Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer...

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Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer cell phagocyti c leukocyte lymph system

Transcript of Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer...

Page 1: Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer cell phagocytic leukocyte lymph system.

Regents Biology 2006-2007

“Fighting the Enemy Within”

Immune System

lymphocytesattackingcancer cell

phagocytic leukocyte

lymphsystem

Page 2: Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer cell phagocytic leukocyte lymph system.

Regents Biology

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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Regents Biology

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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Regents Biology

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

What’s forlunch?!

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Regents Biology

How are invaders recognized? Antigens

chemical name tags on the surface of every cell “self” vs. “invader”

disease-causingbacteria

disease-causingvirus

one of yourown cells

antigens say:“I belong here”

antigens say:“I am an invader”

antigens say:“I am an invader”

Antigens chemical name tags on the surface of

every cell “self” vs. “invader”

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Regents Biology

Viruses

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Regents Biology

Bacteria

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Regents Biology

Lines of defense 1st line:

broad, external defense “walls & moats”

skin & mucus membranes

2nd line: broad, internal defense

“patrolling soldiers” phagocyte (eating) WBCs

3rd line: specific, acquired immunity

“elite trained units” lymphocyte WBCs & antibodies

B & T cells

Non-specific Barriers

Non-specific Patrol

Specific - Immune system

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Regents Biology

Kristen
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Regents Biology

1st Line: Physical Barriers non-specific defense external barriers

skin & mucus membranes excretions

sweat stomach acid tears mucus saliva

“lick your wounds”

Lining of trachea:

ciliated cells & mucus secreting cells

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Regents Biology

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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Regents Biology

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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Regents Biology

- 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

Don’t swallowed bacteria have a good chance of infecting you?

1st Line of Defense Mucus

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Regents Biology

- 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!

1st Line of Defense Stomach Acid

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Regents Biology

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Regents Biology

Second Line of Defense is non-specific INTERNAL defense.

White Blood Cells Inflammation Fever

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Regents Biology

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”

Macrophage “eating” bacteria

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Regents Biology

Type Main Targets

Neutrophilbacteriafungi

Eosinophillarger parasitesmodulate allergic inflammatory responses

Basophil release histamine for inflammatory responses

LymphocyteB cells: releases antibodies and assists activation of T cellsT cells:Natural killer cells: virus-infected and tumor cells.

MonocyteMonocytes migrate from the bloodstream to other tissues and differentiate into tissue resident macrophages.

MacrophageIs 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 cellsIs a monocyte derivative. Main function is as an antigen-presenting cell (APC) that activates T lymphocytes.

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Regents Biology

Lymph systemStorage of white blood cells & traps “foreign” invaders

2nd “circulatory” system lymph node

lymph vessels(intertwined amongst blood vessels)

Tonsils and Appendix are apart

of your LYMPH system. Getting them removed

COULD weaken your immune system

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Regents Biology

Phagocytes

yeastmacrophage

macrophage

bacteria

white blood cells that eat

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Regents Biology

PUS EXPLOSION

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Regents Biology

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… …and after.

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Regents Biology

- 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

The Second Line of Defense for a Virus - Interferon

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Regents Biology

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Regents Biology

histamines increases blood

flow brings more

white blood cells to fight bacteria

brings more red blood cells & clotting factors to repair

Why do injuries swell?

Bacteria

Blood vessel

Chemicalalarm

signals

Pin or splinter Blood clot

Phagocytes

Swelling

Inflammation injured cells release chemical signals

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Regents Biology

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Regents Biology

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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Regents Biology

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Regents Biology

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Regents Biology

3rd line: Lymphocytes Specific defense and

internal responseresponds to specific

invaders recognizes specific

foreign antigens white blood cells

B cells & antibodiesT cells

B cell

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Regents Biology

Interleukin - 1

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Regents Biology

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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Regents Biology

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

Antibodies

macrophageeating tagged invaders

invading germs tagged with antibodies Y

Y

YY

YY

Y

B cells releasing antibodies

Y

YY

Y

Y

Y

Y

Y Y

Y

Y

Y

Y

Y

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Regents Biology

B cells immune responseinvader

(foreign antigen)

Y

Y

Y

Y

B cellsY

YY

Y

Y

YY

Y

Y

YY

YY

YY

YY

YY

Y

Y

YY

YY

YY

Y

“reserves”

memory B cells

Y

Y

Y

Y

Y

YY

YY

YY

Y

Y

B cellsrelease

antibodiespatrol blood

forever

recognition

10 to 17 days

YY

Y

Y

YY YY

Y

Y

Y

YY

YY

YYY

YYYY

Y

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Regents Biology 2006-2007

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

Attackof the

Killer T cells!

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Regents Biology

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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Regents Biology

Thymus

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Regents Biology

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

Perforin puncturescell membrane

cell membrane

Killer T cell

cell membrane

invaded cell

vesicle

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Regents Biology

Immune responseinvader

invaders in blood invaders infect cells

B cells T cells

macrophages

helperT cells

patrollingB cells

memoryB cells

memoryT cells

killerT cells

YYY

Y

YY

Y

YantibodiesY Y Y

skinskininvaders in body

YY

Y

Y

YY

Y

YantibodiesY Y Y

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Regents Biology

Interleukin - 1

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Regents Biology

Macrophage Release

Interleukin - 1

Helper Trelease

Interleukin - 2

Interleukin – 2

activates B-Cell

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Regents Biology

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Regents Biology

What is immunity?

- Resistance to a disease causing organism or harmful substance

- Two types- Active Immunity- Passive Immunity

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Regents Biology

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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Regents Biology

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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Regents Biology

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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Regents Biology

Jonas Salk Developed first vaccine

against polio

1914 – 1995

April 12, 1955

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Regents Biology

Polio epidemics

1994: Americas polio free

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Regents Biology

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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Regents Biology

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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Regents Biology

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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Regents Biology

Breastfeeding (passive) mother’s milk gives baby

antibodies & keeps baby healthy`

Passive Immunity

IMPORTANTPROTECTION

antibodies pass from mother to baby in breast milk

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Regents Biology

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Regents Biology

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

Page 55: Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer cell phagocytic leukocyte lymph system.

Regents Biology

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 life-threatening

- Can show no effects for several months all the way up to 10 years

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Regents Biology

AIDS

Transmitted by sexual contact, blood transfusions, contaminated needles

As of 2007, it affects an estimated 33.2 million people

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Regents Biology

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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Regents Biology

Page 59: Regents Biology 2006-2007 “Fighting the Enemy Within” Immune System lymphocytes attacking cancer cell phagocytic leukocyte lymph system.

Regents Biology

Immune system malfunctions Allergies

over-reaction to harmless compounds allergens

proteins on pollenproteins from dust

mitesproteins in animal

saliva body mistakenly

thinks they are attackers

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Regents Biology

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Regents Biology

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Regents Biology 2009-2010

Blood Typeantigens & antibodies

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Regents Biology

Blood Antigens and Antibodies Red blood cells can have antigens on

their surface. These antigens are carbohydrate markers that identify the cell.

Antibodies are located in the blood plasma. The antibodies will attack antigens that are foreign to the system.

Can you identifythis blood type?

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Regents Biology

Blood type; antigens & antibodies

Matching compatible blood groups is critical for blood transfusions

A person produces antibodies against foreign blood antigens

BLOOD TYPE

ANTIGEN ON BLOOD

CELL

ANTIBODIES IN PLASMA

ANTIBODIES WILL ATTACK

THESE ANTIGENS (cannot mix)

ANTIBODIES WILL NOT

ATTACK THESE ANTIGENS

(can mix)

A

B

AB

O

A antigen

B antigen

A and B antigen

NO antigen

Antibody B

Antibody A

NO Antibody

Antibody A & B

B Antigens(B and AB blood)

A Antigens(A and AB blood)

N/A

A and B Antigens(A, B, AB blood)

A Antigens(A and O blood)

B Antigens(B and O blood)

A & B Antigens(A, B, AB and O blood)

N/A(O blood)

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Regents Biology

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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Regents Biology

Blood donation

clotting clotting

clotting clotting

clotting clotting clotting

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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Regents Biology

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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Regents Biology 2009-2010

Do you bloody wellhave any Questions?