defenses big questions 1.why are defenses against pathogens necessary? 2.how do different...
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Defenses
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Big Questions
1. Why are defenses against pathogens necessary?
2. How do different multicellular organisms defend themselves against infections
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Why an immune system?• Attack from outside
– lots of organisms want you for lunch!– Living systems are a tasty nutrient- & vitamin-packed meal
• cells are packages of macromolecules– animals must defend themselves against invaders (pathogens)
• Viruses: HIV, flu, cold, measles, chicken pox• Bacteria: pneumonia, meningitis, tuberculosis
Lyme disease• Fungi: yeast (“Athlete’s foot”…)• Protist: amoeba, malaria
• Attack from inside– cancers = abnormal body cells
Mmmmm,What’s in your
lunchbox?
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It’s All About MoleculesThe immune system is a great example of the ultimate molecular nature of organismal physiology. Essentially, all immune systems produce molecules in response to molecules.It’s Molecular Warfare!
EcoRI Antibody
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Prokaryotic Immune SystemsRestriction Enzymes!Provide defense against phage DNA.The bacterial genome restriction sites are methylated to prevent cleavage
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Plant Immune Defenses2 major routes of defense:• Large variety of chemical compounds for
defense (ex. alkaloids, toxins)• Molecular recognition & systemic response-
infected cells release chemical signals. Leads to an isolation and destruction of infected tissue.
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A maize leaf “recruits” a parasitoid wasp as a defensive response to an herbivore, an army-worm caterpillar
Recruitment ofparasitoid waspsthat lay their eggswithin caterpillars
4
3 Synthesis andrelease of
volatile attractants
1 Chemicalin saliva
1 Wounding
2 Signal transductionpathway
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Defense responses against an avirulent pathogen
1 Specific resistance isbased on the
binding of ligandsfrom the pathogen
to receptors in plantcells.
2 This identificationstep triggers a
signal transductionpathway.
3 In a hypersensitiveresponse (HR), plant
cells produce anti-microbial molecules,
seal off infectedareas by modifying
their walls, andthen destroy
themselves. Thislocalized responseproduces lesionsand protects otherparts of an infected
leaf.
4 Before they die,infected cells
release a chemicalsignal, probably
salicylic acid.
5 The signal isdistributed to the rest of the plant.
6 In cells remote fromthe infection site,
the chemicalinitiates a signal
transductionpathway.
7 Systemic acquiredresistance isactivated: theproduction of
molecules that helpprotect the cell
against a diversityof pathogens for
several days.
Signal
7
6
54
3
2
1
Avirulentpathogen
Signal transductionpathway
Hypersensitiveresponse
Signaltransduction
pathway
Acquiredresistance
R-Avr recognition andhypersensitive response
Systemic acquiredresistance
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Invertebrate Immune ResponsesInvertebrates only have non-specific defense mechanisms (as far as we can tell).They have a wide variety of innate mechanisms to deal with pathogens, but can not adapt to new pathogens during their life cycle.
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Vertebrate Immune SystemsThe most complex.1. Non-specific defenses
A. External (skin, mucus, lysozyme)B. Internal (Inflammatory response, phagocytic
leukocytes)
2. Specific defensesA. Humoral Response (involves B-Cells)B. Cell Mediated Response (involves T-Cells)
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Avenues of attack Points of entry
digestive system respiratory system urogenital tract break in skin
Routes of attack circulatory system lymph system
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Lymph system Production & transport of leukocytes
Traps foreign invaders
lymph node
lymph vessels(intertwined amongst blood vessels)
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Development of Red & White blood cells
short-lived phagocytes60-70% WBC
develop into macrophages
inflammatory response
fightparasites
Red blood cells
Lymphocytes
Leukocytes
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Lines of defense• 1st line: Non-specific barriers
– broad, external defense• “walls & moats”
– skin & mucous membranes• 2nd line: Non-specific patrols
– broad, internal defense• “patrolling soldiers”
– leukocytes = phagocytic WBC• 3rd line: True immune system
– specific, acquired immunity• “elite trained units”
– lymphocytes & antibodies• B cells & T cells
Bacteria & insectsinherit resistance.
Vertebratesacquire immunity.
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1st line: Non-specific External defense
• Barrier• skin
• Traps• mucous membranes, cilia,
hair, earwax
•Elimination• coughing, sneezing, urination, diarrhea
•Unfavorable pH• stomach acid, sweat, saliva, urine
•Lysozyme enzyme• digests bacterial cell walls• tears, sweat
Lining of trachea: ciliated cells & mucus secreting cells
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2nd line: Non-specific patrolling cells • Patrolling cells & proteins
– attack pathogens, but don’t “remember” for next time
• leukocytes– phagocytic white blood cells– macrophages, neutrophils,
natural killer cells • complement system
– proteins that destroy cells• inflammatory response
– increase in body temp.– increase capillary permeability– attract macrophages
yeast
macrophage
bacteria
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Leukocytes: Phagocytic WBCs • Attracted by chemical signals released by damaged
cells – ingest pathogens– digest in lysosomes
• Neutrophils– most abundant WBC (~70%)– ~ 3 day lifespan
• Macrophages– “big eater”, long-lived
• Natural Killer Cells– destroy virus-infected cells
& cancer cells
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• Natural Killer Cells perforate cells– release perforin protein– insert into membrane of target cell– forms pore allowing fluid to
flow in & out of cell– cell ruptures (lysis)
• apoptosis
Destroying cells gone bad!
perforin puncturescell membrane
cell membrane
natural killer cell
cell membrane
virus-infected cell
vesicle
perforin
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Anti-microbial proteins• Complement system
– ~20 proteins circulating in blood plasma– attack bacterial & fungal cells
• form a membrane attack complex• perforate target cell• apoptosis
– cell lysis
plasma membrane of invading microbe
complement proteinsform cellular lesion
extracellular fluid
complement proteins
bacterial cell
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Inflammatory response• Damage to tissue triggers local
non-specific inflammatory response– release chemical signals
• histamines & prostaglandins– capillaries dilate, become
more permeable (leaky)• delivers macrophages, RBCs,
platelets, clotting factors – fight pathogens– clot formation
– increases temperature• decrease bacterial growth• stimulates phagocytosis• speeds up repair of tissues
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Fever • When a local response is not enough
– system-wide response to infection– activated macrophages release interleukin-1
• triggers hypothalamus in brain to readjust body thermostat to raise body temperature
– higher temperature helps defense• inhibits bacterial growth• stimulates phagocytosis• speeds up repair of tissues• causes liver & spleen to store
iron, reducing blood iron levels– bacteria need large amounts
of iron to grow
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• Specific defense with memory – lymphocytes
• B cells• T cells
– antibodies • immunoglobulins
• Responds to…– antigens
• cellular name tags– specific pathogens – specific toxins– abnormal body cells (cancer)
3rd line: Acquired (active) Immunity
B cell
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“self” “foreign”
How are invaders recognized?• Antigens
– cellular name tag proteins• “self” antigens
– no response from WBCs• “foreign” antigens
– response from WBCs– pathogens: viruses, bacteria, protozoa, parasitic
worms, fungi, toxins – non-pathogens: cancer cells, transplanted tissue,
pollen
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Lymphocytes • B cells
– mature in bone marrow– humoral response system
• attack pathogens still circulating in blood & lymph
– produce antibodies• T cells
– mature in thymus– cellular response system
• attack invaded cells
• “Maturation”– learn to distinguish “self”
from “non-self” antigens • if react to “self” antigens, cells
are destroyed during maturation
bone marrow
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B cells• Attack, learn & remember pathogens circulating in
blood & lymph
• Produce specific antibodies against specific antigen
• Types of B cells– plasma cells
• immediate production of antibodies• rapid response, short term release
– memory cells• continued circulation in body• long term immunity
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Antibodies • Proteins that bind to a specific antigen
– multi-chain proteins – binding region matches molecular shape of antigens– each antibody is unique & specific
• millions of antibodies respond to millions of foreign antigens
– tagging “handcuffs”• “this is foreign…gotcha!”
each B cell has ~50,000
antibodies
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antigenantigen-binding site on antibody
variable binding region
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ss
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Structure of antibodies
light chains
antigen-bindingsite
heavy chains
antigen-bindingsite
lightchain
B cellmembrane
heavychains
lightchain
variable region
antigen-binding siteY
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What do antibodies do to invaders?
macrophageeating tagged invaders
invading pathogens tagged with antibodiesY
Y
YY
YY
neutralize
capture
precipitate
apoptosis
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• Immunoglobulins– IgM
• 1st immune response• activate complement proteins
– IgG• 2nd response, major antibody circulating in plasma• promote phagocytosis by macrophages
– IgA• in external secretions, sweat & mother’s milk
– IgE• promote release of histamine & lots of bodily fluids• evolved as reaction to parasites• triggers allergic reaction
– IgD• receptors of B cells???
macrophageeating tagged
invaders
invading pathogens tagged with antibodies
YY
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YY
Classes of antibodies
Weeks0 2 4 6
IgM IgG
Exposureto
antigen
An
tib
od
y le
vel
s
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macrophage
plasma cellsrelease antibodies
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YY Y
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Y
B cell (aka “humoral”) immune response
tested by B cells
(in blood & lymph)
10 to 17 days for full response
invader(foreign antigen) B cells + antibodies
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recognition
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clones1000s of clone cellsY
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Ymemory cells
“reserves”
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Ycapturedinvaders
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Vaccinations • Immune system exposed
to harmless version of pathogen – stimulates B cell system to produce
antibodies to pathogen• “active immunity”
– rapid response on future exposure– creates immunity
without getting disease!
• Most successful against viruses
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Jonas Salk• Developed first vaccine
– against polio• attacks motor neurons
1914 – 1995April 12, 1955
Albert Sabin1962
oral vaccine
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Polio epidemics
1994: Americas polio free
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• Obtaining antibodies from another individual – maternal immunity
• antibodies pass from mother to baby across placenta or in mother’s milk
• critical role of breastfeeding in infant health– mother is creating antibodies against pathogens baby
is being exposed to
• Injection– injection of antibodies– short-term immunity
Passive immunity
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What if the attacker gets past the B cells in the blood & actually infects (hides in) some of your cells?
You need trained assassins to recognize & kill off these infected cells!
T
Attackof the
Killer T cells!
But how do T cellsknow someone ishiding in there?
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How is any cell tagged with antigens?• Major histocompatibility (MHC) proteins
– proteins which constantly carry bits of cellular material from the cytosol to the cell surface
– “snapshot” of what is going on inside cell– give the surface of cells a unique label or “fingerprint”
T or Bcell
MHC protein
MHC proteinsdisplaying self-antigens
Who goes there?self or foreign?
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How do T cells know a cell is infected?• Infected cells digest some pathogens
– MHC proteins carry pieces to cell surface• foreign antigens now on cell membrane• called Antigen Presenting Cell (APC)
– macrophages can also serve as APC• tested by Helper T cells
MHC proteins displaying foreign antigens
infected
cell
T cell with antigen receptors
TH cellWANTED
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T cells• Attack, learn & remember pathogens hiding in
infected cells– recognize antigen fragments– also defend against “non-self” body cells
• cancer & transplant cells • Types of T cells
– helper T cells• alerts rest of immune system
– killer (cytotoxic) T cells • attack infected body cells
– memory T cells• long term immunity
T cell attacking cancer cell
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T cell (aka “Cell mediated”) response
stimulateB cells &
antibodies
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killerT cell
activatekiller T cells
or
interleukin 1
interleukin 2
interleukin 2
helperT cell
helperT cell
helperT cell
helperT cell
helperT cell
recognition
clones
recognition
APC:activatedmacrophage
APC:infected cell
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Attack of the Killer T cells
Killer T cellbinds toinfected
cell
• Destroys infected body cells– binds to target cell– secretes perforin protein
• punctures cell membrane of infected cell– apoptosis
infected celldestroyed
cell membrane
Killer T cell
cell membrane
target cell
vesicle
perforin puncturescell membrane
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Immune system & Blood type
blood type
antigenon RBC
antibodiesin blood
donationstatus
A type A antigenson surface of RBC anti-B antibodies __
B type B antigenson surface of RBC anti-A antibodies __
ABboth type A & type B
antigens on surface of RBC
no antibodies universal recipient
O no antigens on surface of RBC
anti-A & anti-B antibodies
universal donor
Matching compatible blood groups is critical for blood transfusions
A person produces antibodies against foreign blood antigens
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Immune response
free antigens in blood antigens on infected cells
humoral response cellular response
B cells T cells
macrophages(APC)
helperT cells
plasmaB cells
memoryB cells
memoryT cells
cytotoxicT cells
YYY
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YantibodiesY Y Y
skinskin pathogen invasionantigen exposure
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YantibodiesY Y Y
alert alert
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• Human Immunodeficiency Virus– virus infects helper T cells
• helper T cells don’t activate rest of immune system: killer T cells & B cells
• also destroys helper T cells
• AIDS: Acquired ImmunoDeficiency Syndrome– infections by opportunistic
diseases– death usually from – “opportunistic” infections
• pneumonia, cancers
HIV & AIDS
HIV infected T cell
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How to protect yourself…
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Immune system malfunctions• Auto-immune diseases
– immune system attacks own molecules & cells• Lupus: antibodies against many molecules released by
normal breakdown of cells• rheumatoid arthritis: antibodies causing damage to
cartilage & bone• Diabetes: beta-islet cells of pancreas attacked &
destroyed• multiple sclerosis: T cells attack myelin sheath of brain
& spinal cord nerves• Allergies
– over-reaction to environmental antigens• allergens = proteins on pollen, dust mites, in animal
saliva• stimulates release of histamine
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2009-2010
It’s safe
to Ask Questions!
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Quick Check: Make Sure You Can1. Explain how different lineages of life are able
to defend against pathogens.2. Explain the interplay between the humoral
and cell-mediated responses.3. Demonstrate how the HIV virus leads to a
breakdown of the immune system.4. Explain why a vaccine works.5. Explain the causes of immune system
disruptions and how disruptions of the immune system can lead to disruptions of homeostasis.
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InterpretationHere is a graph of an immune response in a vertebrate:
Explain this data, using your knowledge of the immune system