Immunity Flashcards

1
Q

<p>Immunne system</p>

A

<p>A collection of mechanisms that protect against disease by identifying and killing pathogen and tumour cells, and protection against microbial toxins. </p>

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3
Q

<p class=”large” style=”text-align:center”;>Pathogens</p>

A

<p class=”large” style=”text-align:center”;>Viruses, bacteria, mycobacteria, parasites, fungi. </p>

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3
Q

<p>What are the 5 general characteristics of immunity?</p>

A

<p>Recognition, Specificity, Regulation, Amplification, Memory</p>

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5
Q

<p class=”large” style=”text-align:center”;>Recognition (characteristic of immunity)</p>

A

<p class=”large” style=”text-align:center”;>Distinguish between normal self, altered self, and non-self. </p>

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5
Q

<p>Specificity (characteristic of immunity)</p>

A

<p>Inactivate/destroy/remove material without damaging normal tissues. </p>

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7
Q

<p class=”large” style=”text-align:center”;>Regulation (characteristic of immunity)</p>

A

<p class=”large” style=”text-align:center”;>Control the type, intensity, and duration of reaction and prevent it. </p>

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7
Q

<p>Amplification (characteristic of immunity)</p>

A

<p>The effector (attack) phase of humoral immunity, which is brought by many pathways, can be amplified or activated individually. </p>

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8
Q

<p>Characteristics of innate immunity</p>

A

<p>1) exposure leads to maximal response

2) non-specific
3) doesn't require previous exposure
4) found in nearly all life-forms</p>

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10
Q

<p class=”large” style=”text-align:center”;>Characteristics of adaptive immunity</p>

A

<p class=”large” style=”text-align:center”;>1) pathogen/antigen specific
2) lag between exposure and response
3) cell-mediate and humoral (antibody) components
4) inflammatory response
5) memory
6) found only in jawed vertebrates</p>

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10
Q

<p>What happens in innate immunity?</p>

A

<p>Happens when an organism breaks through the epithelial barriers; phagocytes inject microbes and secrete cytokines to stimulate the inflammatory response. </p>

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12
Q

<p class=”large” style=”text-align:center”;>What two cells act in innate immunity?</p>

A

<p class=”large” style=”text-align:center”;>Cytokines and phagocytes. </p>

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12
Q

<p>Components of innate immunity:</p>

A

<p>1) surface barriers (mechanical, biological, and chemical)
2) Humoral and chemical barriers (inflammation and complement system)</p>

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14
Q

<p class=”large” style=”text-align:center”;>What cells can produce inflammation?</p>

A

<p class=”large” style=”text-align:center”;>Cytokines (i.e., interleukins), prostaglandins, leukotrienes, chemokines, interferons.</p>

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14
Q

<p>What do neutrophils do during inflammation?</p>

A

<p>phagocyte and release enzymes</p>

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16
Q

<p class=”large” style=”text-align:center”;>What do eosinophils/basophils do during inflammation?</p>

A

<p class=”large” style=”text-align:center”;>secrete chemical mediators</p>

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16
Q

<p>What do monocytes/macrophages do during inflammation?</p>

A

<p>engulf pathogens and digest them via lysozomes</p>

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18
Q

<p class=”large” style=”text-align:center”;>What do mast cells do during inflammation?</p>

A

<p class=”large” style=”text-align:center”;>regulate the immune response</p>

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18
Q

<p>What do dendritic cells do during inflammation?</p>

A

<p>phagocyte microbes</p>

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20
Q

<p class=”large” style=”text-align:center”;>What do dendritic cells do during acquired immunity?</p>

A

<p class=”large” style=”text-align:center”;>phagocyte microbes</p>

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20
Q

<p>What do natural killer cells do during inflammation?</p>

A

<p>Kill cells that don't express or inappropriate express MHC class I; produce cytokine interferon-y to activate macrophages.</p>

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22
Q

<p class=”large” style=”text-align:center”;>What do natural killer cells do during adaptive immunity?</p>

A

<p class=”large” style=”text-align:center”;>Recognize and kill IgG-coated cells (antibody dependent cell-mediated cytotoxicity)</p>

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23
Q

<p class=”large” style=”text-align:center”;>What is the complement system?</p>

A

<p class=”large” style=”text-align:center”;>20 proteins that can form many combinations and cause various responses; they are produced in the liver.</p>

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23
Q

<p>What activates the complement system?</p>

A

<p>Proteases, binding with antibodies/carbs that are attached to microbes, endotoxins and mannose residues.</p>

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25
Q

<p class=”large” style=”text-align:center”;>What are the mechanisms of the complement system?</p>

A

<p class=”large” style=”text-align:center”;>- lysis of target cell
- opsonization of target organism
- attraction of other immune cells via peptides
- release in factors that create inflammation (chemoattractants)
- trigger the coagulation system (kinin, fibrinogen)</p>

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25
Q

<p>What is the Toll-like receptor?</p>

A

<p>A receptor on phagocytes that can recognize bacterial products (endotoxins), viruses (dsDNA), and more.</p>

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27
Q

<p class=”large” style=”text-align:center”;>Adaptive immunity depends on:</p>

A

<p class=”large” style=”text-align:center”;>Lymphocytes, antigen presenting cells (APCs), and phagocytes.</p>

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27
Q

<p>How does adaptive immunity achieve specificity?</p>

A

<p>Recognition of specific antigens and expression of MCH.</p>

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29
Q

<p class=”large” style=”text-align:center”;>What drives this system to be so far-reaching?</p>

A

<p class=”large” style=”text-align:center”;>Hypermutation in somatic immune cells and V(D)J recombination of antigen receptor genes creating a huge number of unique antigens, with one on each lympocyte. </p>

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29
Q

<p>Components of adaptive immunity:</p>

A

<p>Lymphocytes (T, B, NK cells), MHC, phagocytes, and antigen presenting cells (dendritic cells and macrophages)</p>

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31
Q

<p class=”large” style=”text-align:center”;>What is the origin of T-Lymphocytes?</p>

A

<p class=”large” style=”text-align:center”;>Originate from primitive stem cells (yolk sac in embyros and bone marrow after birth) and mature in the thymus gland. </p>

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32
Q

<p class=”large” style=”text-align:center”;>What is the function of T-lymphocytes?</p>

A

<p class=”large” style=”text-align:center”;>Recognize specific cell-bound antigen by means of antigen-specific T-Cell Receptor (TCR), which are linked to 5 polypeptide chains called the CD3 molecular complex. </p>

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32
Q

<p>What is the CD3 molecular complex?</p>

A

<p>In T-lymphocytes, they bind to the receptor cytoplasmically and transduce signals into the cell after antigen binding. </p>

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34
Q

<p class=”large” style=”text-align:center”;>What is the CD4 molecular complex?</p>

A

<p class=”large” style=”text-align:center”;>In 60% of mature CD3+ cells, they provide Helper/inducer functionality. </p>

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34
Q

<p>What is the CD8 molecular complex?</p>

A

<p>In 30% of T cells, they provide suppressor/cytotoxic functionality. </p>

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36
Q

<p class=”large” style=”text-align:center”;>What presents antigens to T cells?</p>

A

<p class=”large” style=”text-align:center”;>Antigen presenting cells, namely accessory cells. </p>

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36
Q

<p>T/F: There are more B cells than T cells.</p>

A

<p>False; 60% T cells, 10-20% B cells. The rest are NK cells.</p>

38
Q

<p class=”large” style=”text-align:center”;>Where do B cells originate from?</p>

A

<p class=”large” style=”text-align:center”;>Same as T cells (yolk sac/bone marrow), but they mature in bone marrow as well. </p>

38
Q

<p>What is the mechanism of action of B cells?</p>

A

<p>On antigenic stimulation, they proliferate and form plasma cells that secrete 5 classes of Igs (MGADE), and memory B cells.</p>

40
Q

<p class=”large” style=”text-align:center”;>What kinds of receptors are there on the B-cells?</p>

A

<p class=”large” style=”text-align:center”;>IgM antigen receptor complex (mostly), and complement receptors, IgA and IgE, CD40, and Fc receptors. </p>

40
Q

<p>What do B cells absolutely require for their maturation?</p>

A

<p>T cells and other non-specific factors (i.e., bacterial products)</p>

42
Q

<p class=”large” style=”text-align:center”;>Why are macrophages important in adaptive immunity?</p>

A

<p class=”large” style=”text-align:center”;>As phagocytic cells, they process and present antigens to T cells by engulfing opsonized microbes in humoral immunity.</p>

42
Q

<p>Give an example of cell-mediated immunity where macrophages are imporant:</p>

A

<p>Delayed hypersensitivity (i.e., alergies)</p>

44
Q

<p class=”large” style=”text-align:center”;>What is the difference between humoral and cell-mediated immunity?</p>

A

<p class=”large” style=”text-align:center”;>Humoral has to do with pathogens in the blood stream, while cell-mediated has to do with pathogens in cells. </p>

44
Q

<p>What are the two types of dendritic cells (APCs) and what is the difference between them?</p>

A

<p>Interdigiting - express MHC
Follicular - express Fc receptors for IgG</p>

46
Q

<p class=”large” style=”text-align:center”;>Name the affect of inteferon and prostaglandin on NK cells.</p>

A

<p class=”large” style=”text-align:center”;>Interferon promotes their killing activity, while prostaglandinds suppress them. </p>

46
Q

<p>What two receptors do NK cells bear?</p>

A

<p>CD16 and CD56 only. NOT TCRs.</p>

48
Q

<p class=”large” style=”text-align:center”;>What are the 3 classes of MHC and their function?</p>

A

<p class=”large” style=”text-align:center”;>Class I - present on all nucleated cells and recognized by cytotoxic T-cells and NK cells.
Class II - Antigent presenting cells, B cells, and some activated T cells; recognized by CD4+ helper T cells.
Class III - compliment antigen, not histocompatibility. </p>

48
Q

<p>What is the function of helper T cells?</p>

A

<p>Activate other cell types involved in immunity via cytokines (interleukin-2) and the CD40 ligand</p>

50
Q

<p class=”large” style=”text-align:center”;>What is the function of interleukin-2?</p>

A

<p class=”large” style=”text-align:center”;>Secreted by helper T cells, they cause proliferation of a specific T cell (allowing amplification of response). </p>

50
Q

<p>What to cell types can arise from helper T cells that secrete IL-2?</p>

A

<p>TH1, TH2, and TH17 cells.</p>

52
Q

<p class=”large” style=”text-align:center”;>What is the function of TH1 cells?</p>

A

<p class=”large” style=”text-align:center”;>Release IFN-y, which activates phagocytosis, antibody production in B cells, and production of antimicrobial substances in macrophages. </p>

52
Q

<p>What is the function of TH2 cells?</p>

A

<p>Secrete IL-4/5/13, which activate mast cells and eosinophils. </p>

54
Q

<p class=”large” style=”text-align:center”;>What is the function of TH17 cells?</p>

A

<p class=”large” style=”text-align:center”;>Secrete IL-17, which activates neutrophils. </p>

54
Q

<p>What cell types arise from cytotoxic (CD8+) T cells?</p>

A

<p>Cytotoxic lymphocytes. </p>

56
Q

<p class=”large” style=”text-align:center”;>What is the function of cytotoxic lymphocytes?</p>

A

<p class=”large” style=”text-align:center”;>Recognize infected cells via MHC I and release granules of perforin and granzyme-B into these cells (perforin allows entry of granzyme-B).</p>

56
Q

<p>What does granzyme B do and what secretes it?</p>

A

<p>Cytotoxic lymphocytes, and it causes apoptosis via proteolytic cleavage and activation of capsases. </p>

58
Q

<p class=”large” style=”text-align:center”;>What cells types arise from B cells in humoral immunity?</p>

A

<p class=”large” style=”text-align:center”;>Plasma cells and memory B cells.</p>

58
Q

<p>Can B-cells be activated by non-T-cells?</p>

A

<p>Yes, but lipid or polysaccaride antigens (which may activate several different B cells)</p>

60
Q

<p class=”large” style=”text-align:center”;>What are the five antibodies secreted by B cells in humoral immunity?</p>

A

<p class=”large” style=”text-align:center”;>GMADE!
IgG - opsonize microbe, activate complement (crosses placenta)
IgM - activate complement
IgA - secreted in mucosal tissues
IgD - unknown!
IgE - costs parasites, activates mast cells and eosinophils</p>

60
Q

<p>What is antibody dependent cell-mediated cytotoxicity?</p>

A

<p>Neutrophils, macrophages, and NK cells have surface receptors to the Fc portion (non-variable) of antibodies, which allows them to non-specifically destroy cells/microbes. </p>

62
Q

<p class=”large” style=”text-align:center”;>Which two cells are long lived and allow fast response to recognized antigens?</p>

A

<p class=”large” style=”text-align:center”;>Memory B cells and T-cells.</p>

62
Q

<p>What are the two main forms of disease from hypofunction of the immune system?</p>

A

<p>Defense and Surveillance</p>

64
Q

<p class=”large” style=”text-align:center”;>What are disorders of defense?</p>

A

<p class=”large” style=”text-align:center”;>Increased succeptibility to infection.</p>

64
Q

<p>What are disorders of surveillance?</p>

A

<p>Increase frequency of malignant disease.</p>

65
Q

<p>What is the end result of hypersensitivity?</p>

A

<p>Damage to body tissues.</p>

67
Q

<p class=”large” style=”text-align:center”;>What are the four types of immune reactions that lead to tissue damage or disease></p>

A

<p class=”large” style=”text-align:center”;>Type I: Anaphylactic, Type II: Antibody-mediated, Type III: Immune complexes, and Type IV: Cell-mediated.</p>

67
Q

<p>What is the mechanism of Type I hypersensitivity?</p>

A

<p>Release of vasoactive amines through TH2 helper T-cells, which activate IgE-producing B cell; IgE will stimulate mast cells to release histamine.
Ultimately increases vascular permeability and smooth muscle contraction. </p>

69
Q

<p class=”large” style=”text-align:center”;>What is the mechanism of Type II hypersensitivity?</p>

A

<p class=”large” style=”text-align:center”;>IgG or IgM antibodies are produced; in addition to activating the complement system, they bind to Fc receptors on phagocytes. This causes non-specific engulfing of circulating opsonized cells and imflammation.</p>

69
Q

<p>What kind of reaction occurs in transplant patients?</p>

A

<p>Type II hypersensitivity!</p>

71
Q

<p class=”large” style=”text-align:center”;>What is the mechanism of Type III hypersensitivity?</p>

A

<p class=”large” style=”text-align:center”;>Antigen/antibody complexes are trapped in organs, where they produce injury by complement and neutrophil activation.
Examples: systemic lupus erythematosus, post-streptococcal glomerulonophritis.</p>

71
Q

<p>What is the mechanism of Type IV hypersensitivity?</p>

A

<p>Trick question! There are two types (delayed type mediated by CD4 cells, and T-cell-mediated cytotoxicity mediated by CD8 cells.</p>

72
Q

<p>What is the mechanism of delayed type hypersensitivity?</p>

A

<p>CD4 cells differentiate into either TH1 or TH17 cells. These may then form granulomas if the pathogen persists.
Example: Tuberculosis, poison, etc. </p>

74
Q

<p class=”large” style=”text-align:center”;>What is the mechanism of T-cell-mediated cytotoxic hypersensitivity?</p>

A

<p class=”large” style=”text-align:center”;>CD8 cells destroy cell expressing self-antigens.
Example: Type I diabetes (islet cells in pancreas)</p>

74
Q

<p>Symptoms of autoimmune disease depends on what 3 factors?</p>

A

<p>a) the target (antigen)

b) type of immune reaction (cell-mediated, humoral, or both)
c) secondary changes (due to immune response or loss of organ)</p>

76
Q

<p class=”large” style=”text-align:center”;>What are the clinical symptoms of system lupus erythematosus?</p>

A

<p class=”large” style=”text-align:center”;>a) DNA is the target
b) Type III immune rection (circulating DNA/anti-DNA complexes)
c) Dermatitis, nephritis, arthritis</p>

76
Q

<p>What are the symptoms of Hashimoto's thryroiditis?</p>

A

<p>a) thyroid follicular cells are the target

b) Type II and IV hypersensitivity
c) Hypothyroidism due to destruction of thyroid cells</p>

77
Q

<p>What are the clinical feaures associated with immunodeficiency?</p>

A

<p>1. Chronic infection

2. Recurrent infection
3. Unusual infecting agent (low virulence)
4. Poor resolution or poor response to antibiotic treatment</p>

79
Q

<p class=”large” style=”text-align:center”;>In primary (congenital) immunideficiency, why is pure T cell deficiency unlikely?</p>

A

<p class=”large” style=”text-align:center”;>Because there is also a lack of helper effect on B cells. </p>

79
Q

<p>Give an example of a pure B cell dysfunctive immunodeficiency.</p>

A

<p>Bruton's syndrome (not detected until 5-6 months, because of protection by maternal IgG antibodies. </p>

80
Q

<p>Which Ig can cross the placenta?</p>

A

<p>IgG</p>

82
Q

<p class=”large” style=”text-align:center”;>T/F: Both T and B cell deficiency can occur in the same patient.</p>

A

<p class=”large” style=”text-align:center”;>True (i.e., severe combined immunodeficiency disease)</p>

82
Q

<p>Give an example of a cell-mediate immune deficiency syndrome.</p>

A

<p>DiGeorge syndrome - congenital absence of thymus.</p>

83
Q

<p>What are some primary immunodeficiency disorders affect lymphocyte function (adaptive immunity)?</p>

A

<p>a) X-Linked agammaglobulinemia

b) Common variable immunodeficiency
c) Isolated IgA deficiency
d) Hyper IgM syndrome
e) DiGeorge syndrome
f) severe combined immunodeficiency</p>

85
Q

<p class=”large” style=”text-align:center”;>If a patient has intact B and T cell function, why are recurrent infections still possible?</p>

A

<p class=”large” style=”text-align:center”;>Because there may be defects in the amplification systems </p>

85
Q

<p>Phagocytic dysfunction (absence of lysosomal enzymes in monocytes and granulocytes) can lead to what common disease?</p>

A

<p>Chronic granulomatous disease</p>

87
Q

<p class=”large” style=”text-align:center”;>What are some primary immunodeficiency disorders affect innate immunity?</p>

A

<p class=”large” style=”text-align:center”;>a) Deficiency of complement proteins
b) Chronic granulomatous disease (defect in NADPH oxidase)
c) Rare mutations in Toll-like receptors (TLRs)</p>

87
Q

<p>What are the causes of secondary immunodeficiencies?</p>

A

<p>a) Infections

b) Immunosupressive therapy (cytotoxic drugs, irradiation, anti-lymphocyte serum globulin (ALG)
c) Malignancy
d) Chronic illness
e) Malnutrition
f) Aging</p>

88
Q

<p>Name four common diseases that secondary immunodeficiences caused by infections.</p>

A

<p>Rubella, Measles, Mycoplasma, and HIV</p>