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MICR 270 > Module 3 > Flashcards

Module 3 Flashcards

1
Q

adaptive immune response phases

A
  1. antigen recognition (antigen presentation)
  2. lymphocyte activation
  3. elimination or pathogens or non-self perceived antigens
  4. apoptosis of immune cells (contraction)
  5. establishment of immunological memory
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2
Q

antigen recognition (antigen presentation)

A
  1. PAMPs are seen by APCs such as DCs and macrophages
  2. APCs will present antigens to naive T-cells via their surface MHC proteins
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3
Q

purpose of antigen recognition

A

identify and activate the cells that can recognize and bind the antigen from the specific pathogen that is invading

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4
Q

lymphocyte activation

A

requires a series of cellular interactions (communication) which lead to T-cell and B-cell differentiation and clonal expansion

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5
Q

what does lymphocyte activation include?

A
  1. B-cells (plasmocytes)
  2. T-cells (helper T-cells or cytotoxic T-cells)
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6
Q

purpose of lymphocyte activation

A

produce a large quantity of immune cells specific to the pathogen in order to stop the invasion

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7
Q

clonal expansion

A

production of a large quantity of identical cells from the same original cell

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8
Q

elimination of pathogens or non-self perceived antigens

A

most efficient defenced are unleashed

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9
Q

purpose of elimination of pathogens or non-self perceived antigens

A

to completely destroy the pathogen that invaded

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10
Q

humoral

A

plasmocytes produce antibodies that bind to extracellular pathogens

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11
Q

cell-mediated

A

cytotoxic T-cells destroy cells infected by intracellular pathogens or get activated by antigens presented by APCs

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12
Q

apoptosis of immune cells (contraction)

A

once pathogen is eliminated, the vast majority of activated lymphocytes undergo apoptosis, and the immune response gradually declines

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13
Q

why do cells undergo apoptosis?

A

the cells duty is accomplished and most immune cells are not needed anymore and could produce more damage than good, they die off)

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14
Q

apoptosis

A

programmed cell death that occurs in a way controlled by the cell itself, which generate almost no damage to the surrounding cell

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15
Q

establishment of immunological memory

A
  1. the few immune cells that survive the contraction
    phase turn into memory cells
  2. when re-exposed to the same antigen, these memory
    cells proliferate quickly to generate an immune response that is faster and more robust than first response to the pathogen
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16
Q

ex of immunological memory

A

vaccination

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17
Q

self and non-self recognition

A

the MHC serves as a self-label, and helps identify and recognize self from non-self-molecules, to ensure the immune system does not attack the host (you)

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18
Q

MHC

A

display antigenic peptides on surface of cells
- can be recognized by the TCR and its co-receptors (CD4 or CD8) to initiate an adaptive immune response leading to elimination of foreign antigens

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19
Q

classes of MHC molecules

A
  1. MHC class I (CD8+ cytotoxic T-cells)
  2. MHC class II (CD4+ helper T-cells)
    - distinguish between different recognition patterns
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20
Q

autoimmune disorders

A

arise when the body’s immune response is unable to differentiate between self and non-self, and the immune system begins to attack its own tissue

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21
Q

antigen presenting cells (APCs)

A
  1. internalize pathogens, by phagocytosis or receptor-mediated endocytosis, and process them into peptides (antigens)
  2. antigens are displayed on the MHC on the surface of the APC and can be recognized by T-cells
  3. since T-cells are unable to recognize extracellular pathogens by themselves, APCs present T-cells to the antigen in the body
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22
Q

receptor-mediated endocytosis

A

an endocytic process in which a cell absorbs external material by invagination of the plasma membrane – relies on receptors specific for the material being absorbed

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23
Q

2 types of APCs

A
  1. professional APCs
  2. non-professional APCs
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24
Q

professional APCs

A

most efficient cells that both present antigens through MHC class II and express co-stimulatory signals to activate Helper T-cells

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25
Q

examples of professional APCs

A
  1. macrophages
  2. B-cells
  3. DCs
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26
Q

most effective professional APCs

A

dendritic cells because DCs constitutively express a high level of MHC class II molecules and co-stimulatory molecules

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27
Q

non-professional APCs

A
  1. rarely needed in this specific function and only for short periods of time in case of a sustained inflammatory response
  2. fibroblasts and glial cells
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28
Q

antigen processing

A

each antigen presented by a MHC molecules (class I or II) needs to be processed to form an effective peptide

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29
Q

2 pathways forming cell surface complexes

A
  1. endogenous pathway
  2. exogenous pathway
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30
Q

endogenous ptahway

A

forms peptide – MHC class I complex (recognized by CD8+ Cytotoxic T-cells)
- allows the cell to process self or foreign intracellular
particles and present them at the cell surface in
order to be recognized by T-cell receptors on cytotoxic T-cells

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31
Q

exogenous pathway

A

forms peptide – MHC class II complex (recognized by CD4 Helper T-cells)

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32
Q

5 main steps in exogenous antigen processing

A
  1. antigen engulfment
  2. proteolytic processing
  3. formation of MHC-antigen complex
  4. cell surface expression
  5. recognition by helper T-cell
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33
Q

antigen engulfment

A
  1. APCs engulf the foreign antigen by endocytosis forming an endosome
  2. antigen is generally recognized by PRRs
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34
Q

proteolytic processing

A

foreign antigens inside the endosome are broken down into fragments by proteolytic processing

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35
Q

proteolytic processing

A

protease cleaves one or more bonds in a target protein to modify its activity (activation, inhibition, or destruction of activity)

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36
Q

formation of MHC-antigen complex

A

the vesicle containing the foreign fragments fuses with vesicles containing MHC molecules, forming MHC-antigen complexes

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37
Q

cell surface expression

A

MHC-antigen complex is transported to plasma membrane, where it will be displayed on the surface of the cell

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38
Q

recognition by helper T-cell

A

TCR on surface on a Helper T-cell binds to the MHC-antigen complex on the cell surface of APC, which will initiate an adaptive IR

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39
Q

B-cell receptor (BCR)

A

composed of a membrane-bound antibody and signal transduction molecules (ITAMs)

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40
Q

ITAMs

A

an immunoreceptor tyrosine-based activation motif is composed of a repeated sequence of four amino acids in the cytoplasmic tails of cell surface proteins

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41
Q

T-cell receptor (TCR)

A

formed of membrane-bound antigen-specific molecule and signal transduction molecules (CD3 and ITAMs)
- TCRs in associated with a co-receptor (CD4 or CD8) recognize and bind to peptide: MHC complex

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42
Q

what happens to the immune system with no communication

A

the body is left susceptible to infection and disorders

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43
Q

immune communication system

A

components of the IS communicate between using specific cell surface receptors found on immune cells and a well-developed cytokine network

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44
Q

2 major parts of immune communication system

A
  1. lymphocyte activation
  2. cytokine networks
45
Q

lymphocyte activation

A
  1. involves many interactions with other immune cells, which will mediate the efficiency of the specific IR
  2. macrophage, DCs, B-cell, helper T-cell and cytotoxic T-cell
46
Q

cytokine networks

A

coordinate appropriate IR and modulate the balance between humoral and cell-mediated immunity

47
Q

types of cytokines based on function and structure of receptor

A
  1. chemokines
  2. interleukins
  3. interferons
  4. tumor necrosis factor
  5. growth factor
48
Q

T-cell dependent B-cell activation

A

is an intricate process that involves specific signals essential to production of functional plasmocytes and memory B-cells

49
Q

what does the interaction between T-cell and B-cell induce?

A

exchange of activation signals between the two lymphocytes allowing activation of strong and efficient humoral IR
- upon activation, B-cells can differentiate into antibody-producing cells

50
Q

2 types of antigens that activate B-cells

A
  1. thymus-dependent
  2. thymus-independent
51
Q

thymus-dependent

A

antigens that require a direct interaction between the B-cell and a Helper T-cell (majority)

52
Q

thymus-independent

A

induce the production of antibodies by B-cells without presence of a T-cell

53
Q

T-cell dependent B-cell activation - signalling pathway (3 signals)

A
  1. peptide-MHC class II complex
  2. signal 1:TCR - peptide: MHC complex
  3. expression of co-stimulatory molecules
  4. signal 2: co-stimulation
  5. signal 3: cytokines
  6. outcome of the three signals
54
Q

peptide-MHC class II complex

A
  1. since the antigen binding to BCR on a specific B-cell does
    not produce a strong enough signal to activate the cell, the
    antigen is internalized by receptor-mediated endocytosis,
    processed and displayed on the cell membrane in context of MHC
  2. B-cell is acting as APC and expresses high levels of peptide: MHC complex on cell surface
55
Q

signal 1: TCR - peptide: MHC complex

A
  1. the specific TCR complex and CD4 co-receptor on
    T-cell recognizes and binds to peptide: MHC class II
    complex expressed on B-cell
56
Q

expression of co-stimulatory nolecules

A

signal 1 induces the expression of CD40L on the cell surface of the Helper T-cell

57
Q

signal 2: co-stimulation

A
  1. CD40L and CD28 expressed on T-cell, bind to CD40 and B7
    expressed on B-cell
  2. this induces a co-stimulatory signal in both cells
58
Q

signal 3: cytokines

A

activated helper T-cell secretes cytokines which
bind to their associated cytokine receptor located on both cells (a paracrine and autocrine effect)

59
Q

outcome of the 3 signals

A
  1. the combination of 3 SIGNALS stimulate the proliferation and differentiation of B-cells into plasma cells and memory B-cells
  2. this forms the humoral IR against the specific antigen
60
Q

immune synapse

A

formed by the interaction between a T-cell and an APC

61
Q

when will T-cells not become properly activated?

A

T-cells will not become properly activated if only signal molecules such as T-cell receptor and a peptide: MHC complex interact
- immune synapse must be formed

62
Q

how is an immune synapse formed?

A

via signal molecules and adhesions patterns

63
Q

supra molecular activating clusters (SMAC)

A

“bullseye” pattern with three rings depicting three different cell clusters with similar functions

64
Q

components of an immune synapse

A
  1. signal molecules (cSMAC)
  2. adhesion molecules (pSMAC)
  3. signal regulation molecules (dSMAC)
65
Q

signal molecules (cSMAC)

A

the central SMAC contains the molecules responsible for signaling between the 2 cells such as TCR and peptide: MHC molecules

66
Q

adhesion molecules (pSMAC)

A

the peripheral SMAC contain adhesion proteins, (integrins and cytoskeletal linker proteins) responsible for keeping the cells in contact for long enough for signals to propagate (breed/grow)

67
Q

signal reduction molecules (dSMAC)

A

the distal SMAC consists of proteins with large extracellular domains that are responsible for helping regulate signal transduction

68
Q

immune synapse functions

A
  1. effective activation of the T-cell
  2. hold signal proteins together to form stronger connection, which give enough time for right amount of signals to be produced
  3. leads to reorganization of structures inside the T-cell, directing the release of cytokines close to the target cell
  4. regulates lymphocyte activation
69
Q

primary goal of immune synapse

A

effective activation of the T-cell

70
Q

what would occur if immune synapse activation was incomplete?

A

cell wouldn’t function effectively (anergic phenotype)

71
Q

key role of immune synapse in T-cell activation

A
  1. the attachment of TCR to peptide: MHC complex is too weak to hold connection long enough for signal to be induced
  2. the formation of immune synapse by concentrating signal molecules into a circle surrounded by adhesion molecules holding the interaction between the 2 cells (T-cell and APC) gives enough time to signal activation
72
Q

cytokine networks

A

classification of cytokines can differ depending on which criteria they are organized by… therefore we divide into groups based on function

73
Q

chemokines

A
  1. induce chemotaxis
  2. call in cells to the region of infection or injury
74
Q

key roles of chemokines

A
  1. inflammation; wound healing
  2. cell-mediated and humoral immune responses
  3. hematopoiesis
75
Q

interleukins (IL)

A

contain over 10 subfamilies (IL-1, IL-2, IL-3, etc.)

76
Q

functions of interleukins (IL)

A
  1. regulate immune and inflammatory responses
  2. affect the proliferation and differentiation of various hematopoietic and immune cells
77
Q

interferons (IFN)

A

most common and well-known interferon molecules are IFN-, IFN-, and IFN-y

78
Q

function of interferons (IFN)

A
  1. induce an antiviral state- inhibit replication process of viruses
  2. help regulate an immune response
79
Q

tumor necrosis factor (TNF)

A

most common and well-known are TNF- and TNF-

80
Q

function of tumor necrosis factor (TNF)

A
  1. involved in systemic inflammation (septic shock)
  2. involved in tumor regression
  3. can cause apoptosis (cell death)
81
Q

septic shock

A

serious medical condition associated with a significant drop in blood pressure that can lead to respiratory or health failure and death

82
Q

growth factors

A

regulate a variety of cellular processes such as immune responses

83
Q

growth factors stimulate

A
  1. growth
  2. proliferation
  3. healing
  4. cellular differentiation
    ***T-cells (TH1 and TH2) are used for antifungal protection
84
Q

immunological memory

A
  1. ability of lymphocytes to respond more efficiently to re-infection by a previously encountered antigen
  2. develop a greater and faster IR than first encounter
  3. basis of vaccines
85
Q

what cells contribute to immunological memory?

A

contribution from T-cells in immunological memory, but more is known about B-cells

86
Q

memory B-cells & immunological memory

A
  1. IM occurs when second encounter with an antigen, that induces a heightened state of immune re-activity
  2. mediated by memory B-cells
87
Q

second exposure to an antigen

A
  1. memory B-cells differentiate from naïve B-cells and display the same membrane-bound antibody as their parent cells
  2. one a person becomes re-infected, the immune response is so efficient they never display symptoms
88
Q

memory B-cells

A

have a longer lifespan than naïve B-cells, which contribute to lifelong immunity against many pathogens

89
Q

naive B-cells

A

need to be activated through a series of cell interactions, including antigen presentation on MHC complex, before they can differentiate into plasma cells and memory B-cells

90
Q

difference between naive B-cells and memory B-cells?

A

naive B-cells: must be activated before differentiation into plasma cells
memory B-cells: differentiate immediately into plasma cells, making IR more efficient

91
Q

type of immunological memory

A
  1. natural passive immunity
  2. artificial passive immunity
  3. natural active immunity
  4. artificial active immunity
92
Q

natural passive immunity

A
  1. acquired by fetus or newborn from mother
  2. placental transfer of antibodies during pregnancy or breastfeeding
  3. short-lived immunity (~6 months)
  4. no immunological memory for the recipient
93
Q

ex of natural passive immunity

A

the transfer of placental IgG from the mother to fetus

94
Q

artificial passive immunity

A
  1. acquired by injection of serum containing antibodies
  2. immunity is temporary
  3. no immunological memory for the recipient
95
Q

ex of artificial passive immunity

A

rabis immunoglobin

96
Q

serum

A

fluid portion of the blood, which is free of cells and clotting factors

97
Q

natural active immunity

A
  1. acquired through infection by a pathogen, possibly leading to symptoms/a disease state
  2. development of innate and adaptive immune responses
  3. immunological memory has a significant chance of being developed
98
Q

ex of natural active immunity

A

when the body builds immunity towards the chickenpox virus and thereby cannot get sick with the chickenpox virus again

99
Q

artificial active immunity

A
  1. acquired through vaccination
  2. development of innate and adaptive immune responses
  3. normally, no symptoms/disease states are present
  4. immunological memory has a significant chance of being developed
100
Q

ex of artificial active immunity

A

COVID-19 vaccine

101
Q

challenges with developing novel vaccines

A
  1. determining what your correlate of protection is (what part of immune response neutralizes the pathogen – is it antibody, T-cell, B-cell?)
  2. developing that specific IR
102
Q

chicken pox

A
  1. varicella-zoster virus (VZC)
  2. highly contagious disease causing a skin rash characterized by small, itchy blisters
103
Q

how does transmission of chicken pox occur?

A

occurs from person to person, via direct contact or through airborne agents

104
Q

what happens after being infected with chicken pox once?

A

cannot develop chicken pox again

105
Q

what can second infection of chicken pox manifest as?

A

shingles

106
Q

prevalence of chicken pox

A

95% of population demonstrates serologic evidence of infection by adulthood
- incidence is increasing

107
Q

shingles

A

subsequent reactivation of latent virus of chicken pox
- anyone who has had chickenpox is at risk for shingles, but mostly older individuals and individuals with a poor immune system

108
Q

symptom of shingles

A

painful rash on torso or face

109
Q

shingles vaccine

A
  1. shingles vaccine reduces risk by 50-60% (one dose) (Merck)
  2. new vaccine reduces risk by 95% (two doses) (GlaxoSmithKline)

MICR 270 (5 decks)

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