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  1. immunity
    resistance to disease
  2. what are the two intrinsic systems of the immune system
    • innate (nonspecific) defense system
    • adaptive (specific) defense system
  3. immune system
    • functional system rather than organ system
    • innate and adaptive defenses intertwined 
    • release and recognize many of same defensive molecules
    • innate defenses do have specific pathways for certain substances
    • innate responses release proteins that alert cells of adaptive system to foreign molecules
  4. what are the two lines of defense for the innate defense system
    • first - external body membranes:skin and mucosa
    • second -antimicrobial proteins, phagocytes, other cells: inhibit spread of invaders; inflammation most important mechanism
  5. what is the third line of defense
    • adaptive defense system
    • it attacks particular foreign substances, so it takes longer to react than the innate system
  6. defensins
    antimicrobial peptides which inhibit growth
  7. respiratory system modifications
    • mucus coated hairs in nose
    • cilia of upper respiratory tract sweep dust and bacteria mucus toward mouth
  8. internal defenses: cells and chemicals
    • phagocytes
    • natural killer (NK) cells
    • antimicrobial proteins (interferons and complement proteins)
    • feber
    • inflammatory response (macrophages, mast cells, WBCs and inflammatory chemicals)
  9. phagocytes
    • neutrophils: most abundant but die fighting. become phagocytic on exposure to infectious material
    • macrophages: develop form monocytes -chief phagocytic cells. free macrophages wander through tissue spaces, while fixed macrophages permanent residents of some organ e.g. kupffer cells (liver)
  10. mechanism of phagocytosis
    • phagocyte must adhere to particle
    • some microorganisms evade adherence with capsule.
    • cytoplasmic extensions bind to and engulf particle in vesicle
    • phagosome fuses with lysosome
  11. opsonization
    marks pathogens; coating by complement proteins or antibodies
  12. what cells release respiratory burst and what does it do
    helper t cells cause release of enzymes of respiratory burst, which kill pathogens resistance to lysosomal enzymes.
  13. is defensins a mechanism of phagocytosis
    yes, it pierces the membrane of the pathogen
  14. natural killer NK cells
    • nonphagocytic large granular lymphocytes
    • attack cells that lack "self" cell surface receptors (induce apoptosis)
    • secrete potent chemicals that enhance inflammatory response
  15. apoptosis
    controlled cell suicide
  16. inflammatory response
    • triggered whenever body tissues injured
    • prevents spread of damaging agents
    • disposes of cell debris and pathogens
    • alerts adaptive immune system
    • sets the stage for repair
  17. what are the cardinal signs of acute inflammation
    • redness
    • heat
    • swelling
    • pain
    • sometimes impairment of function
  18. what are the inflammatory mediators
    • kinins, prostaglandins, and complement.
    • -dilate local arterioles
    • -make capillaries leaky
    • -many attract leukocytes to area
    • -some have inflammatory roles
  19. clotting factors form fibrin mesh
    • scaffold for repair
    • isolates injured area so invaders cannot spread
  20. steps for phagocyte mobilization
    • 1. leukocytosis: release of neutrophils from bone marrow in response to leukocytosis inducing factors from injured cells
    • 2. margination: neutrophils cling to walls of capillaries in inflamed area in response to CAMs
    • 3. diapedesis of neutrophils
    • 4. chemotaxis: inflammatory chemicals promote positive chemotaxis of neutrophils
  21. interferon and complement proteins
    • attack microorganisms directly
    • hinder microorganisms' ability to reproduce
  22. interferon
    • family of immune modulating proteins
    • viral infected cells secrete IFNs to warn neighboring cells.
    • IFNs enter neighboring cells, produce proteins that block viral reproduction and degrade viral RNA; also activate NK cells
  23. complement
    • 20 blood proteins that circulate in inactive form
    • major mechanism for destroying foreign substances
    • our cells contain complement activation inhibitors
    • unleashes inflammatory chemicals that amplify all aspects of inflammatory response
    • kills bacteria and certain other cell types by cell lysis
    • enhances both innate and adaptive defenses
  24. what are the three pathways to complement activation
    • classical: antibodies bind to invading organisms and to complement componenets, called complement fixation, first step in activation
    • lectin pathway: lectins produced by innate system to recognize foreign invaders, when bound to foreign invaders can also bind and activated complement
    • alternative: triggered when activated C3, B, D, P interact on surface of microorganisms
  25. fever
    • abnormally high body temperature
    • systemic response to invading microorganisms
    • leukocytes and macrophages exposed to foreign substances secrete pyrogens
    • pyrogens act on body's thermostat in hypothalamus, raising body temperature
  26. what are the benefits of moderate fever
    • causes liver and spleen to sequester iron and zinc
    • increases metabolic rate for faster repair
  27. adaptive immune system
    • protects against infectious agents and abnormal body cells
    • amplifies inflammatory response
    • activates complement
    • must be primed by initial exposure to specific foreign substances (priming takes time)
  28. specific
    recognizes and targets specific antigens
  29. systemic
    not restricted to initial site
  30. have memory
    stronger attacks to known antigens
  31. humoral
    antibody mediated immunity
  32. cellular
    cell mediated immunity
  33. humoral immunity
    • antibodies produced by lymphocytes circulating freely in body fluids
    • bind temporarily to target cells, temporarily inactivate, mark for destruction by phagocytes or complement
  34. immunogenicity
    ability to stimulate proliferation of specific lymphocytes
  35. reactivity
    ability to react with activated lymphocytes and antibodies released by immunogenic reactions
  36. haptens
    • small molecules not immunogenic by themselves 
    • e.g. peptides, nucleotides, some hormones
    • (incomplete antigens)
    • may be immunogenic if attached to body proteins and combination is marked foreign
    • cause immune system to mount harmful attack
    • examples: poison ivy, animal dander, detergents, cosmetics
  37. antigenic determinants
    • only certain parts (antigenic determinants) of entire antigens are immunogenic
    • antibodies and lymphocyte receptors bind tot hem as enzyme binds to substrate
  38. self antigens: MHC proteins
    • protein molecules (self antigens) on surface of cells not antigenic to self but antigenic to others in transfusions or grafts
    • ex. MHC glycoproteins
  39. three types of cells of the adaptive immune system
    • two types of lymphocytes: B (humoral immunity) and T (cell mediated immunity)
    • antigen presenting cells (APCs)
  40. lymphocyte development five general steps
    • origin: all originate in red bone marrow
    • maturation
    • seeding secondary lymphoid organs and circulation
    • antigen encounter and activation
    • proliferation and differentiation
  41. where do t and b cells mature
    • T cells: thymus
    • B cells: bone marrow
  42. immunocompetence
    • lymphocyte can recognize one specific antigen by binding to it.
    • B or T cells display unique receptor on surface when achieve maturity, bind only one antigen
  43. self-tolerance
    lymphocytes unresponsive to own antigens
  44. Positive selection (t cells)
    selects t cells capable of recognizing self-MHC proteins; failures destroyed by apoptosis
  45. negative selection ( t cells)
    • prompts apoptosis of t cells that bind to self antigens displayed by self MHC
    • ensures self tolerance
  46. B cells
    • mature in red bone marrow
    • positively selected if successfully make antigen receptors
    • those that are self reactive are eliminated by apoptosis
  47. when are B and T cells considered naive
    when the immunocompetent B and T cells ahve not yet been exposed to antigens
  48. clonal selection
    • naive lymphocyte's fire encounter with antigen, selected for further development
    • if correct signals present, lymphocyte will complete its differentiation
  49. proliferation and differentiation
    • activated lymphocytes proliferates > exact clones
    • most clones > effector cells that fight infections
    • few remain as memory cells 
    • B and T memory cells and effector T cells circulate continuously
  50. memory cells
    able to respond to same antigen more quickly second time
  51. what determines what foreign substances immune system will recognize
    genes
  52. antigen presenting cells (APCs)
    • engulf antigens
    • present fragments of antigens to T cells for recognition
    • major types: dendritic, macrophages, B cells
  53. dendritic and macrophages
    • dndritic cells phagocytize pathogens, enter lymphatics to present antigens to T cells in lymph node
    • macrophages widespread in lymphoid organs and connective tissues
    • can activate naive T cells
    • present antigens to T cells to activate themselves into voracious phagocytes that secrete bactericidal chemicals
  54. do B lymphocytes activate naive t cells
    no
  55. activation and differentiation of B cells
    • b cell activated when antigens bind to its surface receptors and cross-link them
    • receptor mediated endocytosis of cross linked antigen receptor complexes
    • proliferation and differentiation into effector cells
  56. fate of clones
    • most clone cells become plasma cells: secrete specific antibodies at rate of 2000 molecules per second for four to five days then die
    • antibodies circulate in blood or lymph: bind to free antigens and mark for destruction by innate or adaptive mechanisms
  57. clones that do not become plasma cells become
    • memory cells
    • provide immunological memory
    • mount an immediate response to future exposures to same antigen
  58. primary immune response
    • cell proliferation and differentiation upon first antigen exposure
    • lag period: three to six days
    • peak levels of plasma antibody are reached in 10 days
    • antibody levels then decline
  59. secondary immune response
    • re-exposure to same antigen gives faster, more prolonged, more effective response
    • sensitized memory cells respond within hours
    • antibody levels peak in two to three days at much higher levels
    • antibodies bind with greater affinity
    • antibody level can remain high for weeks to months
  60. what are the two types of humoral immunity
    • naturally acquired: response to bacterial or viral infection
    • artificially acquired: response to vaccine of dead or attenuated pathogens
  61. vaccines
    • most of dead of attenuated pathogens
    • spare us symptoms of primary response
    • provide antigenic determinants that are immunogenic and reactive
    • can cause illness trying to vaccinate against; can cause allergic responses
  62. what are the two types of passive humoral immunity
    • naturally acquired: anitbodies delivered to fetus via placenta or to infant through milk
    • artificially acquired: injection of serum, such as gamma globulin
  63. antibodies
    • immunoglobulins
    • proteins secreted by plasma cells
    • capable of binding specifically with antigen detected by B cells
    • grouped into one of five Ig classes
  64. what are the five Ig classes
    IgM, IgG, IgB, IgA, IgD
  65. IgM
    • pentamer
    • larger than the rest
    • first antibody released
    • potent agglutinating agent
    • readily fixes and activates complement
  66. IgA
    • monomer or dimer
    • in mucus and other secretions
    • helps prevent entry of pathogens
  67. IgD
    • monomer attached to surface of B cells
    • functions as B cell receptor
  68. IgG
    • monomer; 75-85% of antibodies in plasma
    • from secondary and late primary responses
    • crosses placental barrier
  69. IgE
    • monomer active in some allergies and parasitic infections
    • causes mast cells and basophils to release histamine
  70. what are the defensive mechanisms used by antibodies
    • neutralization and agglutination are the most important
    • precipitation and complement fixation
  71. neutralization
    • simplest defensive mechanism
    • antibodies block specific sites on viruses or bacterial exotoxins
    • prevent these antigens from binding to receptors on tissue cells
    • antigen antibody complexes undergo phagocytosis
  72. agglutination
    • antibodies bind same determinant on more than one cell bound antigen
    • crosslinked antigen antibody complexes agglutinate
  73. precipitation
    • soluble molecules are cross linked
    • complexes precipitate and are subject to phagocytosis
  74. complement fixation and activation
    • main antibody defense against cellular antigens
    • several antibodies bind close together on a cellular antigen > complement binding sites on stem regions align which triggers complement fixation into cell's surface to cause cell lysis
  75. does activated complement functions amplify inflammatory response
    yes
  76. do T cells directly kill cells
    some do. others release chemicals that regulate immune response
  77. what are the two types of t cells
    • helper T: CD4 usually become helper T, which activate B cells, other T cells, macorphages, and direct adpative immune response. some beomce regulatory T cells which moderate immune response
    • Memory T cells
  78. CD8 cells become
    • cytotoxic t cells
    • destory cells harboring foreign antigens
    • also become memory T cells
  79. helper cytotoxic and regulatory t cells are all activated T cells, true or false
    true
  80. MHC I
    displayed by all cells except RBC
  81. MHC II
    displayed by APCs (dendritic, macrophages, B cells)
  82. CD8 cells bind to MHC I or MHC II
    MHC I
  83. CD4 bind to MHC I or MHC II
    MHC II
  84. t cell activation
    • antigen binding and costimulation
    • both occur on surface of same APC
    • both required for clonal selection
  85. who produces B7 proteins
    dendritic cells and macrophages produce surface B7 proteins when innate defenses mobilized. it is crucial for a co-stimulatory signal
  86. without t cell co stimulation
    • they become tolerant to that antigen
    • are unable to divide
    • do not secrete cytokines
  87. t cells that are activated
    • enlarge and proliferate in response to cytokines
    • differentiate and perform functions according to their T cell class
  88. cytokines
    • chemical messengers of immune system
    • mediate cell development, differentiation, and responses in immune system
    • include interferons and interleukins
  89. role of helper T cells
    • play central role in adaptive immune response
    • activate both humoral and cellular arms
    • without them, there is no immune response
  90. CD4 cells require helper T cell activation into destructive cytotoxic T cells
    false; CD8 cells do that
  91. cytotoxic cells
    • directly attack and kill other cells
    • activated T cells circulate in blood and lymph and lymphoid organs in search of body cells displaying antigen they recognize
  92. what are the targets of cytotoxic cells
    • virus infected cells
    • cancer cells
    • foreign cells
    • cells with intracellular bacteria or parasite
  93. perforins
    create pores through which granzymes enter target cell
  94. granzymes
    stimulate apoptosis
  95. autografts
    from one body site to another in same person
  96. isofrafts
    between identical twins
  97. allografts
    between individuals who are not identical twins
  98. xenografts
    from another animal species
  99. how many people have died from AIDS
    none; they die from an opportunistic disease because of the weakened immune system due to AIDS
  100. HIV coasted glycoprotein complexes attache to which receptor
    CD4
  101. anaphylactic shock
    • systemic response to allergen that directly enters blood and circulates rapidly
    • basophils and mast cells enlisted throughout body
    • systemic histamine release ay cause constriction of bronchioles, tongue may swell, circulatory collapse and death
    • treatment: epinephrine

Card Set Information

Author:
 swasdo
ID:
 276989
Filename:
 ch 21
Updated:
2014-06-16 22:26:05
Tags:
bio242
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Description:
immunity
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