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MICR 270 > module 3-immune response > Flashcards

module 3-immune response Flashcards

1
Q

overall immune response

A

from the entrance of the pathogen in the body to its elimination
- consists of innate and adaptive

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2
Q

what happens if innate is overwhelmed

A

an antigen specific adaptive immune response will develop against non-self molecules

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3
Q

list the adpative immune responses

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

how many phases are there in the adaptive immune

A

5

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5
Q

phase 1

A

antigen recognition

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6
Q

antigen recognition

A
  • after pathogen has entered body and innate defenses
  • PAMPS are seen by antigen-presenting cells (dendritic cells, macrophages)
  • antigen presenting cells will present antigens to naive T-cells via their surface major histocompatibility complex (MHC) proteins
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7
Q

what is the purpose of the antigen recognition step

A

to identify and activate cells from adaptive immunity that are able to recognize and bind the antigens from the specific pathogen that is indvading

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8
Q

phase 2

A

lymphocyte activation

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9
Q

lymphocyte activation

A
  • requires a series of cellular interactions which lead to t-cell and b-cell differentiation and clonal expansion
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10
Q

clonal expansion

A

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

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11
Q

what is the point of the lymphocyte activation phase

A

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

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12
Q

phase 3

A

eliminations of pathogens

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13
Q

elimination of pathogens

A

depending on the pathogen the most efficient defences are unleashed
humoral immunity- plasmocytes produce antibodies that bind to extracellular pathogens

cell-mediated immunity- cytotoxic t-cell destroy cell infected by intracellular pathogens or get activated by antigens presented by ABCs

completely destroy the pathogen

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14
Q

phase 4

A

contraction

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15
Q

contraction

A

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

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16
Q

apoptosis

A

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

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17
Q

phase 5

A

memory

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18
Q

memory

A

the few adaptive immune cells that survive the contraction phase differentiate into memory cells
- when re-exposed to the same antigen, these memory cells proliferate quickly to generate an immune response that is much faster and more robust than the first response to the pathogen

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19
Q

how many days til phase 5

A

21

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20
Q

how many days til phase 4

A

14-20

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21
Q

how many days phase 3

A

arouind day 14

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22
Q

how many days phase 1-2

A

days 0-7

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22
Q

which process are included in lymphocytes during their activation

A

cell differentiation and clonal expansion

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23
Q

why does adaptive immunity need a process called antigen presentation?

A
  • it contains a countless number of specific immune cells, each able to recognize one specific antigen.
    its necessary to identify which cells should be activated to encounter the specific invader during an infection
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24
Q

why do immune cell cells die after the elimination of the pathogen

A

vast majority aren’t needed
- if they stay alive they consume unnecessary energy in the body that could be better used elsewhere and there is a risk that these extra immune cells could cause additional, non-specific damage

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25
Q

what is the histocompatibility complex (MHC)

A

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

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26
Q

the role of MHC molecules

A

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

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27
Q

classification of MHC molecules

A

there are 2 MHC class I, and MHC class II
- help distinguish between different recognition patterns

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28
Q

what cells is essential in the process to induce an effective adaptive response

A

helper t-cells

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29
Q

are t-cells able to recognize extracellular pathogens by themselves?

A

NO, they require an intermediate to present them the antigen found inside the body.
the intermediates are called Antigen-presenting cells (APCs)

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30
Q

role of APCs

A

internalize pathogen, by phagocytosis or receptor-mediated endocytosis, and process them into peptides
- the peptides (antigens) are displayed on the major histocompatibility complex on the surface of the APC and can be recognized by T-cells

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31
Q

receptor mediated endocytosis

A

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

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32
Q

what are the 2 types of antigen presenting cells

A

professional APCs
nonprofessional APCs

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33
Q

Professional APCs

A
  • macrophage
  • b-cell
  • dendritic cell
    they are most efficient cells that both present antigens through MHC class II and express costimulatory signals to activate help t-cells
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34
Q

non professional APCs

A

some other cells types can be induced to express MHC class II complexes or stimulatory molecules, but normally they don’t

because these cells will rarely be needed in this specific function and only for short periods of time in case of a sustained inflammatory response

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35
Q

exampels of non-professional APCs

A
  • fibroblasts
  • glial cells
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36
Q

antigen processing

A

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

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37
Q

what are the 2 pathways which lead to the formation of these cell surfaces complexes

A

endogenous pathway
exogenous pathway

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38
Q

endogenous pathway

A

forms peptide: MHC class I complex (recognized by CD8+ cytotoxic T-cells)

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39
Q

exogenous pathway

A

forms peptide: MHC class II complex (recognized by CD4+ helper T-cells)

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40
Q

antigen processing by the endogenous pathway

A

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
- turns bacteria into peptide fragment–>to the ER associate with MHC class I__> then to golgi complex, and transported to surface for recognition

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41
Q

what are the 5 steps of antigen processing by the exogenous pathway

A
  1. antigen engulfment
  2. proteolytic processing
  3. fomration of MHC-antigen complex
  4. cell surface expression
  5. recognition by helper T-cell
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42
Q
  1. antigen engulfment
A

antigen presenting cells (macrophages, B-cells, dendritic cells) engulf the foreign antigen by endocytosis forming an endosome

  • antigen is generally recognized by PRRs
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43
Q
  1. proteolytic processing
A

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

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44
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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45
Q
  1. formation of MHC-antigen complex
A

the vesicle containing the foreign fragments fuses with vesicles containing MHC molecules (originating from the endoplasmic reticulum via Golgi), forming MHC-antigen complexes

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46
Q
  1. cell surface expression
A

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

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47
Q
  1. recognition by helper T-cell
A

the t-cell receptor (TCR) on the surface of a helper T-cells binds to the MHC-antigen complex on the cell surface of the APC, which will initiate an adaptive immune response

48
Q

in order to initiate an adptiave response, antigens must be…..

A

recognized by receptors on the surface of these cells

49
Q

what do B-cells and T-cells each express

A

specific receptors called BCR and TCR

50
Q

B-cell receptor (BCR)

A
  • composed of a membrane-bound antibody and signal transduction molecules
  • BCRs recognize and bind to extracellular pathogens or toxins directly
51
Q

ITAMS

A

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

52
Q

T-cell receptor (TCR)

A
  • is formed of a membrane-bound antigen-specific molecules and signal transduction molecules (CD3 and ITAMs)
  • TCRs in association with a co-receptor (CD4 or CD8) recognize and bind to peptide: MHC complex
53
Q

why is communication within the immune system critical

A
  • for the production of a coordinated and effective immune response
54
Q

what happens without proper communication

A
  • the body is left susceptible to infection and disorders of the immune system
  • autoimmunity
55
Q

how does the immune system communicate

A

between themselves using specific cell surface receptors found on immune cells and a well-developed cytokine network

56
Q

communication- lymphocyte activation

A

involves many interaction with other immune cells, which mediate the efficiency of the specific immune response
- macrophage
- dendritic cells
- b-cell
- helper t-cell
- cytotoxic t-cell

57
Q

communication- cytokine networks

A

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

58
Q

how are cytokine networks divided for communcation

A

depending on their functions and the structure of their receptor

59
Q

list the cytokines for communication

A
  • chemokines
  • interleukins
  • interferons
  • tumor necrosis factor
  • growth factors
60
Q

what does CD4+ helper T-cells help with

A

stimulate humoral immunity and the differentiation off B cells

61
Q

after activation of B cells what can they do

A

B-cells can differentiate into antibody producing cells

62
Q

what does t-cell dependent activation of B-cell do

A

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

63
Q

what does the interaction between t-cells and b-cells induce?

A

the exchange of activation signals between the 2 lymphocytes allowing the activation of strong and efficient humoral immune response

64
Q

how many steps are there in the signalling pathwats of t-cell dependent b-cell activation

A

6

65
Q

what are the steps called

A
  1. peptide-MHC class II complex
  2. SINGAL 1: TCR-peptide: MHC complex
  3. expression of co-stimulatory molecules
  4. SINGAL 2: co-stimulation
  5. SIGNAL 3: cytokines
  6. outcome of the three signals
66
Q

how many signals are there in the process of B-cell activation

A

3

67
Q

step 1. Peptide-MHC class II complex

A

as the antigen binding to the 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 the context of MHC
b-cell is acting as a antigen presenting cell

68
Q

step 2. signal 1: tcr-peptide: MHC complex

A

the specific TCR complex and CD4 co-receptor on the t-cell recognizes and binds to the peptide: MHC class II complex expressed on the B-cells

69
Q

step 3. expression of co-stimulatory molecules

A

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

70
Q

step 4. signal 2: co-expression

A

CD40L and CD28 expressed on the T-cell, respectively, bind to CD40 and B7 expressed on the B-cell inducing a costimulatory signal in both cells

71
Q

step 5. Signal 3: cytokines

A

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

72
Q

step 6. outcome of the three signals

A

the combination of these 3 signals ultimately stimulate the proliferation and differentiation of B-cells into plasma cells and memory B-cells, forming the humoral immune response against the specific antigen

73
Q

what forms the immune synapse

A

the interaction between a T-cell and APC will form the structure

74
Q

how would a t-cell become properly activated

A

an immune synapse, consisting of signal molecules and adhension proteins, must be formed

75
Q

components of an immune synapse

A

signal molecules (csMAC)
Adhesion molecules (pSMAC)
Signal regulation molecule (dSMAC)

76
Q

signal molecule (cSMAC)

A

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

77
Q

adhesion molecules (pSMAC)

A

the peripheral SMAC contains adhesion proteins, such as integrins and cytoskeletal linker proteins, responsible for keeping the cells in contact long enough for signals to propagate

78
Q

signal regulation molecules (dSMAC)

A

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

79
Q

what is the pattern/ orientation of the immune synapse?

A

“bullseye”
- three rings depicting three different cell clusters with similar functions, called supra molecular activating clusters (SMAC)

80
Q

can the immune synapse between T-cell and other APCs be arrganged into different patterns with similar components

A

yes

81
Q

function 1 of the immune synapse

A

the primary goal is the effective activation of the T-cell

82
Q

function 2 of the immune synapse

A

the synapse holds signal proteins together to form stronger connections, which give enough time for the right amount of signals to be produced

83
Q

function 3 of the immune synapse

A

leads to the reorganization structures inside the T-cell, directing the release of cytokines close to the target cell

84
Q

function 4 of the immune synapse

A

regulates lymphocyte activation

85
Q

what would happen if immune synapse activation was incomplete

A
  • down regulation of the immune response
  • prevent T-cell proliferation
  • development of anergic phenotype (cell doesn’t function effectively)
86
Q

what are cytokines

A

chemical messengers secreted by immune cells that play a key role in cell-to-cell communication
- function is to regulate immune response processes

87
Q

what are the different types of cytokine

A

chemokines
interleukins (IL)
interferons (IFN)
tumor necrosis factor (TNF)
growth factors

88
Q

chemokines

A

induce chemotaxis
call in cells to the region of ingection or injury

89
Q

what do chemokines play a key role in?

A
  • inflammation, wound healing
  • cell-mediated and humoral immune responses
  • hematopoiesis
90
Q

interleukins (IL)

A
  • contain over ten subfamilies (IL-1, IL-2, IL-4, IL-12, etc)
  • regulated immune and inflammatory responses
  • primarily affect the proliferation and differentiation of various hematopoietic and immune cells
91
Q

interferons (IFN)

A
  • the most common and well-known interferon molecule are IFN-a, IFN b, and IFN y
  • induce an antiviral state- inhibit the replication processes of viruses
  • help regulate immune responses
92
Q

Tumor necrosis factor (TNF)

A

the most common and well-known are TNF-a and TNF b
- involved in systemic inflammation (septic shock)
- involved in tumor regression
- can cause apoptosis (cell death)

93
Q

septic shock

A

a serious medical condition association with a significant drop in blood pressure that can lead to respiratory or heart failure

94
Q

chemotaxis

A

is the movement of an immune cell in direction of an elevated concentration of chemoattractant molecules

95
Q

growth factors

A

stimulate:
- growth
- proliferation
- healing
- cellular differentiation
- regulate a variety of cellular processes such as immune responses

96
Q

name the 3 major signals during T-cell dependent B-cell activation

A

signal 1: TCR- peptide:MHC class II complex

signal 2: co-stimulation

signal 3: cytokines

97
Q

what is the outcome of B-cell activatoin

A

proliferation
differentiation into plasma cells and memory b-cells

98
Q

what is immunological memory

A

is the ability of lymphocytes to respond more efficiently to re-infection by a previously encountered antigen

99
Q

what does immunological memory result in?

A

greater and faster immune response than the first encounter

100
Q

what is immunological memory a part of

A

central to the adaptive immune system and the basis of vaccines

101
Q

memory b-cells

A

immunological memory occurs when there is a second encounter with an antigen.
- it induces a heighted state of immune reactivity.
mediated by memory b-cells

102
Q

if memory cells exist and they stay in the body for decades, why do you think you can get the flu multiple times

A

there is different strains of the virus.
- your immune system only has memory cells for the specific strain you were infected with, every time you are infected with a new strain, your body goes through the full primary response

103
Q

what happens during the second expousre to an antigen (memory b-cells)

A
  • they differentiate from naive b-cells and display the same membrane-bound antibody as their parent cells.
  • these cells have longer lifepsan tha navie b-cells. which contributes to lifelong immunity.
104
Q

how can naive b-cells be activated?

A

through a series of cell interaction, including antigen presentation on MHC complex, before they can differentiate into plasma cells and memory b-cells.

105
Q

what is the other rounte memory b-cells can do

A

differentiate immediately into plasma cells, making immune response more efficient

106
Q

natural passive immunity

A
  • acquired by the fetus or newborn from the mother
  • placental transfer of antibodies during pregnancy or breastfeeding
  • short-live immunity (6 months)
  • no immunological memory for the recipient
107
Q

artifical passive immunity

A
  • aquired by infection of serum containing antibodies
  • immunity is temporary
  • no immulogical memory for the recipient
108
Q

serum

A

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

109
Q

natural active immunity

A
  • acquired through infection by a pathogen, possibly leading to symphtoms of disease state
  • development of innate and adaptive immune responses
  • immunological memory has a significant chance of being developed
110
Q

artifical active immunity

A
  • acquried through vaccination
  • development of innate and adaptive immune responses
  • normally, no symptoms/disease states are present
  • immunological memory has a significant chance of being developed
111
Q

chickenpox

A
  • known as varicella virus
  • constagious disease that causes a skin rash
  • trasmission is person to person via direct contact or through airborne agents
112
Q

can you get chicken pox if you had it once?

A

no. but can get second infection known as shingles

113
Q

what is the chickenpox an example of

A

immunological memory, individual who already been exposed to the virus will have a increased immune response upon secondary exposure and thus wont get sick

114
Q

how can the inicdence rate of chickenpox be so low, when this disease is so contagious

A

vaccines

115
Q

serology

A

an analysis that involves the diagnostic evaluation of blood serum to test for the presense of a host antibody response against a foreign particle/pathogen

116
Q

how could serolgic evidence for chickenpox be so high in the population

A

the majority of the population is now vaccinated aginast it, this means they have been exposed to components of the pathogen, developed a immune response and serologic test return postivie even though people may have never been naturally infection with the virus

117
Q

what is shingles

A
  • the VSV virus remains in the nervous system in an inactive states referred to as latency.
    reactivation of this virus will create shingle
    older people and ppl with poor immune system are at risk

MICR 270 (4 decks)

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