Immunity Study Guide Exam 3

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  1. Phagocytosis
    • cells ingest another cell or an antigen
    • (macrophages, neutrophils)
  2. Respiratory Burst (which cells)
    • Neutrophils* and Macrophages
    • They are attracted by chemical signals to infected areas. Once they arrive to an infected area they kill by respiratory burst
  3. Tolerance
    TRUE
  4. Fever (beneficial?)
    • yes, kills antigens immunity replicates, speed up metabolism, kill them
    • Fever (Pyrexia)- A fever may develop in response to toxins produced by pathogens or due to pyrogens released by leukocytes.  While a high fever is dangerous (1040F), moderate fevers inhibit the growth of some microorganisms. The high body temperature inhibits some microbial growth and speeds up body reactions that aid repair.
  5. Eosinophils (what do they kill?)
    • parasitic worms
    • Contain destructive enzymes in cytoplasm granules which are discharged against the outer covering of the invading pathogen
  6. Cancer cells and virus-infected body cells are killed how? (What do they kill?, who hunts down?)
    • Natural Killer Cells
    • 1. Kill aberrant cells that could form tumors
    • 2. Destroy body's own infected cells, especially those harboring viruses. Are not phagocytic, but attack membrane, causing lysis. NK cell recognizes abnormal cell then secretes perforins, which bind to the enemy cell and make holes in the membranes
    • 3. Theory of Immunological Surveillance
  7. Inflammatory Response (stages, sings & symptoms)
    Inflammatory Response occurs when there is damage to a tissue due to physical injury or infection.

    • Purpose: restore tissue homeostasis by-
    • 1. Protecting and defending by eliminating microbes, toxins, or foreign material from site of injury
    • 2. Preventing the spread of microbes, toxins, or foreign material to other organs
    • 3. Preparing the site for tissue repair

    • Stages:
    • 1. Vasodilation (widening) 
    • 2. Increased permeability of blood vessels
    • 3. Phagocyte migration
    • 4. Repair

    • Symptoms:
    • 1. Redness
    • 2. Pain
    • 3. Heat
    • 4. Swelling
    • 5. Loss of function


  8. Chemotaxis
    Phagocytes are attracted to the damaged tissue by several chemical mediators (chemotaxis)
  9. Phagocytic cells (2 main inflammatory -hystamine and protagladins)
    • Chemical signals are important to initiate inflammatory response:
    • 1. Histamine- released from injured circulating basophils and mast cells in the connective tissue. Released histmaine causes localized vasodilation and the capillaries in the area to become more permeable=leakier
    • 2. Protaglandins- released from WBC and damaged tissues. promotes increased blood flow to the injured area.
  10. Phagocytic cells (Types of WBCs)
    • 1. Neutrophils (60-70%)
    • 1st to arrive at the scene
    • attracted by chemical signals to infected areas methods of killing 1. Phagocytosis 2. Respiratory burst *
    • 2. Monocytes (5%)
    • enter tissue become Macrophages (larger)
    • kill: 1.Phagocytosis * 2. Respiratory Burst
    • Types of Macrophages:
    • 1. Alveolar macrophages- dust cells in the lungs
    • 2. Histiocytes- in connective tissue
    • 3. Kupffer cells- in liver
    • 4. Microglial cells- in neural tissue
    • Dentric cells- in epidermis, oral mucosa, esophagus, vagina, and lymphatic organs

    • 3. Eosinophils (1.5%) limited phagocytic activity
    • 1. Kill Parasitic worms
    • 2. contain destructive enzymes in cytoplasm granules which are discharged against the outer covering of the invading pathogen.
    • see Natural Killer Cells

  11. Basophils
    • Basophills (<1%)
    • store histamine
    • IgE. A Y-shaped monomer. Stem regions attach to receptors on mast cells and basophils; stimulates these cells to release histamine and other chemicals that cause allergic reactions when triggered by an antigen.
  12. ----
  13. Interferon (chemical functions, cytokin-what cell secretes it?)
    • Interferon- Antimicrobial substance
    • against colonization by viruses and bacteria and provide a 2nd line of defense should microbes penetrate the skin and mucous membranes 
    • released by virally infected cells
    • INFs also enhance the activity of phagocytes and NK cells, inhibit cell growth, and suppress tumor formation 
    • most effective against short-term infections (colds, influenza)
    • Cytokines Interferon(chemical messengers)
    • cytokines- chemicals secreted by one cell as a regulator of neighboring cells
    • regulate B and Tcells
    • involved in both humoral and cell-mediated responses
  14. What are antigens?
    foreign to the body
  15. Physical barriers to invasion
  16. Complement
    • Complement proteins, When activated- enhance certain immune, allergic, and inflammatory reactions
    • antimicrobial substance, work against colonization of viruses and bacteria and provide 2nd line of defense should microbes penetrate the skin and mucous membranes
    • group of 20 proteins present in blood plasma and on cell membranes.
  17. Inflammatory Response (signs symptoms and stages)
    see #7
  18. Opsonization
    • (complement Protein way to kill pathogenss in 3 ways 2. Oponization)
    • copperative mechanism in which complement proteins attach to a foreign cell and stimulate phagocytes to engulf the cell
  19. An alarm substance that triggers an inflammatory reaction is ________.
    **Histamine**
  20. Inflammatory Response
    see #7
  21. Vaccination
    • Artificial Active Immunity
    • vaccine consists of either dead or attenuated (weakend) pathogens which can stimulate the body's immune response but normally cause little or no discomfort or disease.
    • long lasting due to memory cells are produced
    • the production of one's own specific immunity cells as a result of vaccination against disease
  22. If a person's bone marrow were destroyed by radiation what cells would be affected?
    **ALL**
  23. Physical barrier to infection
  24. Interleukin-1 (what type?)
    • what type? - *Cytokin*
    • Interleukin-1- secreted by leukocytes

  25. Macrophages
    • derive from Monocytes
    • destroy pathogens by phagocytosis, clean up the remains of damaged tissue cells and dead neutrophils
    • Monocytes (5%) enter tissue become Macrophages (larger)
    • kill: 1.Phagocytosis * 2. Respiratory Burst
    • Types of Macrophages:
    • 1. Alveolar macrophages- dust cells in the lungs
    • 2. Histiocytes- in connective tissue
    • 3. Kupffer cells- in liver4. Microglial cells- in neural tissue
  26. Complement (how it kills?)
    • kills 3ways:
    • 1. Membrane attack complex- the complex lyses the pathogen.
    • 2. Oposonization- cooperative mechanism in which complement proteins attach to a foreign cell and stimulate phagocytes to engulf the cell 
    • 3. Immune adherence- complement proteins and antibodies coat a microbe which causes it to adhere to blood vessels walls and other surfaces' this makes the cell easy prey for circulating phagocytes
  27. The following events occur when the immune system first encounters a pathogen. Place them in a correct sequence, and then choose the answer that indicates that sequence.
    • III. Antigenic determinants from pathogen bind to antigen receptors on lymphocytes
    • IV. Lymphocytes specific to antigenic determinants from pathogen become numerous
    • II. Lymphocytes secrete antibodies
    • V. Only memory cells remain
  28. Plasma cells (function, what pathway AMI plasma cells are effector cells)
    • Antibody Mediated Immunity (AMI) plasma cells are effector cells
    • function- produce and secrete antibodies by other means
    • spleen is a site of B cell proliferation into plasma cells
  29. Cytokines
    • Chemical Messengers
    • cytokines- chemicals secreted by one cell as a regulator of neighboring cellsregulate B and Tcells involved in both humoral and cell-mediated responses
    • Interferon- secreted by virally infected cells
    • Interlukin I&II- secreted by leukocytes
  30. Perforin
    • creates holes in plasma membranes
    • released by Cytotoxic T cells "effector cells" (warriors)
    • lethal cytotoxic chemical
  31. Helper T cells
    • Cell Mediated Immunity
    • Helper T cells promote the action of cytotoxic cells as well as playing key roles in AMI and nonspecific defense. ALL other T cells are in CMI only
  32. Suppressor T cells (function)
    down regulate the immune response
  33. A doctor discovers that her patient can produce antibodies against some bacterial pathogens, but he is unable to protect himself against viral infections. The doctor suspects a disorder in her patient's (what type of cell)
    **T-cells**
  34. MHC (marker 1 why is it important?)
    • distinguishing abilities
    • http://quizlet.com/5421813/microbiology-15-flash-cards/
  35. Which of the folowing is true for both T cells and B cells?
    • lymphocytes
    • effectors
    • produced in bone marrow
  36. Allergy attack
    IgE- a Y-shaped monomer. Stem regiions attach to receptors on mast cells and basophils; stimulates theses to release histamine and otehr chemicals that cause allergic reactions when triggered by an antigen
  37. AIDS
    T-helper cell
  38. Antibodies of the different classes IgM, IgG, IgA, IgD, and IgE differ from each other in ( how do they different? different functions)
    • different functions
    • add more
  39. Clonal Selection
    • CMI1. a macrophage calls the T-helper cells to him by releasing interlukin-1
    • 2. A T-helper cell with the correct surface receptor will hook up with the macrophage. When a T-helper cell binds to antigen-presenting macrophage recognition occurs which causes the T-helper cells to begin to multiply (clonal selection).
    • 3. When the T-helpers multiply we also at this time set some of these aside to become T-helper memory cells.
    • 4. Activated T helpers secrete interlukimn II
    • 5. Interlukin II does two important things:
    •     1) Calls cytotoxic T cells to the infected area so that they can become activated
    •     2) Activates B cells that also have the ability to recognize this particular antigen.
    • 6. Activated cytotoxic T cells go out and destroy infected host cells
    • 7. Once the pathogen has been defeated suppressor T cells down regulate the immune response
  40. Cell-mediated immunity is mostly the function of what type of cell
    **T cell**
  41. Active Immunity v. Active Immunity
    • (active-long lasting since memory cells are produced) 1. Natural Active Immunity- production of one's own specific immunity cells as a result of exposure to an antigen
    • 2. Artificial Active Immunity- production of one's own specific immunity due to vaccination 
    • Passive:
    • 1. Natural Passive Immunity- temporary immunity that results from acquiring antibodies produced from another individual (ex: from mom to fetus or baby) 
    • 2. Artificial Passive Immunity- temporary immunity that results from the injection of an immune serum ontained from another or from an animal that produced antibodies against a certain pathogen (2-3weeks)
  42. Humoral Immunity (Antibody Mediated Immunity AMI)
    • (AMI) B cells are responsible fro the Humoral Immunity (AMI)
    • B cells defend by generating specific antibodies
    • (2-subpathway T-independent- long chains of proteins trigger humoral immune response without macrophage or T cell involvement)
  43. Secondary Immune Response
    • occurs when the body is exposed to a previously encountered antigen response is faster (3-5d) and more prolonged than a primary response.
    • Immuniological memory- (Tcell recall response, anamnestic response (Bcell)
  44. Plasma Cells
    • effectors of AMI pathway
    • function: produce and secrete antibodies to tag antigens for destruction by other means
    • some activated Bcells turn into Plasma cells (proliferation) in the spleen
  45. protection by antibodies that cross the placenta from mother to fetus?
    **passive natural**
  46. Types of T cells
    • Cytotoxic T cells- (EFFECTOR CELLS) of CMI
    • 1. Perforin 2. Lymphotoxin- destroys targets cell's DNA 3. Tumor necrosis factor (TNF) kills cancer cells by unknown mechanisms
    • Helper T cells (ON switch)- promote action of cytotoxic Tcells as well as playing key role in AMI and nonspesific defense. (all others involved in CMI only)
    • Suppressor Tcell (OFF switch)- limit CMI attack and keep the immune system from running out of control (regulatory lymphocytes)
    • Memory T cells- are descended from helper T and cytotoxic T cells and are responsible for memory in CMI
    • Antigen Presenting Cells (APC's)= macrophages and infected body cells
  47. Lymphocytes (characteristics)
    • made in the bone marrow
    • antigen receptors present on both
    • mature- lymph nodes, spleen, other lymph organs
    • B cells- Humoral immune response or AMI generate antibodies, membrane bound antibdy molecuels which recognize specific antigens
    • T cells- CMI response, only respond to antigenic epitopes displayed on surfaces of the body's own cells. T cells cannot detect free antigens in the body fluids. receptors are proteins embedded in the membrane which recognize specific antigens 
  48. Function of CD4 and CB8
    • CD4- interactions T helper and APCs (antigen present cells) 
    • CB8- enhances recognition Cytotoxic T cell and infected cell
  49. Interleukin-I
    • Interleukin I&II- Cytokins
    • Macrophages release Interleukin-I to call T-helper cells to come to him for recognition for clonal selection
  50. Interleukin-II
    • Interleukin  II-released by (Activated T-helper cells)
    • 1. calls Cytotoxic T-cells so they become activated too
    • 2. activates B cells that also have the ability to recognize the particular antigen
  51. Perforin Mechanism
    • released by Cytotoxic T-cell
    • creates holes in the plasma membranes
  52. Plasma cells
    see #28
  53. Antibody production by plasma cells
    • Antibodies made up of Immunoglobulins (Ig)
    • Y-shaped, 4 amino acid chains 
    • (V) VARIABLE REGION not stem
  54. Characteristic of specific defenses include (omit)
  55. immunoglobulins
  56. immunoglobulins
  57. immunoglobulins
  58. immunoglobulins
  59. variable region of an antibody (function) BCR recognition
    (V) is the variable region of an antibody
  60. The binding of an antigen to an antibody can result in?
    • replicate stimulate immune response
    • form antigen-antibody complex which tags the invader for destruction by:
    • 1. Neutralization- simple, blocks viral attachment sites or coats a bacterial toxin, making them ineffective
    • 2. Agglutination- antigens cross-link and hold back clumps of bacteria
    • 3. Precipitation- cross-linking of soluble antigen molecules instead of cells (corner them)
    • 4. Complement fixation- activation of the complement system, combine with complement proteins, result in cell lysis
  61. In order for a lymphocyte to respond to an antigen, the antigen must
    *match*
  62. When an antigen is bound to a class I MHC molecule, it can stimulate a ______ cell.
    **T helper cell**
  63. Class II MHC molecules are found only attached to which of the following
     Macrophages
  64. When an antigen is bound to a Class II MHC molecule, it can stimulate a _______ cell.
    T-helper cell**
  65. B cells are primarily activated by the activities of
    Secreting T-helper cell of Interleukin II
  66. The following are steps in the cell-mediated immune response
    • 2. Antigen is engulfed and presented by a macrophage
    • 4. Undifferentiated T cells with specific receptors recognize the antigen
    • 1. Several cycles of mitosis occur (cloning)
    • 5. T cells differentiate into cytotoxic T cells and T memory cells
    • 3. cytotoxic T cells migrate to site of infection
    • 6. cytotoxic T cells release perforin and/or lymphotoxin
  67. Interlukins (function)
  68. Newborn infants gain most of their immunity from (active or passive mom)
    **Natural Passive Immunity**
  69. Immunoglobulins
  70. allergies (ref. to imunoglobins) Ig[]
    **IgE**

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Author:
 13BlueInkBunnies
ID:
 245872
Filename:
 Immunity Study Guide Exam 3
Updated:
2013-11-09 16:55:36
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Immunity
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Immunity Lymphatics
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