Regents Biology “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

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

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 for lunch?!

Regents Biology How are invaders recognized?  Antigens  chemical name tags on the surface of every cell  “self” vs. “invader” disease-causing bacteria disease-causing virus one of your own cells antigens say: “I belong here” antigens say: “I am an invader”  Antigens  chemical name tags on the surface of every cell  “self” vs. “invader”

Regents Biology Viruses

Regents Biology Bacteria

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

Regents Biology

1 st 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

Regents Biology 1 st 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!

Regents Biology 1 st 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.

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? 1 st Line of Defense  Mucus

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! 1 st Line of Defense  Stomach Acid

Regents Biology

Second Line of Defense  is non-specific INTERNAL defense.  White Blood Cells  Inflammation  Fever

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

Regents Biology TypeMain 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.

Regents Biology Lymph system Storage 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

Regents Biology Phagocytes yeast macrophage bacteria white blood cells that eat

Regents Biology PUS EXPLOSION

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.

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

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 Chemical alarm signals Pin or splinter Blood clot Phagocytes Swelling  Inflammation  injured cells release chemical signals

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

Regents Biology

3rd line: Lymphocytes  Specific defense and internal response  responds to specific invaders  recognizes specific foreign antigens  white blood cells  B cells & antibodies  T cells B cell

Regents Biology Interleukin - 1

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

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 macrophage eating tagged invaders invading germs tagged with antibodies Y Y Y Y Y Y Y B cells releasing antibodies Y Y Y Y Y Y Y Y Y Y Y Y Y Y

Regents Biology B cells immune response invader (foreign antigen) Y Y Y Y B cells Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y “reserves” memory B cells Y Y Y Y Y Y Y Y Y Y Y Y Y B cells release antibodies patrol blood forever recognition 10 to 17 days Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y

Regents Biology 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 Attack of the Killer T cells!

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?

Regents Biology Thymus

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 punctures cell membrane cell membrane Killer T cell cell membrane invaded cell vesicle

Regents Biology Immune response invader invaders in bloodinvaders infect cells B cellsT cells macrophages helper T cells patrolling B cells memory B cells memory T cells killer T cells Y Y Y Y YY Y Y antibodies Y Y Y skin invaders in body Y Y Y Y YY Y Y antibodies Y Y Y

Regents Biology Interleukin - 1

Regents Biology Macrophage Release Interleukin - 1 Helper T release Interleukin - 2 Interleukin – 2 activates B-Cell

Regents Biology

What is immunity? - Resistance to a disease causing organism or harmful substance - Two types - Active Immunity - Passive Immunity

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

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

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

Regents Biology Jonas Salk  Developed first vaccine  against polio 1914 – 1995 April 12, 1955

Regents Biology Polio epidemics 1994: Americas polio free

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

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

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

Regents Biology  Breastfeeding (passive)  mother’s milk gives baby antibodies & keeps baby healthy` Passive Immunity IMPORTANT PROTECTION antibodies pass from mother to baby in breast milk

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

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

Regents Biology AIDS  Transmitted by sexual contact, blood transfusions, contaminated needles  As of 2007, it affects an estimated 33.2 million people

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

Regents Biology

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

Regents Biology

Blood Type antigens & antibodies

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 identify this blood type?

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)

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.

Regents Biology Blood donation 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.

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.

Regents Biology Do you bloody well have any Questions?