* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Download Regents Biology - I Heart Science
Survey
Document related concepts
Homeostasis wikipedia , lookup
Embryonic stem cell wikipedia , lookup
Cell culture wikipedia , lookup
History of biology wikipedia , lookup
State switching wikipedia , lookup
Artificial cell wikipedia , lookup
Organ-on-a-chip wikipedia , lookup
Human genetic resistance to malaria wikipedia , lookup
Regeneration in humans wikipedia , lookup
Hematopoietic stem cell wikipedia , lookup
Neuronal lineage marker wikipedia , lookup
Human embryogenesis wikipedia , lookup
Microbial cooperation wikipedia , lookup
Cell theory wikipedia , lookup
Adoptive cell transfer wikipedia , lookup
Developmental biology wikipedia , lookup
Transcript
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 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 Regents Biology 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” Regents Biology Viruses Regents Biology Bacteria Regents Biology 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 Regents Biology B & T cells Regents Biology 1st Line: Physical Barriers non-specific defense external barriers skin & mucus membranes excretions sweat stomach acid tears mucus saliva “lick your wounds” Regents Biology 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! 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. Regents Biology 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 Regents Biology 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! Regents Biology 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” Regents Biology 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. Regents Biology 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) Regents Biology 2nd “circulatory” system lymph node Phagocytes macrophage bacteria white blood cells that eat macrophage Regents Biology yeast 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… Regents Biology …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 Regents Biology Regents Biology 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 Regents Biology Bacteria Blood clot Swelling Chemical alarm signals Phagocytes Blood vessel 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 Regents Biology 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 Regents Biology B cell 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 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 Y Y Y Y Y Y invading germs tagged with antibodies Regents Biology Y Y Y Y Y Y macrophage eating tagged invaders Y B cells immune response Y Y Y Y Y Y Y Y Y Y “reserves” Y YY Y Y Y Y Y memory B cells Y Y Y Y Y Y Y Y Y Y Y Y recognition B cells Y Y Y Y Y Y B cells release antibodies patrol blood forever Y Y Y Y Y Y Y (foreign antigen) Y Y Y invader Y Y 10 to 17 days Y Y Y Regents Biology Y Y 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 Regents Biology 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? 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 Killer T cell vesicle cell membrane Perforin punctures cell membrane cell membrane Regents Biology 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 Y Y Y Y Y Y Y Y Y Y Y antibodies Regents Biology Y antibodies Y Y Y Y Y Y Y Y Y memory B cells Y patrolling B cells T cells killer T cells Interleukin - 1 Regents Biology Interleukin – 2 activates B-Cell Macrophage Release Interleukin - 1 Helper T release Interleukin - 2 Regents Biology 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 1914 – 1995 Jonas Salk Developed first vaccine against polio 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 Passive Immunity Breastfeeding (passive) mother’s milk gives baby antibodies & keeps baby healthy` IMPORTANT PROTECTION antibodies pass from mother to baby in breast milk Regents Biology 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 lifethreatening - 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 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 Regents Biology Regents Biology 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. Regents Biology 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 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 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 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? Regents Biology 2009-2010