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805 > Lecture 7 (Cut off for Exam 2) > Flashcards

Lecture 7 (Cut off for Exam 2) Flashcards

Third Line Defenses

1
Q

Two Important Adaptive Immunity Characterisitcs

A

Pathogen specific and memory based.

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2
Q

Cellular Immunity

A
  • Mediated by T-cells

- Target and kills cells infected and intracellular pathogen

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3
Q

Humoral Immunity

A
  • Antibodies produced by B-cells

- Target extracellular pathogens

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4
Q

Immune Cell Development

A

Lymphoid Stem Cell&raquo_space; Small Lymphocyte&raquo_space; T-Cell / B-Cell (latter goes into plasma cells)

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5
Q

Cells Involved in Adaptive Immunity Activation (6)

A
  1. Macrophage and dendritic cells
  2. Collectors and informers
  3. Helper T-cells
  4. Cytotoxic T-Cells
  5. B-Cells
  6. Memory B & T-Cells
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6
Q

Collectors & Informers

A
  • ingest and kill microbes
  • antigen presenting and processing
  • activation of adaptive immunity
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7
Q

Helper T-Cells

A
  • Central Orchestrators of humoral and cellular immunity
  • CD4 markers on surface
  • Direct adaptive immunity
  • Interact with APCs using MHCII
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8
Q

Cytotoxic T-Cells

A
  • Assassins
  • CD8 markers on surface
  • Discriminately kill infect host cells (intracellular pathogens)
  • Interact with infected cells using MHCI
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9
Q

B-Cells

A
  • Antibody factories

- Humoral immunity

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10
Q

Memory Cells

A
  • Provide long term immunity

- Programmed for faster and stronger reactions

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11
Q

Antigens

A
  • Antibody Generator
  • Activates specific adaptive immunity
  • Different from PAMP (specificity)
  • Also known as immunogens
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12
Q

Bacterial examples of Antigens

A

Capsule, fimbriae, flagella, LPS, cell wall, toxins

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13
Q

Viral Examples of Antigens

A

Capsid, spikes, envelopes

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14
Q

Epitopes

A

Smallest “recognizable” part of antigen that reacts with T-cells and antibodies. Each antigen has multiple epitopes on it.

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15
Q

Antigenicity Factors (3)

A
  1. Molecular class
  2. Shape
  3. Size
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16
Q

Molecular Class + Antigenicity

A
  • Proteins = most antigenic
  • Carbs = least antigenic
  • Lipids/nucleic acids = not antigenic usually
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17
Q

Shapes + Antigenicity

A
  • 3D shape = important

- Provides epitopes

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18
Q

Size + Antigenicity

A
  • Larger molecules = more antigenic

- Haplens = too small to be antigenic on their own

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19
Q

Proteins + Antigenicity

A

Ex: fimbriae, flagella

  • Cellular and humoral response
  • Longest lasting immune response
  • Programmed memory
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20
Q

Carbohydrates + Antigenicity

A

Ex: Capsule

  • Only humoral response
  • Weaker and shorter immune response
  • Lacks programmed memory
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21
Q

Lymphocyte Receptors

A

-Surface molecules that bind antigen epitopes
-Provide specificity of immune response
Ex: B-Cell and T-Cell receptors

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22
Q

B-Cell Receptors

A
  • Recognize many molecule types
  • Soluble or pathogen-associated
  • Doesn’t undergo phagocytosis, internalizes epitopes after they bind to B-cell receptors
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23
Q

T-Cell Receptors

A
  • Recognize proteins only

- Require antigen presentation

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24
Q

Major Hisocompatibility Complex

A
  • Aka MHC, examples = MHC I & MHC II
  • Cell surface glycoprotein molecules
  • On surface of all nucleated cells
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25
Q

MHC I

A
  • All nucleated cells have it
  • Presents normal, abnormal, and foreign antigens
  • Presents to cytotoxic T-cells and NK cells
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26
Q

MHC II

A
  • Macrophages, dendritic cells, & B-Cells has receptor
  • Presents only abnormal or foreign antigens
  • Presents to helper T-cells
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27
Q

Antigen Presenting Cells

A
  • All nucleated cells present antigens with MHC-I
  • Professional phagocytes = macrophages, dendritic cels
  • APCs present with MHC II to activate helper T-Cells
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28
Q

T-Cell Production

A
  • Produced from multi-potent stem cell

- Differentiate into lymphoblasts in red marrow

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29
Q

T-Cell Maturation

A
  • Lymphoblasts enter blood stream
  • Travel to thymus for maturation over 3 phases
  • Immature in thymus = thymocytes
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30
Q

Phase I T-Cell Maturation

A
  • Negative selection against thymocytes with defective T-cell receptor (TCR)
  • Forces apoptosis to occur (programmed cell death)
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31
Q

Phase II T-Cell Maturation

A
  • Positive selection for MHC interactions
  • Thymocytes that interact with MHC appropriate receive positive signals to move though maturation stages
  • Thymocytes that interact inappropriately are not stimulated and die through apoptosis
32
Q

Phase III T-Cell Maturation

A
  • Occurs in cortex and medulla
  • Negative selection to remove self-reacting thymocytes through apoptosis
  • Referred to central tolerance - minimizes T-Cells in peripheral blood and tissues that would cause autoimmunity
33
Q

Peripheral Tolerance

A

Mechanisms to catch missed self-reacting T-cells

34
Q

Results of Thymic Selection

A
  • 2% of thymocytes allow to make and enter blood stream lymphatic system
  • Travel to secondary lymphatic tissues (tonsils, spleen, lymph nodes) and await to by activated by APCs
35
Q

Diversity of T-Cell Receptors

A
  • need diversity of receptors to have different epitope recognizers
  • need to recognize different parts or types of bacteria and viruses
  • different regions of receptor have different coding possibilities to make up the receptor diversity
36
Q

Types of T-Cells

A
  • *1. Helper
    2. Regulator
  • *3. Cytotoxic
  • *Focus on these**
37
Q

Regulatory T-Cell

A

Have CD4. Interact with APCs with MHCII. Act on peripheral tolerance.

38
Q

Activation of Helper T-Cells

A
  • Naive Helper T-Cells interact with APC which activate the helper cell
  • CD4 on Helper T-Cell anchors the MHCII in place
  • Proliferates and differentiates into TH1, TH2, and memory helper T-Cells
39
Q

TH1 Functions

A
  • Stimulate Cytotoxic T-Cells to kill more effectively
  • Stimulates memory CTC production
  • Stimulates macrophages and PMNs to kill more effectively
  • Stimulates NK cells to kill more effectively
40
Q

TH2 Functions

A
  • Stimulate B cell differentiation into plasma and memory cells
  • Direct antibody class switching in B cells
41
Q

TH17 Function

A

Stimulate immunity to chronic mucocuntaneous candidiasis

42
Q

Memory TH Functions

A
  • Remember specific pathogens

- Programmed to respond faster and stronger to pathogens that are encountered again

43
Q

Activation of Cytotoxic T Cells

A
  • Naive cytotoxic T-Cells interact with MHCI on infected cells, CD8 anchors in the interaction
  • Cycotoxic T-Cell is then activated and releases perforins and granzymes
  • Release of these cytotoxins can a controlled destruction of the infected cell via apoptosis
44
Q

Perforins

A

Create membrane pores in infected cells

45
Q

Granzymes

A

Enzymes that enter the infected cell and induce apoptosis.

46
Q

Do Cytotoxic T-Cells and NK Cells have the same mechanism of killing?

A

Yes.

47
Q

Do Cytotoxic T-Cells and NK cells have the same role in protection?

A

No.

48
Q

Superantigens

A
  • Bacterial or viral proteins that stay locked onto T-Cells
  • Create a non-specific bridge between TCR & MHCII
  • Leads to uncontrolled, excessive activation of Helper T-Cells
49
Q

Cytokine Storm

A

What occurs when superantigens bind to Helper T-cells. Causes high fever, circulatory collapse, lowered blood pressure, shock, and death.

50
Q

Production/Maturation of B-Cells

A
  • produced in bone marrow like T-Cells
  • Also mature in bone marrow, unlike T-Cells
  • Cell that pass selection travel to spleen for final maturation
51
Q

Selection Process of B Cells

A
  • Positive Selection - cells with functional receptor
  • Negative selection - against self-reacting cells, causes them to undergo apoptosis, receptor editing, or induction of anergy.
52
Q

T Cell Receptors V.S. B Cell Receptors

A

T-Cell

  1. Antigen presented by APC
  2. Protein Antigens

B-Cell

  1. Free antigen OR antigen on intact pathogen
  2. Can be carbohydrate, lipid, or protein
53
Q

Antibody Functions (5)

A
  1. Complement activation
  2. Neutralization
  3. Agglutination
  4. Opsonization
  5. ADCC
54
Q

Antibodies + Complement Activation

A

Activates protein cascade that leads to increased inflammation, opsonization, and cytosis

55
Q

Antibodies + Neutralization

A

Antibodies bind to parts of the pathogen that causes it to lose its ability to bind, move, etc.

56
Q

Antibodies + Agglutination

A

Causes pathogens or foreign cells to be grouped together and more easily undergo phagocytosis

57
Q

Antibodies + Opsonization

A

Binding to pathogen can opsonize it for better binding to macrophage receptors to undergo phagocytosis.

58
Q

Antibodies + ADCC

A

Aka Antibody-Dependent Cell-Mediated Cytotoxicity

Binds to pathogen to increase its binding to NK cells that will kill it with cytotoxins.

59
Q

B-Cell Activation Types (2)

A
  1. T-Cell Dependent

2. T-Cell Independent

60
Q

T-Cell Dependent Activation

A
  • Protein antigens
  • Requires presentation of epitope to Helper T-Cell or B-Cell
  • Diversity of antibody classes
  • Strongest, longest, and memory immunity
61
Q

T-Cell Independent Activation

A
  • Carbohydrate, lipid, etc antigens
  • No T-Cell Involvement
  • Almost exclusively produced IgM antibodies
  • Weaker, shorter, and no memory immunity
62
Q

T-Cell Dependent Activation Process

A

B-Cell interacts with T-cell to release cytokines and then undergoes clonal expansion into memory and plasma cells. The latter makes antibodies, most commonly IgG

63
Q

T-Cell Independent Activation Process

A

B-Cell interacts with pathogen cell on its own and is activated. Then releases mostly IgM antibodies.

64
Q

Antibody Class Switching

A
  • Directed by TH2 cells (T-Cell Dependent)
  • Cytokines tell activated B-Cells to switch antibody classes based on needs
  • Only changes the CONSTANT region, the antibody specificity/affinity is untouched
65
Q

Mechanisms of Acquiring Immunity (4)

A
  1. Passive Natural - antibodies through breast milk or placenta
  2. Passive Artificial - Antibodies given through IV or injection that are harvested from humans or other animals
  3. Active Natural - gained through illness and recovery
  4. Active Artificial - gained via vaccines
66
Q

Live, Attenuated Vaccines Advantages

A
  • Multiply within host, more natural exposure
  • Stimulates both cellular and humoral immunity
  • May be life-long immunity from memory
  • Use smaller doses with no boosters
  • Spreads to others for “herd” immunity
67
Q

Live, Attenuated Vaccines Disadvantages

A
  • Preparations may be unstable, hard to store, hard to transport
  • Risk of serious infections in immuno-compromised individuals
  • Risks a reversion to virulent form
68
Q

Inactived Vaccines Advantages

A
  • Stable over longer period of time
  • Easier to transport
  • No active disease in immuno-compromised
  • Can’t revert to virulent form
69
Q

Inactivated Vaccines Disadvantages

A
  • Larger and multiple doses
  • Increases risks of side effects
  • ONLY humoral defense, no cellular
70
Q

Acellular/Subunit Vaccines

A
  • Purified key antigens from pathogens
  • Acellular = bacterial
  • Subunit = viral
71
Q

Acellular/Subunit Advantages and Disadvantages

A

Advantages
-Side effects are less likely

Disadvantages

  • Activation of adaptive immunity may be weaker
  • Immunity may be shorter
72
Q

Toxoid Vaccines Definition/Advantages/Disadvantages

A

Inactivated bacterial toxins

Advantages

  • Side effects are less likely
  • Humoral immunity used to neutralize toxins

Disadvantages

  • Doesn’t prevent bacterial infection
  • Similar for subunit vaccines
73
Q

Conjugate Vaccines Definition/Advantages/Disadvantages

A

Capsule polysaccharide conjugated to proteins

Advantages

  • T-Cell dependent response to carbohydrate
  • Immune response in young children achieved

Disadvantages

  • Costly to produce
  • No Protection against antigenic variation
74
Q

DNA Vaccines

A
  • Cells take up naked DNA
  • Display foreign antigens with MHCI
  • Secrete antigens
  • Well rounded response
75
Q

Vector Vaccines

A
  • Attenuated virus introduces genes

- Attenuated bacteria express genes for virulence

805 (18 decks)

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