Transcript Regents Biology - I Heart Science

phagocytic
leukocyte
“Fighting the
Enemy Within”
Immune System
Regents Biology
lymphocytes
attacking
cancer cell
lymph
system
2006-2007
Think the flu is no big deal?
- Think again…
- In 1918, a particularly
deadly strain of flu,
called the Spanish
Influenza, spread
across the globe
- It infected 20% of the
human population and
killed 5%, which came
out to be about 100
million people
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Avenues of attack
 Points of entry
digestive system
 respiratory system
 urinary system
 genitals
 break in skin

 Pathways for attack
circulatory system
 lymph system

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Why an immune system?
 Attack from the outside & inside


lots of organisms want you for lunch!
we are a tasty vitamin-packed meal
 cells are packages of proteins, carbohydrates & fats


animals must defend themselves against invaders
 viruses
 HIV, flu, cold, measles, chicken pox, SARS
 bacteria
 pneumonia, meningitis, tuberculosis
 fungi
 yeast
 protists
 amoeba, Lyme disease, malaria
cancer cells
 abnormal body cells
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What’s for
lunch?!
How are invaders recognized?
 Antigens

chemical name tags on the surface of
every cell
 “self” vs. “invader”
one of your
own cells
disease-causing
virus
disease-causing
bacteria
antigens say:
“I belong here”
antigens say:
“I am an invader”
antigens say:
“I am an invader”
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Viruses
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Bacteria
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Lines of defense
 1st line:Non-specific Barriers

broad, external defense
 “walls & moats”

skin & mucus membranes
 2nd line: Non-specific Patrol

broad, internal defense
 “patrolling soldiers”

phagocyte (eating) WBCs
 3rd line:Specific - Immune system

specific, acquired immunity
 “elite trained units”

lymphocyte WBCs & antibodies
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 B & T cells
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1st Line: Physical Barriers
 non-specific defense
 external barriers


skin & mucus membranes
excretions
 sweat
 stomach acid
 tears
 mucus
 saliva
 “lick your wounds”
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Lining of trachea:
ciliated cells &
mucus secreting
cells
1st Line of Defense
 Skin
- The dead, outer
layer of skin, known
as the epidermis,
forms a shield
against invaders
and secretes
chemicals that kill
potential invaders
- You shed between
40 – 50 thousand
skin cells every day!
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1st Line of Defense
 Skin
 When it comes to burn victims, the
main reason for mortality is due to
bacteria infections, not necessarily
damage to the skin.
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1st Line of Defense
 Mucus
- As you breathe in, foreign
particles and bacteria
bump into mucus
throughout your
respiratory system and
become stuck
- Hair-like structures called
cilia sweep this mucus
into the throat for
coughing or swallowing
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Don’t swallowed bacteria have a
good chance of infecting you?
1st Line of Defense
 Stomach Acid
- Swallowed bacteria are broken
down by incredibly strong acids
in the stomach that break down
your food
- The stomach must produce a
coating of special mucus or this
acid would eat through the
stomach!
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Second Line of Defense
 is non-specific INTERNAL defense.
White Blood Cells
 Inflammation
 Fever

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2nd: Generalist, broad range patrols
 Patrolling white blood cells

attack invaders that get through the skin
 recognize invader by reading antigen
 surface name tag

phagocyte cells
 macrophages
 “big eaters”
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Macrophage “eating” bacteria
Type
Main Targets
Neutrophil
bacteria
fungi
Eosinophil
larger parasites
modulate allergic inflammatory responses
Basophil
release histamine for inflammatory responses
Lymphocyte
B cells: releases antibodies and assists activation of T cells
T cells:
Natural killer cells: virus-infected and tumor cells.
Monocyte
Monocytes migrate from the bloodstream to other tissues and differentiate into
tissue resident macrophages.
Macrophage
Is a monocyte derivative. Phagocytosis (engulfment and digestion) of cellular
debris and pathogens, and stimulation of lymphocytes and other immune cells
that respond to the pathogen.
Dendrites cells
Is a monocyte derivative. Main function is as an antigen-presenting cell (APC)
that activates T lymphocytes.
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Storage
Tonsils
and of white blood cells
traps
invaders
Appendix
are “foreign”
apart
of your LYMPH
system. Getting
them removed
COULD weaken your
immune system
Lymph system
&
lymph vessels
(intertwined amongst blood vessels)
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2nd
“circulatory” system
lymph node
Phagocytes
macrophage
bacteria
white blood cells that eat
macrophage
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yeast
PUS EXPLOSION
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What about Viruses?
Viruses enter body cells, hijack their organelles, and turn
the cell into a virus making-factory. The cell will
eventually burst, releasing thousands of viruses to infect
new cells.
Cell before infection…
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…and after.
The Second Line of Defense for a Virus - Interferon
- Virus-infected body
cells release
interferon when an
invasion occurs
- Interferon –
chemical that
interferes with the
ability of the
viruses to attack
other body cells
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Why do injuries swell?
 Inflammation

injured cells release chemical signals
Pin or splinter
 histamines
 increases blood
flow
 brings more
white blood
cells to fight
bacteria
 brings more red
blood cells &
clotting factors
to repair
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Bacteria
Blood clot
Swelling
Chemical
alarm
signals
Phagocytes
Blood vessel
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Fever
 When a local response is not enough

full body response to infection

raises body temperature

higher temperature helps in defense
 slows growth of germs
 helps macrophages
 speeds up repair of tissues
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3rd line: Lymphocytes
 Specific defense and
internal response

responds to specific
invaders
 recognizes specific
foreign antigens
 white blood cells
B cells & antibodies
T cells
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B cell
Interleukin - 1
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B cells & antibodies
 B cells
white blood cells that attack
invaders in blood
 mature in Bone marrow

 Patrolling B cells

make antibodies against invader immediately
 Memory B cells
remembers invader
 can make antibodies quickly the next time

 protects you from getting disease more than once
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Antibodies
 Proteins made by B cells that tag invaders
in the blood so macrophages can eat them

tag says “this is an invader”  gotcha!
 biological “handcuffs”

antibody attaches to antigen of invader
B cells
releasing antibodies
Y
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invading germs tagged
with antibodies
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macrophage
eating tagged invaders
Y
B cells immune response
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“reserves”
Y YY Y
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Y Y memory B cells
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recognition
B cells
Y
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B cells
release
antibodies
patrol blood
forever
Y
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(foreign antigen)
Y
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invader
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10 to 17 days
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What if the attacker gets past
the B cells in the blood &
infects some of your cells?
You need trained assassins
to kill off these infected cells!
T
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Attack
of the
Killer T cells!
2006-2007
T cells
 T cells mature in Thymus
 Helper T cells

sound the alarm for rest
of immune system
 Killer T cells

destroy infected body cells
 Memory T cells

remembers invader & reacts
against it again quickly
Where’s that?
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Thymus
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Attack of the Killer T cells
 Killer T cells destroy infected body cells
T cell binds to invaded cell
 secretes perforating protein

 punctures cell membrane of infected cell
 cell bursts
Killer T cell
vesicle
cell
membrane
Perforin
punctures
cell membrane
cell
membrane
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invaded cell
Immune response
invader
skin
invaders in body
invaders in blood
skin
invaders infect cells
macrophages
helper
T cells
B cells
memory
T cells
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Y antibodies
Regents Biology Y antibodies
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memory
B cells
Y
patrolling
B cells
T cells
killer
T cells
Interleukin - 1
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Interleukin – 2
activates
B-Cell
Macrophage
Release
Interleukin - 1
Helper T
release
Interleukin - 2
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What is immunity?
- Resistance to a disease causing
-
organism or harmful substance
Two types
- Active Immunity
- Passive Immunity
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Active Immunity
- You produce the antibodies
-
Your body has been exposed to the
antigen in the past either through:
- Exposure to the actual disease causing
antigen – You fought it, you won, you
remember it
- Planned exposure to a form of the antigen
that has been killed or weakened – You
detected it, eliminated it, and remember it
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How long does active immunity last?
 It depends on the antigen
 Some disease-causing bacteria
multiply into new forms that our
body doesn’t recognize, requiring
annual vaccinations, like the flu
shot
 Booster shot - reminds the
immune system of the antigen
 Others last for a lifetime, such as
chicken pox
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Vaccinations (Active)
 Exposure to harmless version of germ
stimulates immune system to produce
antibodies to invader
 rapid response if
future exposure

 Most successful
against viral diseases
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1914 – 1995
Jonas Salk
 Developed first vaccine

against polio
April 12, 1955
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Polio epidemics
1994:
Americas polio free
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Vaccines
 Pros and Cons of Vaccines

advantage
 don’t get illness
 long term immunity
 produce antibodies for life
 works against many viruses
& bacteria

disadvantage
 not possible against all invaders
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Fighting Bacterial Disease (Active)
 Antibiotics = medicine

advantage
 kill bacteria that have successfully
invaded you
 make you well after being sick

disadvantage
 use only after sick
 only good against bacteria
 possible development of
resistance by bacteria
(if don’t use correctly)
 can get sick again
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Passive Immunity
 You don’t produce the
antibodies

A mother will pass immunities
on to her baby during
pregnancy - mainly through the
placenta

These antibodies will protect
the baby for a short period of
time following birth while its
immune system develops.
(thymus)

Lasts until antibodies die
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Passive Immunity
 Breastfeeding (passive)

mother’s milk gives baby
antibodies & keeps baby healthy`
IMPORTANT
PROTECTION
antibodies pass
from mother to
baby in breast
milk
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Diseases of the immune system
 HIV: Human Immunodeficiency Virus
infects helper T cells
 helper T cells can’t activate rest of
immune system

 body doesn’t hear the alarm
 AIDS:
Acquired ImmunoDeficiency Syndrome
immune system is weakened
 infections by other diseases
 death from other invading
diseases or cancer

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AIDS The Modern Plague
- The HIV virus doesn’t kill
you – it cripples your
immune system
- With your immune system
shut down, common
diseases that your
immune system normally
could defeat become lifethreatening
- Can show no effects for
several months all the way
up to 10 years
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AIDS
 Transmitted
by sexual
contact, blood
transfusions,
contaminated
needles
 As of 2007, it
affects an
estimated 33.2
million people
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Immune system malfunctions
 Auto-immune diseases

immune system attacks own cells
 lupus
 antibodies attack many different body
cells
 rheumatoid arthritis
 antibodies causing damage to
cartilage & bone
 diabetes
 insulin-making cells of pancreas
attacked & destroyed
 multiple sclerosis
 T cells attack myelin sheath of
brain & spinal cord nerves
 fatal
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Immune system malfunctions
 Allergies

over-reaction to harmless compounds
 allergens
 proteins on pollen
 proteins from dust
mites
 proteins in animal
saliva
 body mistakenly
thinks they are
attackers
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Blood Type
antigens & antibodies
Regents Biology
2009-2010
Blood Antigens and Antibodies
 Red blood cells can have antigens on
their surface. These antigens are
carbohydrate markers that identify the
cell.
Can you identify
this blood type?
 Antibodies are located in the blood
plasma. The antibodies will attack
antigens that are foreign to the system.
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Blood type; antigens & antibodies
ANTIGEN
BLOOD
ANTIBODIES
ON BLOOD
TYPE
IN PLASMA
CELL
ANTIBODIES
WILL ATTACK
THESE
ANTIGENS
(cannot mix)
ANTIBODIES
WILL NOT
ATTACK THESE
ANTIGENS
(can mix)
B Antigens
A Antigens
(B and AB blood)
(A and O blood)
A
A antigen
Antibody B
B
B antigen
Antibody A
A Antigens
B Antigens
(A and AB blood)
(B and O blood)
AB
A and B
antigen
NO Antibody
N/A
A & B Antigens
O
NO antigen
Antibody
A&B
A and B Antigens
N/A
(A, B, AB blood)
(O blood)
(A, B, AB and O blood)
Matching compatible blood groups is critical for blood transfusions
A person
produces antibodies against foreign blood antigens
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Blood Antigens and Antibodies
 When a blood antigen and their antibody
mix, let’s say blood type A, with
antibody A (antibody A is found in the
plasma of blood type B) then clotting will
occur.
 If clotting occurs there will be a
blockage in circulation and death will
occur.
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x, let’s say blood type A, with antibody A (antibody A is found in the plasma of blood type B) then clotting will occur. If clotting occurs there will be a
Blood donation
clotting clotting
clotting
clotting
clotting clotting clotting
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Hey, wait a minute!
 Blood type O is a universal donor, but
there are A and B antibodies in the blood
plasma, why doesn’t it form a clot when
mixed with A and B blood antigens?
Two Reasons:
1. The amount of antibodies is so small it
doesn’t make a difference
2. Doctors can remove blood plasma if
necessary and just give recipients the RBCs.
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Do you bloody well
have any Questions?
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2009-2010