Immunity

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emmayarewhy
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273143
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Immunity
Updated:
2014-05-05 00:09:57
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immunity
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Final Exam
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Immunity
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  1. 1. What is immunity?

    2. What is the immune system? Immune response?

    3. What is the immune system associated with? (5)

    4.  What are the two processes involved in innate immunity?
    1. Immunity  - resistance to infectious disease

    2. Immune system - collection of tissues, cells, molecules that mediate resistance to an intruder (prevention of infection and eradication of established infection)

    Immune response is the action of these tissues/cells/molecules

    3. Defense against infection, tumors, allergy, autoimmunity, and transplant rejection

    4. Blocking (skin, eyes, GI tract, respiratory pathways --> barrier to pathogens) and rapid, nonspecific elimination of intruders (inflammatory response)
  2. 1.Describe inflammatory response (3)

    2. What are the 3 types of cells involved in the innate immune system? 

    3. What are antigen-presenting cells (APCs)? (3)

    4. What are the 3 types of phagocytes?
    1. Injury induces inflammation:

    1. chemical signaling (histamine release stimulating blood vessel dilation and capillary leakiness) and cytokines stimulate release/attraction of WBCs to injury

    2. Dilation of small blood vessels - allows for increased blood supply, redness, heat, swelling--> helps phagocytic cells move to site of injury. Phagocytic cells engulf microorganisms and clean debris

    3. Role of clotting proteins & platelets in the blood - repairs/seals infected area preventing spread of infection

    2. Phagocytic cells, natural killer cells, and mast cells

    3. Dendritic cells (lymph), B cells, and monocytes/macrophages

    4. Neutrophils, monocytes/macrophages, dendritic cells (lymph)
  3. Describe the 3 types of phagocytic cells.

    1. Neutrophils (5)

    2. Monocytes macrophages (4)

    3. Dendritic cells
    1. Neutrophils ((1) 50% of WBCs, (2) first cells to respond to infections, (3) mainly target bacteria and fungi, (4) engulf and self-destruct, and (5) short-lived - few hours/days)

    2. Monocytes and macrophages (1. 2-10%) 2. immature macrophages are monocytes --> blood monocytes become tissue macrophages. 3. Stimulate cells of adaptive immune response esp Th cell proliferation) and 4.  live much longer than neutrophils


    3. Dendritic cells - (1) phagocytic, antigen-presenting cell. (2) Links between innate and adaptive immune system (3) Function - takes up antigen, processes them, presents them to adaptive immune system cells for development of adaptive system

  4. 1. Which cells respond first to infection?

    2. Which cells make up the majority of WBCs?

    3. What is pus?

    4. What do neutrophils target?

    5. Which phagocytes are the shortest-lived?

    6. Link between innate and adaptive?
    1. Neutrophils

    2. Neutrophils (~50%)

    3. Dead cells, debris, and fluid

    4. Bacteria and fungi

    5. Neutrophils

    6. Dendritic cells (but also macrophage)
  5. 1. Describe natural killer cells

    2. How does granulation occur? What does it affect? What does it cause?

    3. Do they directly kill microorganisms? What do they act upon?

    4. What are they important for?

    5. Do they have antigen-specific cell surface receptors?
    1. Natural killer cells = cytotoxic lymphocytes part of the innate immune system. 

    2. NKs release perforin and granenzyme --> degradation of cel membrane --> cell lysis

    3. No, they act on infected cells

    4. Very important in viral infection and cancer

    5. No - but they can recognize change in cell surface proteins
  6. 1. What are mast cells?

    2. Where are they found?

    3. What happens when they're activated?

    4. What does this attract? (2)

    5. Can mast cells be phagocytic?
    1. Resident granulocyte (not lymphocyte or monocyte) containing granules of histamine & heparin

    2. Connective tissue & mucous membranes

    3. They release granules of histamine, heparin, and cytokines

    4. Neutrophils and macrophages to aid in defense mech

    5. Yes
  7. 1. How do phagocytes recognize the intruder before attacking/engulfing it? Be specific

    1.5 How do lymphocytes recognize intruders?

    2. What is the complement system?

    3. Name 4 functions of the complement system

    4. How is the complement system activated?
    1. Through surface receptors that are specific to a broad class of microbial products (toll-like receptors) and other receptors like mannose and cytokine receptors. These signals lead to activation of the phagocyte

    1.5. Through receptors on plasma membranes, but recognize specific receptors for a particular site on particular molecule. 

    2. Biochem/enzymatic cascade that aids ability of antibodies & phagocytes to clear pathogens or mark them for destruction by other cells. 

    • 3. (1) Coating/promoting binding to antibodies and phagocytes
    • (2) Chemotaxis - attracting macrophages and neutrophils to sites of injury
    • (3) Clumping of foreign agents -  making it easier for cells to clear debris 
    • (4) cell lysis (via membrane attack complex - MAC)

    4. (1) Classical pathway - triggered by antibody binding (involving adaptive immunity)

    (2) Alternative pathway - doesn't require antibodies - part of innate response, involving direct binding of C3B to microbe.

    (3) Lectin pathway - triggered by binding lectin to mannose residues of microbial glycoproteins
  8. 1. What are cytokines?

    2. What is adaptive immunity comprised of? (2)

    3. What does an infection usually activate?

    4. What are the key cells of adaptive immunity?

    5. What are the two main types of lymphocytes?
    1. Soluble proteins that mediate immune/inflammatory rxns by acting as tools of communication between leukocytes and other cells (including leukocytes)

    2. Cell-mediated and humoral immunity

    3. Innate immune system and lymphocytes

    4. Lymphocytes

    5. B cells (humoral immunity) - antibody production and T cells (cell-med immunity) - helper t cells and cytotoxic t cells.
  9. T cells and T Receptors

    1. What is the structure of a T cell receptor (TCR)?
    2. What do B and T cells recognize?
    3. How many antigen binding sites does a T cell receptor have?

    4. How many antigen receptors does a B or T cell have?

    5. What are the only types of antigens that T cells can "see?"
    1. A-B chain linked by a disulfide bridge. 

    2. Antigens bound to MHC molecules

    3. 1

    4.  100,000 identical antigen receptors

    5. Antigens that have been processed and presented by other cells via MHC molecules.
  10. 1. What do CD8+ cells also go by?
    2. What binds to CD8+ cells?
    3. What type of cell can display peptide antigens via MHC1?
    4. Which cells kill other cells? (2)
    5. How do Tc cells kill other cells?

    6. Which cells attack foreign transplant/tumor cells?
    • 1. Cytotoxic T cells
    • 2. MHC1
    • 3. Any kind
    • 4. Tc and NK
    • 5. By attacking membrane - releasing granules causing perforin causing cell to lyse. 
    • 6. Tc
  11. 1. What do Helper T cells do? (2)

    2. Who makes MHC2 molecules? When?

    3. In antigen presenting cells, what is the role of MHC2?

    4. What specifically do Helper T cells recognize?

    5. What does binding of Helper T cells to cell cause?

    6. What are the types of helper T cells and what do they act on? 1-4, 2-4
    1. Release cytokines that stimulate b cells to differentiate into effector cells that can produce antibodies OR facilitate proliferation of Tc cells

    2. Antigen-presenting cells (APCs - dendritic cells, macrophages/monocytes, B cells). Constitutitively

    3. MHC2 binds to peptides derived from foreign materials that have been phagocytized,  tagging the cell attached to the antigen as "self" 

    4. Helper T cells recognize the antigen in the context of MHC2 by APCs

    5. binding of Th cell to APC causes release of cytokines stimulating growth and division of Th cell ---> other functions (B cell differentiation, Tc proliferation)

    6. Th1 - active against bacterial and protozoan infections, autoimmunity. Acts on CD8+ cells, macrophages, IgG B cells, 

    Th2 - active against helminths and allergies. Acts on basophils, eosinophils, mast cells, IgE B cells
  12. 1. How are B cells activated? By who?

    2. what happens to the B cell after activation? Who do they target?

    3. What happens when the B cell binds to a pathogen with epitopes that match its receptor?

    4. What do plasma/effector cells do? At what rate do they produce?
    1. After binding to antigen-presenting cell and proliferating, helper T cells bind to B cells activating them. 

    2. Growth and proliferation. A specific antigen

    3. Clonal selection - B cells proliferate and differentiate into effector (mostly) and memory cells.

    4. Become factory for antibody productio, producing as many 2000 antibody molecules per second for 4-5 day lifespan of the plasma cell
  13. 1. What is an effector B cell?

    2. What is a memory cell?

    3. What are the functions of antibodies? (3)

    4. What are the 5 types of antibodies?
    1. Effector B cell = plasma cell - factory for creating antibodies until it dies (4-5 days)

    2. Memory cell = long-lasting cells bearing receptors for the same antigen (REMEMBERED)

    3. To (1) bind to antigen and (2) assist in elimination of that antigen by activating complement system, activating other effector cells (macrophages, neutrophils, dendritic cells, etc) and aggluginating cells together to make it easier to get rid of the pathogen

    (1) neutralization - blocks pathogens from carrying out damage bc phagocytes can recognize antigen-antibody complex

    (2) agglutination - crosslinks foreign molecules together to make it easier for phagocytes to find and engulf antigen-antibody complex

    (3) Activation of complement - eventually leads to cell lysis

    4. IgM, IgG, IgA, IgE, IgD
  14. 1. What does IgM do? (2) where is it found?
    2. IgG? (2)
    3. IgA? (1) Where is it found? (2)
    4. IgE? (2)
    5. IgD? (2)
    6. Which is most abundant?
    7. Passive immunity?
    8. Major antibody in colostrum?
    1. IgM - early response, only in blood, activates complement system 

    2. IgG- comes later, diffuses through placenta for passive immunity for fetus, activates complement 

    3. Prevents pathogen from colonizing. Found in mucosal surfaces & colostrum

    4. IgE - allergic reaction and triggers histamine release

    5. IgD - antigen receptor on B cells, involved in innate cell activation - mysterious



    6. IgG

    7. IgG
  15. 1. What is the primary immune response?  How long does it take?

    2. What is the secondary immune response? How long does it take? How does it differ from primary (3)? 

    3. What do the characteristics of the secondary immune response indicate?

    4. Are antibodies part of humoral or cell-med immune system? 

    5. Name the 3 mechanisms by which antibodies mark antigen-bearing invaders?
    1. Selective proliferation and differentiation of lymphocytes that occur the first time the body is exposed to an antigen. 10-17 days

    2. A second exposure to same antigen at later time. 2-7 days. faster response, greater magnitude, will last longer.

    3. Immunological memory

    4. Humoral

    5. (1) neutralization - blocks antigen from carrying out damage  (2) agglutination (3) activation of complement leading to cell lysis
  16. 1. What is most common disorder of immune system? Affects how much of population?

    2. What are 8 most common food allergens? 

    3. Define allergy

    4. Where can allergy occur?

    5. What is allergy mediated by? (2)

    6. What are 4 common types of allergies?
    1. Allergy - 20%

    2. Peanuts, tree nut, shellfish, egg, fish, wheat, soy, milk

    3. Allergy - rapid, hypersensitive response of the body's immune system to certain antigenes (allergens)

    4. skin, GI tract, respiratory tract, etc

    5. IgE cells and mast cells

    6. Food allergens, seasonal allergens, exercise-induced allergens, exercise-induced food allergens
  17. 1. Causes of allergies? (3)

    2. Describe mechanism in allergies (5)

    3. What causes symptoms of allergies? What interferes with action of histamines?

    4. What is anaphylaxis?
    1. Strong genetic component (70% twins, 40% non-identical twins), over-hygiene, and imbalance between Th1 (pro-inflammatory) and Th2 (anti-inflammatory) 

    2. (1) B cells produce IgE antibody in response to allergen (in predisposed individual)

    (2) IgEs bind to mast cells at Fc region (process called sensitization)

    (3) IgEs re-encounter antigen. Cross-linking occurs betwen bound IgEs and introduced allergen

    (4) Cross-linking leads to degranulation (release of mast cell mediators)

    (5) Degranulation (release of mast cell mediators) - release of histamine, proteases, and other inflammatory mediators which cause inflammation including dilation and leakiness of blood capillaries and tissue damage. Released cytokines recruit LEUKOCYTES!!!!!

    (3) Degranulation (release of mast cell mediators)


    (4) Anaphylaxis is the most severe form of immediate hypersensitivity. Cuased by widespread and sudden mast cell degranulation in response to allergen --> abrupt dilation of peripheral blood vessels causes sharp drop in blood pressure --> can be lifethreateing and countered with epinephrine.
  18. 1. Are food tolerances IgE-mediated?
    2. What are they caused by? (4) Name examples for each.

    3. What is autoimmunity? Who does it occur in more often?

    4. What factors must be in place in order for autoimmune disorder to be expressed?

    5. What is ^ generally associated with production of? (5)
    1. No

    2. Enzyme deficiency (lactose, alcohol), inability to absorb nutrients (fructose -transporter), biochemical/pharmacologic reaction to food (aspirin), non-IgE immune response to food (celiac disease, gullian barre disease)


    3. Lack of proper recognition to self due to improper immune response against self-antigens. Women

    4. Needs environment, antibody, and target organ/cell to be malfunctioning in some way (multiple-hit phenomenon)


    5. Autoreactive B and T cells, autoantibodies (IgG, IgM, IgA)
  19. 1. Describe pathogenesis of celiac disease.

    2. What activates innate immune response? (2)
    • 1. Gluten protein gets through epithelial barrier to lamina propia stimulating immune system
    • 2. Gluten peptide encounters transaminase 2 --> deamidation --> glutamic acid (highly immunogenic, attracting APCs)

    3. APCs process glutamic acid and presents antigen in context of HLA-DQ2/8 of the MHC2 molecule.

    4. T cell sees this and produces cytokines--> activating B cells to produce antibodies to transaminase 2 and gluten. As well as release of  cytokines from Th1 and Th2

    5. Th1 cytokines cause release of inflammatory molecules and matrix metalloproteinases that cause cell death and cell degradation. 

    6. Response to gluten also activates innate immune system as eptihelial cells secrete IL-15 and MHC-1 molecules ---> activating CD8+ cells expressing NK receptors which further target/destroy epithelial cells. 


    2. A-amylase/protease inhibitors of wheat through engagement of toll-like receptor
  20. 1. Difference between celiac disease, wheat allergy, and non-celiac gluten sensitivity (NCGS)?

    2. What can celiac disease and NCGS cause? Why? Symptoms? (4)
    1. Celiac diseaes - anti-TG2, anti-D-gliadin antibodie. Gluten only

    2. Wheat allergy - wheat-specific IgE antibodies. Clinical symptoms, skin prick tests (gluten AND non-gluten)

    3. NCGS - negative for CD serologic markers, IgE antibodies, but many are positive for anti-gliadin antibody (not sure if trigger is gluten and/or other wheat proteins). 

    2. Neurological problems. Anti-gliadin antibodies are associated with neuropsychiatric diseases bc the antibodies bind to neural cells and synapsin causing their phagocytosis. 

    Symptoms include ataxia, peripheral neuropathy, schizophrenia, bipolar, autism, etc. May not have intestinal symptoms.
  21. 1. Primary target in guillain barre syndrome?

    2. Trigger? Where is it found?

    3. Is there a genetic component? What is the immune response? 

    4. Symptoms? (3)

    5. Treatment? 

    6. Mechanism?
    1. Peripheral nervous system

    2. Trigger - C. jejuni in raw meat

    3. Yes. Humoral (antibody to peripheral nerve glycolipids)


    4. Symptoms: weakness, paralysis, fatality

    5. Plasma exchange

    6. Surface of c. jejuni contains polysaccharides that resemble glycoconjugates of human peripheral nerve tisuse, so single B or T cell receptor will trigger antibodies/T cells that attack both bacteria and nerve tissue.
  22. 1. What are common methods of antibody detection? (4)

    2. What antibodies biomark infection? (2) ALlergy? (1)? Autoimmune? (3)

    3. What can this information tell us?
    1. ELISA, Western BLot (WB), immunohistochemistry, microarray immunoassay

    2. Infection (IgG, IgM), allergy (IgE), autoimmune (IgG, IgM, IgA) -  same as infection + A

    3. Diagnosis of disease
  23. 1. Kwashiorkor vs. marasmus?

    2. How do protein-calorie and micronutrient deficiency affect immune system (7)
    1. Both are protein def, but kwashiorkor is sufficient calories. 

    2. (1) Atrophy of lymph organs (2) T cell deficiency (primarily impairment of cell-med immunity) (3) decreased phagocyte/NK function (4) defects in mucous membrane barrier (5) decreased cytokine response (6) decreased antibody production (7) Increased risk in frequency and severity of infection
  24. 1. What leads to increase in protein reqs?

    2. What proteins are important in immune system? (2)

    3. Deficiency in essential FAs leads to what? (2)

    4. What can increased fat intake lead to? (2) Why?

    5. What do diets high in w-6 vs. w-3 do?
    • 1. Immunological stress
    • 2. Glutamine - most abundant AA --> lymphocyte prolif against antigen. 

    Arginine - enhances lymphocyte function (essential in infants and highly stressed people)

    3. Lymphoid atrophy and depressed antibody responses. 

    4. Suppressed immune system (esp complement synthesis and cell-mediated immune function) bc these processes are mediated by products of lipid metabolism

    5. High in w-6 --> increased productions of prostaglandin EG (PGE2) --> inhibits complement synthesis and depresses cell-mediated immune function

    High in w-3 --> inhibits production of PGE2 and enhances immune function
  25. What do deficiencies in:

    1. Zinc
    2. Iron
    3. Copper
    4. Magnesium
    5. Selenium

    do?
    1. Zinc - MHC-1 component, altered T cells, thymic atrophy, decreased IgG response

    2. Iron - T cell defects, decreased IgG response, decreased phagocyte activity

    3. Copper - essential for neutrophil function, decreased antibody production 

    4. Magnesium - increased inflammatory cytokines, histamine, reduced complement activity

    5. Selenium - decreased antibody production, reduces Tc and lymphocyte proliferaiton part of glutathione reductase,
  26. What do the following vitamin deficiencies do in terms of effect on immune system?
    1. Vitamin A - lymphopenia, decreased mucosal barrier function, decreased T cell, phaocytes, NK function

    2. Vitamin C - decreased phagocyte function, decreased tumor resistance

    3. Vitamin B - lymphopenia, reduction of antibody response

    4. Vitamin D

    5. Vitamin E
  27. 1. HOw does obesity affect the immune system? (4)

    2. Why are newborns susceptible to infection? (5)

    3. How does breast milk help? (3)
    1. Greater incidence of infection (mortality), delayed wound healing, lower antibody production in response to vaccination (limited data) 

    2. Functional immaturity of immune system - (1) mucosal/epithelial barriers,  (2)low circulation of complement proteins, (3) immature neutrophils, (4) impaired macrophage activation, (5) antimicrobial effector function is short


    3. Prevents infection, enhances immune function, may protect against allergies/autoimmune disorders
  28. What are the immunoprotective components of milk? (3)

    3-6
    1. Immunoglobulins (sIgA - recognize a variety of microorganisms in respiratory tract and intestine)

    2. Leukocytes (primarily in colostrum and early lactation)

    3. Antimicrobial factors  - (1) lactoferrin, (2) lactoferricin,  (3)lysozyme (lysis of bacterial walls), (4) epithelial growth factor (decreasing permeability to infectious agents), (5) oligosaccharides, (6) variety of factors with anti-inflammatory activity (antioxidants, protease inhibitors, anti-inflammatory cytokines, casein subunits)

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