2. Dispatch 1)Take out April calendar and pick up a book -Today is the review (nut/lunch and afterschool) -This Sat is the AP Exam #1 8-11 or Wed, April 16 3-6 -Today we have reading quiz Chapter 43 2) Share with your tablemates what you did during break. Combine what all members did in one word Example: Magicbeachshopping 3) Study notes chapter 43

3. Ms. Morris went to Zion, Utah

4. Chapter 43 ~ The Body’s Defenses lymphocytes attacking cancer cells phagocytes

5. Exit Quiz 1.Explain the inflammatory response 2.What are the main advantages and disadvantages of a physical barrier against infection? 3.Sketch a B-cell receptor. Label V + C regions of light and heavy chains. Mark positions of antigen-binding sites, disulfide bridges and transmemebrane regions. 4.If a child were born without a thymus what cells and functions would be deficient. Explain. 5.HIV targets include all of the following EXCEPT: A Macrophage B Cytotoxic T-cells C Helper T-cells D Brain cells

6. Exit Quiz Answers 1) The inflammatory response (inflammation) occurs when tissues are injured by bacteria, trauma, toxins, heat, or any other cause. The damaged cells release chemicals including histamine, bradykinin, and prostaglandins. These chemicals cause blood vessels to leak fluid into the tissues, causing swelling. This helps isolate the foreign substance from further contact with body tissues.swelling The chemicals also attract white blood cells called phagocytes that "eat" microorganisms and dead or damaged cells. This process is called phagocytosis. Phagocytes eventually die. Pus is formed from a collection of dead tissue, dead bacteria, and live and dead phagocytes. 2) What are the main advantages and disadvantages of a physical barrier against infection? A physical barrier often provides a very effective defense against infection. However it is necessarily incomplete because animals need openings in their bodies for exchange with the environment. 3) Sketch a B-cell receptor. Label V + C regions of light and heavy chains. Mark positions of antigen-binding sites, disulfide bridges and transmemebrane regions. 4) If a child were born without a thymus he/she would not have functional T-cells. Without helper T-cells to help activate B-cells, child would be unable to produce antibodies against bacteria. Without T-cells or helper t-cells the child would be unable to kill viruses. 5) HIV targets include all of the following EXCEPT: B Cytotoxic T-cells

7. Lines of Defense Nonspecific Defense Mechanisms……

8. 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

9. 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

10. 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

11. 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) Destroying cells gone bad! perforin punctures cell membrane cell membrane natural killer cell cell membrane virus-infected cell vesicle perforin

12. 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 proteins form cellular lesion extracellular fluid complement proteins bacterial cell

13. 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

14. 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

15. Dispatch 1)Draw a label a heart 2)How is 02 transported to mitochondria? 3)How is CO2 transported from mitochondria? This Sat in this room. Be here at 7:50 am. Part I 100 multiple choice in 1.5 hours. Part II 4 FRQs If your name is on the board, clear up your N

16. FLT I can compare the circulatory system and the urinary system with the skeleton baby - Heart -1 Artery along arm -1 Vein along arm -Urinary system (kidney, urethra, ureter, bladder)

17. Immune System Play While actors are practicing, copy immune chart pg 848

22. After play 1) Fill in the T-chart with 3 or more difference between a bacteria and virus. 2) A B-cell has antibodies. These antibodies are used to______________________ 3) The role of a T-cell is to__________ 4) What is the first line of defense our body has against pathogens?______________ 5) How is a virus attack handled differently than a bacterial attack by the body?_______

23. 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

24. “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

25. Lymphocytes B cells –mature in bone marrow –humoral response system “humors” = body fluids attack pathogens still circulating in blood & lymph –produce antibodies T cells –mature in thymus –cellular mediated 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

26. 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

27. 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 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 Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y antigen antigen- binding site on antibody variable binding region

28. s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s s Structure of antibodies light chains antigen-binding site heavy chains antigen-binding site light chain B cell membrane heavy chains light chain variable region antigen-binding site 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

29. macrophage plasma cells release antibodies Y Y Y Y Y Y Y Y Y Y Y Y Y B cell immune response tested by B cells (in blood & lymph) 10 to 17 days for full response invader (foreign antigen) B cells + antibodies 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 Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y recognition Y Y Y Y Y Y Y Y clones 1000s of clone 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 Y Y Y Y Y Y Y Y Y Y Y Y memory cells “reserves” 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 Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y YY Y Y captured invaders

30. Induction of Immune Responses Primary immune response: lymphocyte proliferation and differentiation the 1st time the body is exposed to an antigen Plasma cells: antibody-producing effector B-cells Secondary immune response: immune response if the individual is exposed to the same antigen at some later time ~ Immunological memory

31. 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

32. 2007-2008 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 Attack of the Killer T cells! But how do T cells know someone is hiding in there?

33. 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 B cell MHC protein MHC proteins displaying self-antigens Who goes there? self or foreign?

34. 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 T H cell WANTED

35. 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

36. T cell response stimulate B cells & antibodies 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 Y Y Y Y Y Y Y Y YY Y Y killer T cell activate killer T cells or interleukin 1 interleukin 2 helper T cell recognition clones recognition APC: activated macrophage APC: infected cell

37. Attack of the Killer T cells Killer T cell binds to infected cell Destroys infected body cells –binds to target cell –secretes perforin protein punctures cell membrane of infected cell infected cell destroyed cell membrane Killer T cell cell membrane target cell vesicle perforin punctures cell membrane

38. Abnormal immune function I Allergies hypersensitive responses to environmental antigens (allergens); mast cells release histamine causes dilation and blood vessel permeability, epinephrine Antihistamines can relieve symptoms anaphylactic shock: life threatening reaction to injected or ingested allergens.

39. Abnormal immune function II Autoimmune disease: –The system turns against the body’s own molecules Examples: multiple sclerosis, lupus, rheumatoid arthritis, insulin-dependent diabetes mellitus Rheumatoid arthritis

40. Abnormal immune function III Immunodeficiency disease: Immune components are lacking, and infections recur Ex: SCIDS Severe combined immunodeficiency (bubble-boy); A.I.D.S., Acquired Immunodeficency syndrome

41. Abnormal immune function IV 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 infected T cell