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Chapter 39 Immunity: A Summary AP Biology Spring 2011.

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Presentation on theme: "Chapter 39 Immunity: A Summary AP Biology Spring 2011."— Presentation transcript:

1 Chapter 39 Immunity: A Summary AP Biology Spring 2011

2 Integrated Responses To Threats
Immunity: body’s capacity to resist and combat infection, began when multicelled eukaryotic species evolved from free-living cells

3 Integrated Responses To Threats
Mutations introduced molecular patterns in membrane proteins that were unique to cells of a given type Mutations led to mechanisms of identifying those proteins as belonging self- one’s own body And ability to identify nonself

4 Integrated Responses To Threats
Antigen: any molecule that the body recognizes as nonself that revokes an immune response Most are proteins, lipids, and oligosaccharides Pattern receptors: used to detect patterns that are present mainly on pathogenic cells Anything that became bound to hem induced an animal cell to release complement (a set of about 30 proteins) which circulate in blood and destroy microbes or tag them for phagocytes

5 Integrated Responses To Threats
The microbial pattern receptors and complement offered innate immunity- fast, off-the-shelf responses to a fixed set of nonself cues Does not protect against novel or unrecognized threats , adapting to them isn’t possible in an individual’s lifetime


7 Integrated Responses To Threats
Evolution of cytokines and lymphocytes Lymphocytes: specialized class of WBC Together these signals and cells could tailor defenses to an astounding array of specific threats that an individual encountered during its lifetime Adaptive immunity


9 Three Lines of Defense Pathogens cannot do damage unless they can enter the internal environment Intact skin and lining of body tubes and cavities Physical and chemical protection Innate immunity Starts immediately after antigen has been detected or after a tissue has become damaged WBC, complement, acute inflammation, and fever Adaptive immunity Large populations of WBC form, all sensitized to a specific threat


11 The Defenders Leukocytes: all WBC that arise from stem cells in bone marrow

12 The Defenders Many kinds
Neutrophils: most abundant of WBC, fast acting phagocytes Macrophages: slower, bigger eaters, can get rid of as many as 100 bacterial cells Dendrite cells: alert immune system to the presence of antigen

13 The Defenders Many kinds:
Basophils and Mast Cells: circulate in blood (basophils) and tissues (mast cells) and release enzymes and cytokines in response to antigen or injury Eosinophils: secrete enzymes and toxic proteins that are good at punching holes in larvae of parasitic worms B and T Lymphocytes: are central to adaptive immunity Natural killer cells: innate immune response, also participate in adaptive immunity, directly kill body cells that are infected, stressed, or mutated, as by cancerous transformations


15 Immunalogy
Watch the video Draw a diagram to separate innate and adaptive immunity

16 Surface Barriers- The First Line of Defense
Your skin is teeming with about 200 different kinds of microbes Skin is waterproof covering of dead, keratin packed epithelial cell layers Normal skin resident populations of microbes have neutral or helpful impacts on health Staphylococcus epidermidis , the most common species on skin and a leading cause of bacterial infections

17 Linings of Tubes and Cavities
Body has defenses that normally keep microbes outside on the surface of linings Mucus: coating on free surface of epithelial linings Consists of glycoproteins (mucins) and salts in water Lysozyme: enzyme that cleaves peptidoglycans in bacterial cell walls and disrupts their structure Tears have lysozymes

18 Linings of Tubes and Cavities
Breathing in air: Mucus coated epithelial lining of airways Coughing expels many cells, lysozymes in mucus kill others Lining has ciliated cells, cilia beat in synchrony at its free surface, which sweeps the bacteria laden mucus to throat for disposal

19 Linings of Tubes and Cavities
In the mouth If microbes make it to the stomach, low pH kills most If make it to small intestine bile salts in intestinal lumen usually kill them If make it to large intestine, must compete with 500 or so established species and if they do displace the residents a flushing mechanism (diarrhea) usually gets rid of them

20 Linings of Tubes and Cavities
Urinary tract and vagina Lactic acid, byproduct of fermentation by Lactobacillus Helps keep vaginal pH beyond range of tolerance for most bacteria and fungi Flushing action of urination normally keeps most pathogens from colonizing in urinary tract

21 Uneasy Balance Must keep microbes outside body
Surface barriers are vulnerable When we become sick or weak with age, changes in physiology may compromise them Examples: Acne Plaque deposits, periodontitis

22 Innate Immune Response
Phagocytes: Macrophages arrive first: engulf and digest anything other than undamaged body cells Their pattern receptors recognize and bind to pathogen secreting cytokines which signal more macrophages and neutrophils

23 Innate Immune Response
Complement Proteins: Also arrive first Bind to circulating microbes or to antigen being displayed at phagocyte’s surface which causes a positive feedback mechanism One bound molecule becomes activated  then activates a few molecules of a different type of complement  then activates some of a different type, etc. Cascading reactions yield high concentrations of activated complement in localized tissue region

24 Innate Immune Response
Activated complement proteins have many effects Chemotactic: attract phagocyte cells (phagocytes follow gradients to site of damage, where complement is most concentrated) Some bind to microbes: microbes coated with complements will get recognized and engulfed faster by phagocytes Some assemble into attack complexes in cell wall or plasma membrane and promote bacterium’s lysis Also function in adaptive immunity

25 Innate Immune Response
Acute Inflammation: swift response from to tissue irritation or tissue damage Cytokines secretions from macrophages and activated complement trigger this Symptoms: redness, warmth, swelling, pain

26 Innate Immune Response
Steps of acute inflammation Mast cells respond to complement cascades or to antigen Secrete histamine and cytokines into interstitial fluid Histamine makes arterioles in tissue dilate  increases blood flow to the area (causes warmth and redness) Histamine makes blood capillaries in the tissue “leaky” to plasma proteins that usually do not leave blood Causes endothelial cells of capillary wall to shrink, cells pull further apart at clefts between them Plasma proteins and phagocytes slip out

27 Innate Immune Response
Steps of acute inflammation continued Osmotic pressure in interstitial fluid rises, fluid balance across the capillary wall shifts, localized edema (swelling) Swollen tissue cause free nerve endings to give rise to sensations of pain; suppresses voluntary movements (allows for tissue repair) Other plasma proteins leaking into interstitial fluid include clotting factors, macrophage secretions activate them

28 Innate Immune Response
Fever: rise in body temperature above the normal set point on a built in thermostat in hypothalamus Macrophages bring about fever as innate immune response Secrete pyrogenic cytokines which stimulates brain to synthesize and release several kinds of prostaglandins Prostaglandins act in hypothalamus to raise thermostat set point Fever of 39 degrees C, enhances immunity by increasing enzyme activity and speeding metabolism (formation and action of phagocytes accelerates, so does tissue repair) Also pop. Of many microbes grow slowly at high temp.s

29 Features of Adaptive Immunity
Four characteristics of vertebrate active immunity Self/nonself recognition Specificity Diversity Memory

30 Features of Adaptive Immunity
Self versus nonself recognition Every cell or virus has its own identity Human cells have markers: human leukocyte antigens (HLA), also known as MHC markers (major histocompatibility complex) T cells have TCRs: antigen receptors at their surface T cells normally do not target body cell that has bare MHC markers, but will act against it if those markers have antigen bits attached

31 Features of Adaptive Immunity
Specificity New B or T cell makes receptors for one kind of antigen Diversity: Refers to collection of antigen receptors on all B and T cells is the body Potentially billions of different antigen receptors, gives potential to counter billions of different threats

32 Features of Adaptive Immunity
Memory Immune system’s capacity to “remember” antigen that it vanquished First time lymphocytes recognize an antigen, takes a few days to for their populations to form When the same antigen shows up again, system makes faster, hightened response

33 First Step: The Antigen Alert
Recognition stimulates repeated mitotic cell divisions Result is large populations of B and T cells, primed to recognize antigen

34 First Step: The Antigen Alert
Macrophages, B cells, dendritic cells are antigen presenting cells and find antigens and present them to T cell (receptors recognize antigens) First engulf anything bearing antigen, vesicles move into the cytoplasm Vesicle fuses with lysomes, enzymes digest antigens Some fragments bind to MHC markers Antigen-MHC complexes shuttled to plasma membrane and are displayed

35 First Step: The Antigen Alert
When a cell’s MHC markers become paired with antigen fragments, it becomes a call to arms Odds are at least one T cell has receptors that can bind Binds, becomes activated and secretes cytokines that induce divisions of B or T cells sensitive to same antigen Effector cells: differentiated lymphocytes that act immediately against antigen Memory cells: long lived B and T cells that develop during first exposure and set aside for future encounters

36 Two Arms of Adaptive Immunity
Antibody Mediated Immune Response Pathogens in blood or interstitial fluid intercepted by phagocytes and B cells B cells execute most of this response T cells support

37 Two Arms of Adaptive Immunity
Cell mediated immune response Intracellular pathogens Vulnerable only for brief time when they slip out of one cell and infect another This response does not acquire antibodies Starts after antigen becomes positioned at surface of infected or altered body cells where phagocytes and cytotoxic T cells detect it

38 Intercepting and Clearing Out Antigens
After engulfing antigen, dendritic cells and macrophages enter a lymph node In lymph node, both kinds of phagocytes alert the T cells to the threat Free antigen in interstital fluid enters lymph vessels which deliver it to lymph nodes where it passes B cells, macrophages, and dendritic cells that can bind, process, and present it to T cells Lymph nodes trap most antigen- some could circulate to blood! Spleen helps filter again!

39 Intercepting and Clearing Out Antigens
During infection: Antigen-presenting T cells become trapped briefly in lymph nodes Swollen lymph nodes sign of illness and lymphocyte activity Immune response subside once antigen is cleared away

40 B Cells: The Antibodies
Antibodies: proteins synthesized only by B cells that encounter and bind antigen Many Y shaped Most circulate in blood and enter interstitial fluid during inflammation Each acts spcifically against the antigen that promoted its synthesis

41 B Cells: The Antibodies
Structure of Antibodies: Four polypeptide chains Two identical “light” ones Two identical “heavy” ones Each chain has constant region, forms molecules backbone One end of each chain has variable region- domain for one antigen

42 B Cells: The Antibodies
5 structural classes of antibodies called Immunoglobulins (Igs) IgG IgA IgM IgE IgD B cell secretes them, circulate alone or in clumps

43 B Cells: The Antibodies
IgG 80% of all immunoglobulins in blood Induces complement cascades, neutralizes toxins Crosses placenta, protects fetus with mother’s aquired immunities Secreted into early milk (colostrum)

44 B Cells: The Antibodies
IgA Main immunoglobulin in exocrine gland secretions Tears, saliva, milk In mucus of respiratory, digestive, and reproductive tracts

45 B Cells: The Antibodies
IgE Induces inflammation after pathogen invasions Constant regions of its heavy chains become anchored to mast cells, basophils, monocytes, or dendritic cells Makes these cells release histamines and cytokines Factor in allergic reactions and HIV infection

46 B Cells: The Antibodies
IgM First to be secreted in primary response and first made by newborns Surface of each new B cell is covered with hundreds of thousands of IgM or IgD antibodies, each of which recognizes the same antigen Antibodies are B cell receptors, surface immunoglobulins that function as B cell’s antigen receptors

47 The Making of Antigen Receptors
B cells Before new B cell leaves bone marrow, already synthesizing unique antigen receptors Constant region of each is positioned in lipid bilayer of B cell’s plasma membrane Two variable arms project above it B cell will have 100,000 antigen receptors “naïve” B cell- has not yet met its antigen

48 B Cells: The Antibodies
T cells: Form inside bone marrow Do not mature until they take a tour through thymus gland After exposure to thymic hormones, get receptors for MHC proteins Also get TCR’s, unique antigen receptors by gene splicing These recombination’s are random , some TCRs end up recognizing MHC markers rather than antigen, many will not

49 B Cells: The Antibodies
To get a functional set of T cells Thymus cells produce small peptides that are derived from a variety of the body’s proteins Peptides get attached to MHC markers, act as built in quality controls to weed out “bad” TCRs Any T cell that binds too tightly to one of complexes, has TCRs that recognize self peptide T cells that do not bind at all cannot recognize MHC markers Both types die By the time naïve T cells leave the thymus, their surface contains functional TCRs

50 The Antibody Mediated Response
Main targets of antibody mediated response are extracellular pathogens and toxins freely circulating in blood and interstitial fluid Nick your finger, staphlococcus aureus invades Complement in interstitial fluid latches on to carbohydrates in their bacterial cell wall and activates cascading reactions Complement coats bacteria Bacteria move through lymph vessels to lymph node, where paraded past naïve B cells

51 The Antibody Mediated Response
B cells bear immunoglobulins that bind to peptidoglycan in bacterium’s cell wall Bears complement receptors that bind to complement that coats the invading cell These 2 events provoke B cell to begin receptor-mediated endocytosis Bacterium enters B cell, which is no longer naïve, now activated

52 The Antibody Mediated Response
Meanwhile, more S. aureus cells have been secreting chemotactic factors into interstitial fluid around cut Secretions attract phagocytes Dendritic cell engulfs some bacteria, then migrates to the lymph node It has digested the bacteria cell and displays antigen fragments bound to MHC markers on its surface

53 The Antibody Mediated Response
Naïve T cells travel through the lymph nodes at all times, inspect dendritic cells One of T cells has TCRs that tightly bind to S. aureus antigen-MCH complexes on dendritic cell For the next 24h, two cells interact Transcription factors activated in T cell Two cells disengage, T cell returns to circulatory system

54 The Antibody Mediated Response
Theory of clonal selection S. aureus antigen “chose” that T cell because it bears a receptor that can bind to it After T cell is activated, many descendents form by mitotic cell divisions They are clones- one lineage of genetically identical cells Differentiates into helper T cells, all with identical TCRs specific for S. aureus antigen

55 The Antibody Mediated Response
Back to the B cell in lymph nodes Fragments of S. aureus are bound to MHC markers and displayed at the B cells surface Two cells latch on to each other and exchange costimulatory signals Helper T cells secretes several interleukins- cytokines that signal B cell to divide and differentiate

56 The Antibody Mediated Response
When cells disengage, B cell divides, its clonal descendents form huge populations, with identical receptors Differentiate into effector and memory cells

57 The Antibody Mediated Response
Effector cells work immediately in primary immune response or against initial exposure to antigen Instead of making membrane bound IgM as B cell receptors, they switch antibody classes Start making and secreting IgG, IgA, or IgE instead Each of secreted antibody molecules has same antigen specificity as original B cell receptor

58 The Antibody Mediated Response
Great numbers of antibody molecules specific for S. aureus are now circulating through body Bind bacterial cells remaining in blood stream and interstitial fluid Prevent them from attaching to body tissues and also tag them for disposal for NK cells and complement Neutralize toxic agents

59 The Cell-Mediated Response
As long as virus, bacteria, fungi, and protists hide in host cell, antibody mediated response cannot be initiated During acute inflammatory response, cell mediated defenses against these menacing threats get under way in interstitial fluid Usually plasma membrane of infected body cell displays antigen- peptides of intracellular pathogen or self proteins that were altered by cancerous tranformation

60 The Cell-Mediated Response
Dendritic cells recognize, engulf, and digest these antigens as bits of diseased or abnormal cells or their remains Dendritic cells then travel to lymph nodes, where antigen-MCH complexes on their surface are presented to 2 different populations of naïve T cells Both types are activated when their receptors bind to antigen-MCH complexes on the dendritic cells Clonal decendents of one population differentiate into effector helper T cells, which secrete interleukins and other cytokines These signal induce other type of T cell to divide and differentiate into cytotoxic T cells

61 The Cell-Mediated Response
Cytotoxic T cells circulate through body in blood and interstitial fluid Bind to any cell bearing original antigen that is complexed with MHC markers Inject it with perforin and proteases These toxins poke holes into cell and induce it to die by apoptosis Cytotoxic T cells are body’s primary weapons against infected body cells and tumors Also cause rejection of tissue and organ implants

62 The Cell-Mediated Response
Cytokines secreted by some helper T cells enhance macrophage action Stimulate these phagocytes to secrete more inflammatory mediators and toxins that help kill tumor cells and larger parasites Helper T cell cytokines also stimulate cell divisions of NK cells

63 The Cell-Mediated Response
Natural killer cells attack cells that are tagged for destruction by antibodies Also detect Stress markers on infected or cancerous body cells Cell that has normal MCH markers is not killed Cell with MCH markers that have been altered will die NK cells and macrophages are crucial in killing such cells; neither depends on presence of MCH markers

64 Defenses Enhanced or Compromised
Immunization: processes that may promote immunity Active immunization: preparation that contains antigen (a vaccine) is administered orally or injected into body First injection elicits primary immune response Second one, booster, elicits secondary response Additional effector and memory cells form for lasting protection

65 Defenses Enhanced or Compromised
Vaccines can be made from Weakened or killed pathogens or inactivated bacterial toxins Harmless viruses that have genes from other pathogens inserted into their DNA or RNA Passive Immunization Helps if hepatitis B, tetanus, rabies, have already started Based on injections of antibody purified from blood of a person who already fought disease Antibodies do not activate body’s immune system, memory cells do not form Protection ends when body disposes of injected antibody

66 Defenses Enhanced or Compromised
Allergies: hypersensitivity to an allergen Exposure to harmless proteins that stimulates immune response Allergen: any substance that is ordinarily harmless yet provokes immune response Antihistamines or anti-inflammatory drugs relieve symptoms as can desensitization programs (allergy shots) Anaphylactic shock: life threatening response to allergen

67 Defenses Enhanced or Compromised
Autoimmune Disorders When lymophocytes and antibody molecules fail to discriminate between self and nonself Autoimmune response: misdirected attack against one’s own tissues Ex. Rheumatoid arthritis, Graves disease, multiple sclerosis

68 Defenses Enhanced or Compromised
Deficient Immune Responses Loss of immune function can have lethal outcomes Primary deficiencies, present at birth, are outcomes of mutant genes or abnormal developmental steps Ex. SCIDs, ADA Secondary deficiencies are losses of immune function after exposure to some outside agent Ex. AIDS

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