q

macrophages

A
  • located in tissue
  • identify/eliminate pathogens by phagocytosis
  • remove dead cells and cell debris
  • secrete cytokines
  • act as antigen presenting cells
29
Q

dendritic cells

A
  • located in tissues
  • mobile cells that identify pathogens
  • secrete antiviral cytokines
  • present in skin, surface lining
  • also act as antigen-presenting cells
30
Q

eosinophils

A
  • defense against larger parasites

- attacks using toxic chemicals released from granules

31
Q

basophils (mast cells)

A

release histamines as part of inflammatory response

-play role in allergic reactions

32
Q

phagocytosis steps

A
  • pathogen identified by pattern recognition receptor on surface of phagocyte
  • engulfed by outfoldings of plasma membrane
  • pathogen is enclosed in phagosome
  • lysosome fuses with phagosome and releases toxic chemicals that attack pathogen
  • pathogen is digested
  • indigestible material is discharged from phagocytic cell by exocytosis
33
Q

natural killer cells and degranulation

A
  • degranulation-release of anti-microbial and toxic molecules from membrane granules stored in cytoplasm of some innate immune cells
  • NKC release granules- to destroy virus infected body cells and cancer- because NK cells can recognise normal or missing HLA markers on virus infected cells and cancer cells- thus eliminates them
34
Q

degranulation steps

A
  • Natural Killer cells recognise missing or abnormal HLA markers on virus-infected cell or cancer cell
  • NK cells have don’t kill and kill receptors on cell surface
  • if NK cell comes into contact with cell missing or possessing abnormal HLA markers- killer activating receptor is uninhibited
  • NK cells degranulate
  • release active protease enzymes (granzymes) and pore forming protein perforin
  • when combined, these destroy the cell
35
Q

complement proteins

A
  • 20 major complement proteins
  • inactive enzymes circulating in blood
  • activated by making contact with pathogen
  • activation of one kind of complement protein results in cascade effect
  • activation of one kind of complement protein causes cascade effect- each activated complement protein then activates another and so on down the chain
36
Q

ways complement proteins assist phagocytes

A
  • opsonise to invading pathogens- makes them more susceptible to elimination by phagocytosis
  • stimulates phagocytes to become more active via chemotaxis
  • attract phagocytes involved in inflammatory response to infection site
  • destroy plasma membrane of invading microbes- form membrane attack complexes- form pores and induce lysis- causing pathogen death
37
Q

interferons

A
  • antiviral agent secreted by body cells infected with virus

- acts on uninfected cells making them more resistant to virus

38
Q

ways interferons achieve resistance

A
  • induce transcription of specific genes- encode for production of anti-viral enzymes- block synthesis of viral proteins and destroy viral RNA
  • make plasma membrane less fluid- making it difficult for virus to infect cells.
  • cause virus infected cells to undergo apoptosis
  • activate immune cells- such as natural killer cells- eliminate infected virus cells via apoptosis.
39
Q

inflammatory response

A
  • reaction that develops in local tissue when cells are damaged or killed by infection, burns or wounds.
  • area becomes red, hot, swollen and tender- results from increase in blood flow to the area
  • increase in blood flow results in more phagocytes being brought to the area of injury.
  • these phagocytes release chemicals- such as histamines which promotes vasodilation- increases blood flow and brings more phagocytes to area
  • phagocytes engulf and destroy bacteria
40
Q

stages of inflammation

A

increased diameter and permeability of blood vessels-
-blood vessels increase diameter and permeability to area of damage- increase blood flow/phagocytes to the area.- aids in removal of destroyed microbes and toxins
phagocyte migration and phagocytosis- within one hour, phagocytes appear at infection site
- they squeeze between cells of blood vessel walls to reach damaged area, where they destroy microbes.
Tissue repair- functioning cells/supporting connective cells replace dead or damaged cells- some repairs easily while others not at all

41
Q

third line of defence

A
  • presence of specific foreign antigen in body will initiate third line of defence
  • involves specific response to particular pathogen by immune response and results in adaptive/acquired immunity
  • specific immunity acquired is generally long lasting
  • involves b/t lymphocytes, antibodies (immunoglobulins)
  • lymph nodes where b/t cells are activated
42
Q

lymphocytes

A

type of white blood cell involved in adaptive immunity

43
Q

similarities and differences of B and T lymphocytes

A

similarities- made in bone marrow, migrate to lymph nodes when they mature, have receptors that recognise only one antigen, retain memory of antigen met previously
differences- b cells mature in bone marrow, t cells mature in thymus, t cells are activated by exposure to antigens presented to them on surface of other cells, b cells are activated by direct exposure to raw antigens, t cells differentiate into various types of t cells including cytotoxic t cells, helper t cells, b cells develop into plasma membrane that produce specific antibodies against specific antigen

44
Q

two ways of adaptive immunity operating

A

humoral immunity- involves action of antibodies that identify and bind to extracellular pathogens, toxins and other extracellular antigens.
-products of special b cells called plasma cells
cell-mediated immunity- involves various actions of t cells
-cytotoxic t cells eliminate body cells infected by pathogens or have abnormal or missing self markers
-cell mediated immunity doesn’t directly attack pathogens
- they instead remove infected cells and eliminate intracellular pathogens

45
Q

humoral immunity

A
  • b cells have immunoglobulin proteins on membrane- identify antigens- called antibodies
  • some b cells produce and secrete antibodies in response to foreign antigen
  • all about producing antibodies
46
Q

antibodies

A
  • have specific structure and only recognise one kind of antigen
  • specific antigens in extracellular fluid bind to matching antigen and target pathogen for destruction by macrophages.
47
Q

types of antibodies and key features

A

IgG-able to cross placenta, found in breast milk,
IgA- found in breast milk
IgE- involved in allergic reactions

48
Q

how do antibodies act on antigens

A

neutralisation-antibodies bind to surface antigens on pathogens and forms a coating that neutralises pathogens
agglutination- antibodies bind to bacterial toxins, animals toxins and venoms neutralises effect of toxin
activation of complement proteins- tag pathogens for destruction and elimination is carried out by complement proteins or phagocytic cells

49
Q

gene rearrangement for antibody production

A

-b cells can produce approximately 10 million different kinds of antibodies- each one being able to recognise one specific antigen

50
Q

how is diversity of b cells generated

A
  • b cells are produced from immature/naive b cells- genes rearrange during b cell development
  • dna from mature b cells have been re arranged- resulting in removal of some DNA
  • gene rearrangement allows for millions of different types of antibodies to be produced
  • once mature, each b cell leaves bone marrow displaying different antibody on cell surface- act as antigen receptor
  • any b cell that recognises self antigen undergoes apoptosis
51
Q

clonal selection theory of antibody production

A
  • when antigen reaches lymph nodes- comes into contact with many naive b cells that don’t recognise it
  • eventually specific b cell meets antigen, recognises it and binds to it
  • when b cell binds to foreign antigen, b cell is activated - replicates rapidly and produces large clone of cells-clonal expansion
  • all clones produced will have same genetic material and produce same antibodies
  • these cells then differentiate into plasma cells- produce same kind of antibody
  • b cells reproduce to form b memory cells- have sam antibody-antigen specificity as parent b cell but survive for several years
  • if second infection occurs of same pathogen containing same antigen- b memory cells react faster and more vigorously than initial b cell reaction at first infection- responds so quickly, few or no symptoms are shown
52
Q

b cell activation and antibody production process

A
  • b cell with specific antigen receptor on cell membrane binds to antigen on pathogen
  • b cell ingests pathogen and displays pathogens antigen with MHC 2 on cell membrane
  • an effector helper t cell binds to b cell displaying specific antigen on MHC 2 with matching antigen receptor
  • binding between these 2 cells causes t helper cell to release interleukins that stimulate b cell clonal expansion
  • b cell reproduces many times, producing many clones of itself via mitosis
  • b cells differentiate into plasma cells and memory cells
  • plasma cells secrete antibodies, which are specific for antigen of that pathogen
  • antibodies bind to antigen on pathogen in extra cellular fluid
  • forms antibody-antigen complexes, which are recognised by phagocytes that engulf and destroy the complex
53
Q

memory cells

A
  • immunological memory enables more rapid responses to future infections by same pathogen
  • most cells involved in adaptive immune response-removed by apoptosis after pathogen elimination
  • memory cells remain
  • action of b memory cells produces faster and greater production of antibodies on second exposure to same antigen as compared to initial exposure
54
Q

cell mediated immune response

A
  • t lymphocytes assist with b lymphocyte function
  • t cells can also recognise self from non-self- due t specific membrane bound receptors on cell membrane that have different antigen binding sites
  • many types of t cells made due to random gene shuffling
  • after encountering specific antigens- reproduce rapidly and also produce t memory cells- don’t make antibodies
  • t cells don’t bind with antigens directly- bind with antigens presented on MHC markers of APC- dendritic cells
55
Q

helper t cells

A

have specific receptors- detect antigens displayed on MHC class II- APC cells

  • have cell surface markers- CD4-aids in binding to foreign antigens
  • t cells produce cytokines- induce activated t cell or b cell to divide and give rise to effector cells and memory cells- also stimulate macrophages to engulf invading cells more rapidly
  • without t helper cells- b/t cells would not be stimulated - b cells wouldn’t produce antibodies
56
Q

activation t helper cells

A
  • in tissues dendritic cell phagocytose and destroy pathogen
  • dendritic cell acts as antigen-presenting cell
  • antigens from pathogen are combined with MHC class II and sent to cell membrane- displayed as antigen-MHC complexes
  • dendritic cell migrates to lymph nodes
  • T helper cell with matching MHC II antigen receptor bind to MHC II antigen complex on APC
  • binding stimulates dendritic cell to secrete interleukins- stimulates clonal expansion of T helper cells- produces effector t helper cells and memory t helper cells
  • t helper cell also secrete interleukins which stimulate its own clonal expansion
  • effector t helper cell binds to b cell displaying specific antigen on MHC class II with matching antigen receptor
  • binding between these cells cause t helper cell to secrete interleukins- stimulates b cell clonal expansion
  • effector t helper cell also secretes interleukins- stimulate clonal expansion of activated cytotoxic t cells
57
Q

suppressor t cells

A
  • known as regulatory t cells
  • play role in regulating action of lymphocytes
  • suppress action of phagocytes- slow production of antibodies and Tc cells
  • essentially turns off immune response after pathogen is absent
58
Q

cytotoxic t cells

A
  • have receptors that detect specific antigen presented on MHC class II of infected body cells
  • Tc cells kills body cells infected with virus- destroy eukaryotic cells
  • recognise infected body cell by viral antigen presented on MHC class I on outside of cell
  • Tc cells kill infected cells by releasing powerful cytokinins and perforins- punch holes in membrane and allows contents to seep out
  • Tc cells will only divide with signal from Th cell
59
Q

cell mediated response

A

-in tissues dendritic cell phagocytose and destroy pathogen
-dendritic cell acts as antigen-presenting cell
-antigens from pathogen are combined with MHC class II and sent to cell membrane- displayed as antigen-MHC II complex
-dendritic cell migrates to lymph nodes
Tc cell with matching antigen receptor binds to dendritic cell at its MHC II-antigen complex
-effector t helper cell secretes interleukins- stimulate division and differentiation of Tc cells into effector and memory cells
-effector Tc cell migrates to tissues
-then body cell infected with same virus signals infection-displays viral antigen on MHC class I
-effector Tc cells recognise infected cell using MHC I antigen receptor
-binding results in Tc cell secreting perforins and that punch holes in membrane and other cytokinins- induce apoptosis and cell death of infected cells
-Tc cell can then attack other infected cells