Topic 8 Flashcards
immunity
resistant to infectious disease
what is essence of immune defence
-the ability of immune system to distinguish between body’s own cells and molecules from foreign cells and molecules that carry non-self antigens
human immune system
collection organs, tissues, cells and molecules- protect us from various damaging agents around us
where do cells of immune system come from
multipotent stem cells in bone marrow
lymphatic system
- consists of thin walled lymphatic vessels that contain lymph
- reaches all tissues of body and interconnects lymphoid organs
bone marrow
- forms soft tissue in hollow centre of long bones
- source of multipotent stem cells
thymus
- located just behind sternum of ribcage
- site of T cell development
- shrinks with age
spleen
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
lymph
- fluid that circulates throughout lymphatic system
- formed when interstitial fluid is collected through lymph capillaries
lymph vessels
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
primary lymphoids
bone marrow and thymus- site of B and T cell maturation
secondary lymphoids
lymph nodes and spleen- activation site of B and T cells
lymph nodes
- 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
innate immune system features
- 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
adaptive immunity
- 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
first line of defense
- strategies that have been evolved to stop pathogens entering at body’s surface
- includes both physical and chemical barrier to prevent pathogen’s entry
types of physical barriers
intact skin
- mucous membranes
- cilia
- blood clots
- ear wax
chemical barrier
mucous
- tears
- saliva
- sebum
- natural micro-flora
intact skin features
- 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
mucous membrane features
- 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
presence of normal micro-flora
non-pathogenic bacteria that are established in parts of the body
-presence of harmless bacteria inhibits growth of pathogenic microbes
plants physical barriers (first line of defence)
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
plants chemical barriers (second line of defence)
- 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
second line of defence
- 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
phagocytes
-engulf and destroy microorganisms and other foreign material that enters body via phagocytosis
types of phagocytes
neutrophils macrophages dendritic cells eosinophils basophils(mast cells)
neutrophils
- located in blood
- identify and mount phagocytic attacks on microbes
- kills engulfed microbes by toxic chemicals
- first to arrive at infection site
macrophages
- located in tissue
- identify/eliminate pathogens by phagocytosis
- remove dead cells and cell debris
- secrete cytokines
- act as antigen presenting cells
dendritic cells
- located in tissues
- mobile cells that identify pathogens
- secrete antiviral cytokines
- present in skin, surface lining
- also act as antigen-presenting cells
eosinophils
- defense against larger parasites
- attacks using toxic chemicals released from granules
basophils (mast cells)
release histamines as part of inflammatory response
-play role in allergic reactions
phagocytosis steps
- 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
natural killer cells and degranulation
- 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
degranulation steps
- 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
complement proteins
- 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
ways complement proteins assist phagocytes
- 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
interferons
- antiviral agent secreted by body cells infected with virus
- acts on uninfected cells making them more resistant to virus
ways interferons achieve resistance
- 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.
inflammatory response
- 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
stages of inflammation
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
third line of defence
- 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
lymphocytes
type of white blood cell involved in adaptive immunity
similarities and differences of B and T lymphocytes
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
two ways of adaptive immunity operating
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
humoral immunity
- 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
antibodies
- 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.
types of antibodies and key features
IgG-able to cross placenta, found in breast milk,
IgA- found in breast milk
IgE- involved in allergic reactions
how do antibodies act on antigens
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
gene rearrangement for antibody production
-b cells can produce approximately 10 million different kinds of antibodies- each one being able to recognise one specific antigen
how is diversity of b cells generated
- 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
clonal selection theory of antibody production
- 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
b cell activation and antibody production process
- 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
memory cells
- 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
cell mediated immune response
- 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
helper t cells
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
activation t helper cells
- 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
suppressor t cells
- 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
cytotoxic t cells
- 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
cell mediated response
-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
