Unit 3 Lecture Objectives Flashcards

1
Q

Describe the structure and function of lymphatic capillaries and vessels, and explain how the lymph capillaries drain excess ISF and return it to the systemic circulation

A
  • Lymphatic vessels and capillaries structure
    • Vessels originate in “close-ended” lymph capillaries which lie adjacent to the blood capillaries
    • Lymphatic capillaries are larger than regular blood capillaries
    • Vessels have one way valves
  • Function
    • Lymphatic vessels drain excess ISF and return it to the blood stream
  • Lymph capillaries drain excess ISF through the following process:
    1. Blood flows through blood capillaries
    2. Interstitial spaces (space between cells) fill with excess ISF
    3. Lymphatic capillaries pick up the excess ISF now known as lymph
    4. Lymphatic vessels carry the lymph
    5. Lymphatic trunks or ducts recieve the lymph
    6. At the junction of the internal jugular and subclavian vein the lymph is mixed with the blood
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2
Q

List the body’s non-specific defenses and describe the components and mechanisms of each

A
  • Body’s non-specific defenses include:
    1. Physical barriers (first line of defense)
      • Mechanism:
        • Skin (sweat glands, pores), mucus membranes (secreted by goblet cells), hairs and cilia (mucus-coated hairs), acid levels (2.0 in tummy), and tears (contains lysozyme) all protect against bacteria getting into our body from the outside
    2. Fever
      • Mechanism:
        • Body’s thermostat is reset upward in response to pyrogens (their job is to increase temp)
        • Moderate fever causes liver and spleen to hold onto iron and zinc which is needed by microorganisms to grow
        • Also speeds up rate to repair tissue
    3. Inflammation
      • Mechanism
        • Prevents spread of damaging agents, disposes of cell debris, and pathogens, sets stage for repair
    4. Cells and Chemicals
      • Mechanism
        • Attacks microorgansims directly or by hindering their ability to move, produce, and grow
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3
Q

Describe and diagram the functions of the complement system

A
  • Refers to over 30 specific proteins that “complement” or enhance the action of antibodies
  • Complement proteins attach to antibody-antigen complexes
  • End result of attachment of membrance attack complex (MAC) which punches holes in bacterial cell membranes
  • Steps:
    • C3 is the complement protein that auto-cleaves by 3 different pathways
    • C3b coats microbes to help them better undergo phagocytosis and stimulates C5 to cleave
    • C3a and C5a attach to mast cells to help secrete histamines
    • C5b then helps to prodcue C6,7,8,9 which all help to form the a channel in invading cell so that extracellular fluid rushes in and bursts cell (Cytolysis)
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4
Q

Describe how NK cells kill virus-infected cells or tumors

A
  • Specialized class of T-lymphocytes (T-cells from thymus) which kill tumor cells and some virus-infected cells
  • NK cells release perforin which helps perforate the membrane and kill by cytolysis
    1. NK cell recognizes abnormal cell and adheres to it
    2. Golgi apparatus adjusts itself so that it is situated closes to the abnormal cell
    3. Golgi apparatus releases perforin and pores form on abnormal cell
    4. Abnormal cell lysis
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5
Q

Discuss the importance of interferons in disease prevention

A
  • Produced by virus-infected body cells, T-lymphocytes, natural killer cells, and macrophages
  • They are chemical messengers called cytokines
  • How they work
    1. Virus infects cell and that virus-infected cell will release interferons
    2. Interferons bind to receptor of non-infected cell
    3. Virus gets inside the non-infected cell making it infected
    4. Newly infected-cell can’t divide now because interferon is on the receptor
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6
Q

Describe the function, percent circulating WBCs, response, etc. for Neutrophils, Lymphocytes, Monocytes, Eosinophils, and Basophils.

A
  • Neutrophils
    • 60-70%, responds to bacterial infections
    • Fast and direct action against bacteria
    • Releases: lysozymes to digest cell wall, defensin to act as antibiotic and put pores in cell wall, and strong oxidant to destroy bacteria
  • Lymphocytes
    • 20-25%, responds to viral infections
    • Involved in adaptive immunity (B-cells and T-cells)
    • Natural killer cells involved in innate immunity
  • Monocytes
    • 3-8%, respond to fungal/viral infections
    • Wander around, destroy microbes, clean up dead tissue following infection
  • Eosinophils
    • 2-4%, reponds to parasitic infections or allergic reactions
    • Attacks parasites, phagocytizes antibody-antigen complexes, releases histaminase in ISF
  • Basophils
    • <1%, responds to allergic reaction
    • Highten inflammatory responses (eosinophils slow this response down)
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7
Q

Compare and contrast the general features of cell-mediated and antibody-mediated immunity

A
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8
Q

How can proteins from other organisms be identified as different from human proteins?

A

After phagocytosis, the residual body is sifted through and if the the peptide fragment is longer than 8 amino-acids in length, then that means that it can be checked to see if it is for sure a human cell, if it is shorter than 7 amino-acids, it is either a bacteria or human cell but cells can’t distinguish unless longer than 8.

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9
Q

What two sources of information provide us with information about invading organisms’ (bacterial or viral) proteins?

A
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10
Q

What are MHC proteins, and how are they used for the sharing of protein sequence information?

A

MHC proteins are a unique collection of genes that display information in the form of peptides (pieces of protein) to the immune system and this helps the immune system determine if the body they got the peptide from is foreign or part of the person

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11
Q

Compare and contrast the functions of MHC I and MHC II

A
  • MHC II: Antibody-mediated immunity
    • Protein presents processed antigen from protein components of material engulfed and digested by phagocytes: this is displaying extracellular antigen
    • Helper T cells come over with their T cell receptors and determine if the presented antigen is foreign or not
      • It is not MHC II’s job to determine if the presented antigen is foreign
  • MHC I: Cell-mediated immunity
    • Proteins present small fragments of protein called processed antigen
    • Presented antigen is from random-sampled proteins inside cell: this is displaying intracellular antigen
    • Cytotoxic T cells have T cell receptors whose job it is to interact with the peptide chain and determine if its foreign
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12
Q

What receptor protein enables the immune system to identify non-self antigen?

A

T cell receptors enable a T cell to determine if the presented antigen is one’s self or foreign. The TCR is unique meaning it fits like a key to the unqiue presented antigen meaning that it is indeed the body’s own cell. When this tight fit occurs, it is called recognition and an immune response is initiated. The thymus regulates which T cells with certain unique TCRs are allowed to be in circulation so that incorrect recognition doesn’t happen

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13
Q

How are T cells trained to identify only non-self antigen?

A
  • Negative selection: eliminates T cells that are strongly anti-self
  • Positive selection: selects T cells with a weak response to self-antigens, which thus become both immunocompetent and “Self tolerant”
  • Once the T cell with its TCR can tell that the self-MHC protein is itself, it can move onto decide if peptides are self or not. If the T cell with its TCR moderately binds to a self peptide it can finally leave the thymus (it is now immunocompetent) but if it tightly bonds to self peptides, it will dies because we don’t want a T cell with its TCR that will tightly bond to a self peptide because it will then have an immune response.
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14
Q

Compare and contrast the general features of cell-mediated and antibody-mediated immunity

A
  • Cell-mediated immunity: Depends on T-cell receptors (TCRs) that are expressed on the surface of cytotoxic T cells (every T cell is boarn with a unique TCR)
    • MHC I proteins present the foreign antigen that lives within our cells
    • Antigens presented by infected body cell (random sampling)
    • Proliferates Killer T cells
    • Use CD8 for costimulation
      • Activated by IL-2 that is released from helper T cell (effector cell)
  • Antibody-mediated immunity: Depends on T cell receptors (TCRs) that are expressed on the surface of helper T cells, in addition to other proteins used by B cells
    • MHC II proteins present the foreign antigen from outside our cell
    • Antigens presented by Antigen-Presenting Cell (APC)
    • Proliferates other T cells
    • Use CD4 for costimulation
      • Activated by tight binding between antigen and TCR
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15
Q

Describe the 4 major cell surface receptors that take part in immune response

A
  • TCR
  • CD4 (MHC II)
  • MHC II
  • CD8 (MHC I)
  • MHC I
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16
Q

Diagram the processes that leads to activation, proliferation and differentiation of killer and helper T cells

A
  • Antibody-mediated Immunity (MHC II)
  1. Antigen Presentation: Dendritic cells are the antigen presenting cells and they present antigens to T cells
  2. Antigen Recognition: Helper T cells express CD4 and they bind to MHC II molecules
  3. Activation: If the receptor (TCR) tightly bonds to the foreign antigen and correctly recognizes that it is foreign, then costimulators can cause T cells to complete their activation and they can then proliferate and differentiate (helper or cytotoxic)
    • Without costimulation, T cells become tolerant to that antigen and would be unable to divide, don’t secrete cytokines
    • Cytokines costimulate T cells and T cell proliferation
    • Interleukin 1 (IL-1) is a cytokine released by macrophages and it costimulates helper T cells
      • This releases interleukin 2 (IL-2)
        • Starts a positive feedback loop that encourages T cells to divide
      • Synthesize more IL-2 receptors
  4. Proliferation and Differentiation: Once helper T cells recognize presented antigen and become activated
    • Stimulate proliferation of T cells into effector helper T cells (secretes IL-2 for cell mediated immunity) and memory helper T cells
  • Cell-Mediated Immunity (MHC I)
  1. Antigen Presentation: Infected body cells present endogenous antigens in association with MHC-I molecules (random sampling)
  2. Antigen Recognition: CD8 are expressed by Cytotoxic T cells and they bind to MHC I molecules
  3. Activation: Costimulation by IL-2 released by the effector: helper T cell which activated the cytotoxic T cell
  4. Proliferation and Differentiation: Proliferates effector cytotoxic T cells (attack infected body cells) and memory cytotoxic T cells
  5. Action: destruction of the infected cells by circulating throughout the body
17
Q

Explain how killer T cells destroy infected cell

A

Tc Cells circulate throughout the body in search of body cells that display the antigen to which they have been sensitized (this is immune surveillance)

  • Tc cells are the only that have the ability to directly attack and kill other cells of our body
  1. Tc Cells recognize antigens from an infected body cell
  2. Infected body cell…
    • Undergoes apoptosis and the microbes within the popped infected cell disperse and are eaten up by phagocytes
    • Undergoes cytolysis by perforins
18
Q

Discuss the importance of co-stimulation and the role of helper T cells in the immune response

A
  • After surviving the thymus (immature T cell and it’s TCR recognize self-MHC proteins but not self-peptides) its goes out and tight bonds (co-simulates) with a foreign antigen, which is always a good thing. This activates the T cell which leads to proliferation (enabling them to make many, many copies of themselves) and they differentiate
19
Q

Diagram and explain all steps involved in an antibody-mediated immune response

A

1.

20
Q

Explain how antibodies initiate destruction of infected cells and antigens

A
21
Q

Draw the structure of a “typical” antibody, and label all key regions

A
22
Q

Explain “immunological memory”

A
23
Q

Compare and contrast cell-mediated and antibody-mediated immune responses

A