Microbio Final part 1

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  1. What are some of the factors that play into Natural Resistance/Innate Immunity?
    1. Phagocytes (IE: Macrophages)

    2. Mechanical Barriers (IE: Skin and Mucus Membranes)

    3. Chemical Factors
  2. Describe the various chemical factors that play into Natural Resistance/Innate Immunity
    Fatty Acids → Effective against Gm(-) on Skin

    Bile Salts → Effective against Gm(+) on GI Tract (Gall bladder, liver, intestines, etc...)

    Interferon → Effective against Viruses

    Lysozyme → More efective against Gm(+) than Gm(-)

    Phagocytins → Bacteriocidal substance - leukocytes

    Complement → Can cause microbial cells and some cancer cells to lose physical integrity and lyse (this is done by complement proteins attaching to pathogen surfaces, attracted by IgM or IgG antibodies bound to the pathogen. Complement proteins can form a pore)
  3. Where are complement proteins found, and what do they result in?
    Complement proteins are bound by complement receptors called C3 Receptors (C3R) found on the surface of phagocytes (IE: neutrophiles, macrophages), resulting in enhanced opsonization
  4. After an antibody binds to an antigen on the surface of a bacteria, what occurs next? (in respect to phagocytes)
    After antibody binds to antigen, complement proteins (red) are attracted to the cell. Complement may form pores and directly lyse the cell. In addition, phagocytes such as neutrophils and macrophages have receptors that bind antibodies (FcR; green) or complement (C3R; yellow). Interactions with these receptors enhance phagocytosis, a phenomenon called opsonization.

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  5. What may Myeloid Precursors generate?
    1) Granuolcytes 

    Includes: Mast Cells, Esinophils, Phasophils, and Neutrophils ("Actively motile granuolcyte" containing large numbers of lysozymes; contains a segmented nucleus and granular cytoplasm)

    2) Monocytes (which are circulating precursors of macrophages)

    Includes: Dendritic Cells and Macrophages (another phagocyte; injests and destroys most pathogens and foreign molecules that invade the body, they also initiate adaptive immunity by presenting antigens to T-lymphocytes)

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  6. What can Lymphoid Precursors generate?
    1) T-Cells (mature in the thymus)

    2) B-Cells (mature in bone marrow or fetal liver)

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  7. Once engulfment of a pathogen occurs by a phagocyte, how may it kill the pathogen?
    1. Exposure to toxic oxygen compounds (causing oxidation of cellular components) like the following:

    • Hydrogen Peroxide (H202)
    • Superoxide Anions (O2-)
    • Hydroxyl Radical (*OH)
    • Singlet Oxygen (1O2)
    • Hypochlorous Acid (HOCL)
    • Nitric Oxide (NO)

    2. Within the phagolysosome, you may also have Lysozymes, Proteases, Phosphatases, Nucleases, or Lipases
  8. How may bacteria such as Staph. aureus and Mycobacterium tub. counter phagocytosis?
    Staphylococcus aureus: May employ Cartenoids (which can quench singlet oxygen) or Coagulase (which can wall off the growing bacterial population from phagocytes)

    Mycobacterium tuberculosis Is able to grow and persist inside of macrophages (and phagocytic cells in general). May also use their cell wall glycolipids to absorb hydroxyl radicals and superoxide anions)
  9. How may pyogenic bacteria prevent phagocytosis?
    Pyogenic bacteria are able to produce Leukocidins, which are able to kill white blood cells (Leukocidins makes up most of the material called "pus")

    Staph aureus and Staph pyogenes are two examples of bacteria that make produce leukocidins
  10. On what bacteria may M-Proteins be found, and what can they do?
    M-Proteins, found on the surface of Staphylococcus pyogenes, alter the surface of the bacterial cell and inhibits phagocytosis
  11. Consider how Adaptive Immunity breaks up into separate categories of Naturally or Artificially Acquired...(flow chart)
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  12. What are the different separated aspects of Immunity as a whole? (flow chart diagram)
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  13. What does Induced Immunity require?
    Induced Immunity requires prior contact or exposure to the antigen
  14. Humoral Immunity is mediated by _____. Cellular Immunity is mediated by ______.
    Humoral Immunity is mediated by antibodies, which are produced by B-lymphoctes that can differentiate into plasma cells (which produce antibodies in mass quantities) or memory cells

    Cellular Immunity is mediate by cells such as T-cells and NK cells
  15. Describe TH cells (what receptors do they have and are there different types?)
    TH cells contain CD4 receptors, which are associated with the MHC Class II, which is associated with B-lymphocytes, Macrophages, and Dendritic cells (basically all dedicated APCs)

    There are two types:

    1) TH1 - produce cytokines that stimulate macrophages to increase phagocytic activity, and promote inflammation

    2) TH2 - Activate B cells (and thus AB production)
  16. Describe TC cells
    TC cells contain the CD8 receptor, which is associated with MHC Class I, which is associated with all nucleated cells 

    Cells displaying foreign antigens via MHC Class I are killed by TC cells (IE: a virally infected cell wall presents part of the peptide as an antigen, marking the cell for termination via TC cells)

    They also release performins (which create pores in cellular walls) and granzymes (which cause apoptosis)
  17. Describe Natural Killer (NK) Cells
    NK cells are a type of lymphoid cell that is capable of killing tumor cells, virally infected cells, bacteria, fungi, and parasites (realize that they are quite unspecific) 

    They are involved in the Innate Immune Response

    • They target cells by initiating apoptosis in the target cell (releasing performin and granzymes) 
    • They also produce cytokines (specifically TNF, a granuolcyte-macrophage stimulating factor) 

    Do not use Toll-like receptors

    They function as a protective mechanisms, taking place in the interval before the more powerful adaptive immune response is active
  18. What are the characteristics of Adaptive Immunity?
    Adaptive immunity is the acquired ability to recognize and destroy a particular pathogen or its products that is dependent on exposure to that antigen.

    • Specificity: Recognition of specific antigens.
    • Memory: Reaction is faster upon second infection.
    • Tolerance: Immune cells are not able to react with self antigen.
  19. Briefly describe the PAMP-to-PRR interactions of the Innate Immunity
    Phagocytes interact with pathogens by recognizing pathogen-associated molecular patterns (PAMPs) with specific preformed pattern recognition receptors (PRRs). The interactions activate the phagocyte to ingest and destroy the pathogen and to produce cytokines that attract and activate other cells.

    • Examples of PAMPS: Lipopolysaccharide, flagellin, double stranded RNA of certain viruses.
    • Examples of PRRs: PRR to LPS found on all phagocytes.

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  20. What is the general purpose of inflammation?
    To isolate pathogens, and limit tissue damage.
  21. True or false: Inflammation is only a result of the Innate immune system

    Inflammation can be a result of both innate or adaptive immune response.
  22. If inflammation becomes deloacalized, what can result?
    Inflammation can cause septic shock if the reaction is not localized & it spreads through circulatory and lymphatic system.

    Septic shock causes increased vascular permeability (leading to efflux of fluids from vascular tissue), loss of blood pressure, severe edema, loss of blood volume.
  23. PRRs were first observed in ______ and were called ______.
    PRRs were first observed by Drosophila and were called Toll receptors.
  24. What is the specific pathogen recognition receptor (PRR) to the LPS layer of certain bacteria?
    TLR-4 is the PRR specific to LPS layers (PAMP)
  25. True or False: All Immunogens are Antigens, but not all Antigens are Immunogens
  26. Differentiate between Antigens and Immunogens
    Antigens: Substances that react with antibodies or TCRs (T Cell Receptors)


    • Substances that are characterized by their high molecular weight, complexity (polymers>monomers), and form (aggregate>solube, insoluble proteins/antigens are readily taken up by phagocytes). 
    • Illicit an immune response
    • Foreign to the responder
  27. Give an example of a substance that is an antigen, but not an immunogen

    Although it can interact with antibodies or TCRs, it will not activate them. Hapten must be complexed with a high molecular weighted material to elicit an immune response. When this happens, an antibody can respond to separate epitopes on both Hapten and the carrier it is complexed with. 

    Thus, the next time Hapten enters the body, it acts as an antigen and can react
  28. Where and how are antibodies produced at the cellular level? (in depth)
    At the cellular level, complex interactions between T cells and B cells produce antibodies that provide effective antigen-specific immunity. 

    B cells initially function as antigen-presenting cells. They interact with antigen via the antigen-specific Ig receptor, promoting endocytosis of the antigen–antibody complex, and leading to antigen degradation and processing. After processing, antigen is presented to the TH2 cell by the B cell’s class II MHC molecule. The TH2 cell is then activated to transcribe and translate genes for cytokines. The T cell cytokines then spur the same B cell to divide and form plasma cells (antibody producers) or memory cells. Plasma cells produce antibody. Memory cells quickly convert to plasma cells after a later antigen exposure.

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  29. How are antibodies produced at the cellular level? (briefly describe)
    Antibodies are synthesized by plasma cells, that result from activated B cells, which are activated by the release of IL-4 and IL-5 cytokines from TH2 cells from interaction with antigens presented by a B cell via MHC Class II.
  30. True or False: Antibodies or TCRs may react with ay region on an antigen

    Antibodies or TCRs do not interact with the entire antigen, rather at certain regions called epitopes (formerly antigenic determinatives).

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  31. What does MHC stand for, and where can it be found? What are they used for?
    MHC stands for Major Histocompatibility Complex, and they are found on host cell surfaces. All host cells display MHC I proteins, and APCs (macrophages, dendritic cells, and B cells) also display an additional antigen-presenting protein, MHC II. 

    The function of MHC molecules is to bind peptide fragments (antigens) derived from pathogens and display them on the cell surface for recognition by the appropriate T cells.
  32. True or False: There are cicumstances where T-Cells may recognize foreign antigens in the absence of MHC proteins

    T-Cells cannot recognize foreign antigens unless they are presented in the context of an MHC protein
  33. What is the structure of an Antibody?
    Antibodies, or immunoglobulins (Igs), are soluble proteins that interact with antigens and are produced by B lymphocytes. Antibodies consist of four polypeptides, two heavy chains (H) and two light chains (L), arranged as a pair of heterodimers. Each heterodimer consists of a light-chain heavy-chain pair and is a complete antigen-binding unit. The heavy and light chains are further divided into C (constant) and V (variable) domains.

    • The C domains are responsible for common functions such as complement binding.
    • The V domains of one H and one L chain interact to form an antigen-binding site

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  34. What is the function(s) of an Antibody?
    Antibodies function in three distinct ways:

    1) They bind directly to antigens, effectively coating the surface of the invader, in order to prevent pathogens from entering or damaging healthy body cells.

    2) Antibodies can also stimulate other parts of the immune system (e.g. complement proteins) to destroy the pathogens.

    3) Antibodies can mark pathogens through a process called opsonization so that the pathogens can be identified and neutralized by other immune cells.
  35. Where and how are antibodies produced at the genetic level?
    At the genetic level, B cells use unique mechanisms to generate unique antigen-binding receptors. 

    Antibody production starts with stepwise rearrangements of the Ig-encoding genes. During development of B cells in the bone marrow, both heavy-chain and light-chain genes rearrange.

    The genes are recombined (individual gene pieces are mixed and matched in various combinations) by gene splicing and rearrangements in the differentiating B cells, a process called somatic recombination.
  36. Where and how are antibodies produced at the cellular level?
    At the cellular level, complex interactions between T cells and B cells produce antibodies that provide effective antigen-specific immunity. 

    B cells initially function as antigen-presenting cells. They interact with antigen via the antigen-specific Ig receptor, promoting endocytosis of the antigen–antibody complex, and leading to antigen degradation and processing. After processing, antigen is presented to the TH2 cell by the B cell’s class II MHC molecule. The TH2 cell is then activated to transcribe and translate genes for cytokines. The T cell cytokines then spur the same B cell to divide and form plasma cells (antibody producers) or memory cells. Plasma cells produce antibody. Memory cells quickly convert to plasma cells after a later antigen exposure.

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  37. B cells mature in the ____ and differentiate into _____ to produce ______ . T-cells must be ______ to promote immunity.
    B cells mature in the bone marrow and differentiate into plasma cells to produce antibodies . T-cells must be matured in the thymus to promote immunity.
  38. Comare/contrast Cellular Immune response and Humoral Immune response.
    The humoral response (or antibody‐mediated response) involves B cells that recognize antigens or pathogens that are circulating in the lymph or blood (“humor” is a medieval term for body fluid).

    The cell‐mediated response involves mostly T cells and responds to any cell that displays aberrant MHC markers, including cells invaded by pathogens, tumor cells, or transplanted cells.
  39. Describe the process of the Humoral Immune Response.
    1) Antigens bind to B cells.

    2) Interleukins or helper T cells (specifically TH2) co-stimulate B cells. In most cases, both an antigen and a co-stimulator are required to activate a B cell and initiate B cell proliferation.

    3) B cells proliferate (grow+divide) and produce plasma cells. The plasma cells bear antibodies with the identical antigen specificity as the antigen receptors of the activated B cells. The antibodies are released and circulate through the body, binding to antigens.

    4) B cells produce memory cells. Memory cells provide future immunity.

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  40. Describe the process of the Cell-mediated Immune Response.
    1) Self cells or APCs displaying foreign antigens bind to T cells.

    2) Interleukins (secreted by APCs or helper T cells) co-stimulate activation of T cells.

    3) If MHC‐I and endogenous antigens are displayed on the plasma membrane, T cells proliferate (grow+divide), producing cytotoxic T cells. Cytotoxic T cells destroy cells displaying the antigens.

    4) If MHC‐II and exogenous antigens are displayed on the plasma membrane, T cells proliferate, producing helper T cells. Helper T cells (specifically TH1) release interleukins (and other cytokines), which stimulate B cells to produce antibodies that bind to the antigens and stimulate nonspecific agents (NK and macrophages) to destroy the antigens.

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  41. Briefly describe MHC Class I
    MHC Class I proteins are found on the surface of all nucleated cells.

    They work with intracellular pathogens (i.e. viruses) and TC cells.

    They are assembled in the endoplasmic reticulum.
  42. How are MHC Class I proteins made?
    MHC I proteins are stabilized in the endoplasmic reticulmn (ER) by chaperones until antigen is bound.

    1) Internal foreign antigens within the cell are degraded by the proteasome in the cytoplasm and the peptide fragments are transported into the ER through a pore formed by the TAP proteins. 

    2) The peptides bind to MHC I are transported to the cell surface 

    3) The antigens interact with T cell receptors (TCRs) on the surface of TC cells.

    4) The CD8 coreceptor on the Tc cell engages MHC I, resulting in a stronger complex. The Tc cells then release cytokines and cytolytic toxins (perforins and granzymes), killing the target cell.

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  43. Briefly describe MHC Class II proteins
    MHC Class II proteins are found only on the surfaces of B lymphocytes, macrophages, and dendritic cells.

    They work with extracellular pathogens and are assembled in the endoplasmic reticulum.
  44. How are MHC Class II proteins made?
    1) MHC II proteins in the ER are assembled with Ii (an invariant protein chain), preventing MHC II from complexing with peptides in the ER.

    2) Lysosomes containing MHC II then fuse with phagosomes, forming phagolysosomes where the Ii and foreign proteins, imported from outside the cell by endocytosis, are digested.

    3) The MHC II protein then binds to the digested foreign peptides, and the complex is transported to the cell surface 

    4) The complex then interacts with TCRs

    5) The complex then interacts with the CD4 coreceptor on TH cells. The TH cells then release cytokines that act on other cells to promote an immune response.

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  45. Briefly describe TC Cells
    T-cytotoxic (TC) cells, also known as cytotoxic T lymphocytes (CTLs), are CD8 T cells that directly kill cells that display foreign surface antigens.  

    The TC cells respond by releasing granules that contain perforin (forms pore) and granzymes (proteins that cause apoptosis), cytotoxins that perforate the target cell and cause apoptosis, respectively.

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  46. Intracellular parasites are best killed when _______
    Intracellular parasites are best killed when the host cell is destroyed (via the help of TC cells)
  47. Briefly describe TH1 Cells
    TH cells are T-Inflammatory cells that are activated by antigens presented in the context of MHC Class II

    TH cells produce cytokines that stimulate macrophages (they can also kill intracellular bacteria that would normally multiply). They also secrete cytokine IL-2 (the 2nd signal needed for activation of T-Cells)

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  48. Briefly describe TH2 cells
    TH2 cells activate B-Cells that can differentiate into plasma cells that produce antibodies (or memory cells).

    The B-Cell is covered with antibodies that act as antigen receptors, the antigen is endocytosed and degraded, then presented via MHC II to TH2.
  49. A B-cell is activated via the release of ______. The purpose of simulation is to differentiate into plasma cells by _______.
    A B-cell is activated via the release of IL-4 & IL-5. The purpose of stimulation is to differentiate into plasma cells via IL-6.
  50. Which form of immunity is most likely to by stimulated by an intracellular pathogen? Extracellular pathogen?
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  51. How does TH1 stimulate TC cells?
    By secreting cytokine IL-2, thus TH1 cells can be involved in cellular immunity.
  52. Where are antibodies (immunoglobulins) found?
    They are found in the serum, & other body fluids such as gastric secretions and breast milk (colostrum).
  53. Compare/Contrast the 4 Immunoglobulins
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  54. Briefly describe Papain
    • Papain is a nonspecific thiol endopeptidase that enzymatically cleaves IgG above the hinge region to create 2 Fab and 1 Fc regions. Fab fragments bind antigen; Antibody-bivalent
    • Aids in structural study, histochemical study, etc.
  55. Describe the process of Immediate Hypersensitivity
    • Allergens are presented by APC to TH cells and B-Cells.
    • B-Cells make IgE to antigen, which then bind to mast cells.
    • Subsequent exposure to allergen causes mast cell to degranulate releasing histamines, & serotonin (among others) by crosslinking to two IgEs.
    • Causes dilation of blood vessels and contraction of smooth muscle.

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  56. Following a latent period, specific Antibodies appear in the blood, gradually ______, then slowly _______.
    Following a latent period, specific Antibodies appear in the blood, gradually increase, then slowly decrease.
  57. Plasma cells produce large amounts of what antibody?
    Plasma cells produce large amounts of IgM
  58. Plasma cells can live for _____, and Memory Cells can live for _______.
    Plasma cells can live for roughly a week, and Memory Cells can live for several years.
  59. Upon re-exposure to immunizing agent, what happens to memory cells?
    Upon re-exposure to immunizing agent, memory cells skip T-Cell activation, and quickly transform to plasma cells that produce IgG.
  60. Consider the time frame difference in Primary and Secondary response for vaccination injections
    The antigen injected at day 0 and day 100 must be identical to induce a secondary response. The secondary response, also called a booster response, may be more than 10-fold greater than the primary response. Note the class switch from IgM production in the primary response to IgG production in the secondary response.

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  61. What happens if humoral immunity is compromised?
    In Chickens: Remove the bursa in – failure to produce antibodies, more susceptible to bacterial or extrinsic invaders.

    In Humans: Burton’s Agammaglobulinaemia – children fail to produce antibodies, MALT/GALT functionality compromised.

    Cellular immunity is intact, and hosts are no more susceptible to viral/intrinsic infections as a result of these pathologies.
  62. What happens if cellular immunity is compromised?
    In Mice:

    • Removal of thymus in mice causes them to be more susceptible to viral infections or intrinsic parasites (M. tuberculosis).
    • Increased rate of tumor production
    • Failure to reject transplanted tissue

    In Humans:

    • Nonfunctional thymus in Humans
    • DiGeorge’s Syndrome - 10,000x greater chance of malignancy, not more susceptible to extrinsic infections.
  63. What does Vaccination involve?
    Vaccinations involve inoculation of host with inactive or weakened pathogens or pathogen products to stimulate immunity, this involves attenuated strains, chemically or physically inactivated strains (Ex: the polio virus with formaldehyde to yield the Salk polio vaccine).

    Can also be Products of pathogens (i.e. toxins → toxoids) Example: Protective factor of anthrax

    Can also be Recombinant vector vaccine (Antigen cloned from a virus into a vaccinia genome)

    Can also be a DNA vaccine. Bacterial plasmid with cloned DNA injected intramuscularly into host animal resulting in T cells and antibodies made to the protein encoded by the cloned DNA

    Can also be Chemotherapeutic agents
  64. What does attenuation refer to?
    (viral) Strains that have lost their virulence but retain immunogenicity (still viable)

    Effective for viral vaccines.

    May prove to be a danger to immunocompromised individuals, attenuated strains may cause active disease.
  65. Acquired Immunity (artificial, passive) is ____ compared to active
    Acquired Immunity (artificial, passive) is short lived compared to active
  66. What are examples of artificial passive Acquired Immunity?
    Tetanus antiserum given to passively immunize an individual suspected to have been exposed to Clostridium tetani.

    Pooled human gamma globulin given to patients exposed to hepatitis A.
  67. What are examples of natural, passive Acquired Immunity?
    Placental transfer of IgG from mother to fetus.

    IgA transferred from mother to baby via breast milk (colostrum).
Card Set:
Microbio Final part 1
2015-05-03 23:53:58
Microbio Final

Microbio Final part 1
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