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Immunology > Chapter 3 part 2 > Flashcards

Chapter 3 part 2 Flashcards

sections 3-7

1
Q

Within Dendritic Cells

A

peptides from the pathogen are bound by glycoprotiens of host origin called MHC molecules

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2
Q

Major Histocompatibility complex

A

genes that encode for MHC molecles

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3
Q

Dendritic cell Peptide

A

in the DC the peptide from the pathogen is loaded onto a MHC molecule and placed on the DC’s surface (Antigen presentation) (figure 3.7)

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4
Q

antigen presentation

A

the loading of the pathogen peptide, via the MHC molecule, and placing on the DC surface

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5
Q

peptide (from pathogen)

A

MHC molecules interact with TCR that is specific for that peptide Antigen

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6
Q

Dendritic Cells

A

are very important and very effective antigen presenting cells as they are the cells that start off a primary T cell Immune response

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7
Q

Steps of DC presentation

5 steps

A
  1. dendrictic cells takes up pathogen for degradation
  2. pathogen is taken apart (degraded) inside the dendritic cell to release pathogen protein
  3. pathogen proteins are unfolded and cut into small pieces
  4. (pathogen proteins aka) peptides bind to MHC molecules and the complexes go to the cells surface (aka loading)
  5. T -cell receptors bind to peptide: MHC complexes on dendritic cell surface to form a dimer
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8
Q

2 types of MHC

A 
MHC Class I (pirate look peg leg)
MHC class II (normal legs)
different alleles for each of these MHC classes (most people have at least two aleles for each MHC class i.e. are heterozyous for these MHC alleles)
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9
Q

Individual expression of MHC

A 
each individual can express a few different types of MHC molecules
-MHC class I or II
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10
Q

Each MHC molecule

A

has the ability to bind many type of Antigen peptides.(however there are binding limitations in terms of peptide size)

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11
Q

MHC genes are highly polymorphic

A

This is the basis of tissue typing and for most transplants. This forces the physicians to look for a donor with a compatible MHC match (i.e. kidney compatablity)
* if the transplanted tissue is not well- matched then the recipients immune system recognizes it as foreign and rejects the tissue

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12
Q

Reason that MHC molecules are highly polymorphic

A

they are polymorphic within the human population for survival of the species.
* since everyon in the population will likely present the pathogen’s antigen in a different way (dur to differeing MHC molecules among the individuals in the population)there is more chance someone in the population will survive b/c of their Antigen presentation was favorable to the immune response

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13
Q 
What classes of MHC  do Nucleated cells present
What are these nucleated cells
Where is this class present
A 
ClassI
T and B cell
Marphages
dendritic cells 
Neutrophils
 in the 
Thymaic epithelium
Liver hepatocytes
Kidney epithelium
Brain
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14
Q

lymph cells present the majority of
What are these cells
Where is this class present

A 
class II
few T cells
most B cells 
some macrophages
most Dendritc cells
All in Thymic epithelium
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15
Q

MHC class I molecules

A 
present Antigens of intracellular pathogens
-due to loading of cytosolic degraded antigen onto MHC class I  molecules in ER
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16
Q

MHC class II molecules

A

present antigen of Extracellular pathogens

-due to laoding of MHC Class II molecules with Antigen degrated in the endosome

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17
Q

CD

A

clusters of differentiation

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18
Q

CD#

A

the fact that there are molecules of a certian type expressed on a cell’s surface

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19
Q

Two major classes of T cells

A

CD8 cells and CD4 cells

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20
Q

mature T cells

A

are either CD8 or CD4 (of the t-cells circulating 1/3 are CD8 cells and 2/3 are CD4 cells

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21
Q

the most abundant type of CD cells present in body

A

CD4

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22
Q

CD8 cells

A 
cytotoxic t cells
*have a CD8 co-receptor on their surface binds to MHC class I from Antigen Presenting Cell
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23
Q

CD4 cells

A
  • helper T cells

* have a CD4 co-receptor on their surface (, binds to MHC class II from Antigen Presenting Cell

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24
Q

MHC class I molecules

A
  • cytotoxic T Cells (CD 8 cells) recognize Antigen presented by MHC class I molecules
  • This is insred b/c CD8 T cells have a CD 8 co receptor that ONLY interacts with MHC class I
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25
Q

MHC Class II molecules

A
  • helper T cells (CD4 cells) recognize Antigen presented by MHC class II molecules
  • this is insured b/c CD4 T cells have a CD4 co-receptor that only interacts with MHC class II molecules
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26
Q

MHC class I reacts only with _____

A

CD8 cells (cytotoxic cells)

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27
Q

MHC class 2 reacts only with

A

CD4 Cells (helper cells)

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28
Q

Antigen interaction between MHC class I and CD8 cells from infection of DC to apoptosis of infected cells *8 steps

A

1.Infected DC travels to draining LN
2.as infection progresses in DC, viral proteins are produced on ribosomes of DC are degraded by cytosolic proteases
3.These peptides are Transported to Endoplasmic Reticulum where they bind MHC class I molecules
4 antigen MHC class I leaves Endoplasmic Reticulum travels to golgi apparatus and then to the plasma membrane
5. it is now accessable to be presented to naive T cells that are circulating in LN
6. CD8 Tcells with a TCR specific for the Antigen being presented engage the DC and the T cell becomes activated
7. the T cells then proliferate(stick together to produce cytokines) which leads to clonal expansion occurs and differentiation into cytotoxic T cells leave LN to lygate infected (MHC I displaying) cells
8.TCR and CD8 bind to these MHC I molecules of infected cell CD8 cell stimulates the production of toxic chemicals that induces apoptosis in infected cells

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29
Q

Cytosolic proteases

A

within infected DC that degrade viral proteins in prep for binding with MHC class I

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30
Q

Cells that can express MHC class I

A 
since most cells can be infected by some sort of virus most can express MHC class I 
 but not RBC
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31
Q 
Infected cell MHC class I presentation
5 Steps
A

1virus infects cell
2 viral proteins synthesized in cytoplasm
3 the peptide fragments of viral proteins bound by MHC class I in ER
4 bound peptides transported by MHC Class I to cell surface
5 Cytotoxic T cell recognizes comples of viral peptide with MHC class I and induces apoptosis in infected cell

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32
Q

differentiation into Effector T-cells (helper T-cells)

A

when naive CD4 cells encounter their antigen (MHC class II complex)

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33
Q

effector CD4 cells

A

following differentiation of CD4 T-cells into effector/ helper T cells the CD 4 cells secrete cytokines and “help” augment the activity of the other immune cells

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34
Q

what cells do CD4 cell cytokines activate

A

B cells and macrophages

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35
Q

MHC class II development and movement

A
  1. DC’s take up tathogens by endocytosis,
  2. then degrade their proteins and load these onto the MHC class II molecules located on the endosome inner membrane surface(MHC made in ER and then transported to endocytic vesicles)
  3. the Ag: MHC classII molecule moves to the DC surface while DC moves to draining LN
  4. in LN TCR of CD4 Tcell interacts iwth its specific Ag MHC class II molecule complex and the co- receptor interact
  5. CD4 T cell is activated and becomes one of several types of helper T cells
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36
Q

some activated CD4 T cells produce cytokines to

A

help neutrophils
monocytes and
macrophages
to be more efficient in phagocytosis

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37
Q

once activated CD4 helper T cells do 2 things

A
  • some of these travle to infected tissue and produce cytokines to help neutrophils, monocytes and macrophages to be more efficient
  • some stay in LN and help activate B cells to antibody production
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38
Q

B cell activation

A

Helped by helper T cell, B cell proliferates and differentiates into a plasma cell

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39
Q

Plasma cell

A

differentiated / mature B cell that only produces antibodies, these antibodies are of the same specificity as the Ig (BCR) present on the B cell

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40
Q

MHC class II molecules present on what types of cells

A

cells of the immunesystem
macrophages, B cells, DC
not somatic cells

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41
Q

Activation of macrophage(immune cells) by MHC class II molecule steps

A
  1. macrophage in infected tissue engulfs and degrades bacterium, producing peptides
  2. bacterial peptides bound by MHC classII in vesicels
  3. Bound peptides transpored by MHC class II to the cell surface
  4. Helper T cell recognizes complex of peptide antigen with MHC class II and activates macrophage
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42
Q

Some B cell receptors and antibodies recognize..(other ways of recognizing pathogen, 2)

A
  • parts of native structure of molecules on the outer surface of the pathogen
  • bind extracellular toxins released by pathogen
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43
Q

DC in tissue ___

A

carry pathogens with them into LN or pathogen enters via lymph

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44
Q

protiens on pathogens

A

can interact with BCR of circulating naive B cells

Those B cells with specific BCRs for the pathogen bind it and stay in LN while those not specific to the protien leave.

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45
Q

Receptor-mediated endocytosis

A 
caused by the binding of BCR and pathogen, The pathogen is killed inside of the B cell and proteins are degraded in the endosome
there the MHC class II molecule is loaded with peptided of pathogen and is then presented on the surface of the B cell (figure 3.13)
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46
Q

Following presentation of MHC class II peptide by B cell

A

MHC class II complex presents to CD4 cells (helper t cells) that are specific for this peptide (this CD4 cell has already been activated by the peptide from DCs)

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47
Q

B cell + T cell interaction of MHC class II and CD4 results in

A

CD4 secretion of cytokines

activation of B cell

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48
Q

Steps of B cell MHC class II presentation

A 
1 Cell-surfacej immunoglobulin of B cell binds bacteria; the cell engulf and degrades them, producing peptides (antigens of pathogen present to and warn other cells)
2 baterial peptides bound by MHC class II in endocytic vesicles
3 bound peptides trasported by MHC class II to the cell surface
4 helper T cell recognizes complex of peptide antigen with MHC class II and activates B cell
(B and T cell are specific for the same pathogen but receptors are often interacting with different components of the same pathogen)
49
Q

Immunity due to Ab is called humoral immunity

know each and job description

A 
there are Five classes (isotypes ) of antibodies produced by B cells and plasma cells
IgG
IgM
IgA
IgD
IgE
50
Q

All anti-bodys within a class share

A 
similar constant regions on their heavy chains
each class has certain functions and at times this and this constant region even determines the antibodies location
51
Q

antibodies found in blood,lymph and intercellular fluid

A

IgM, IgA, IgG,

52
Q

Most abundant antibody in blood, lymph and intercellular fluid

A

IgG

53
Q

What Antibodiy can be transported across the placenta

A

IgG

54
Q

What antibody is found in mother’s breast milk?

A

IgA

55
Q

What antibody is produced within the baby

A

IgM it is evidence of an interuteral infection the baby experienced

56
Q

first antibody made during the primary reaction

A

IgM

57
Q

C3b deposition

A

is deposited and binds with IgM and then facilitates the phagocytic uptake

58
Q

Important opsonins to assist in phagocytic uptake

A

IgG

59
Q

Antibody transported transplacentally

A

IgG

60
Q

Anti toxin, defends against toxin

A

IgG

61
Q

can activate complement

A

IgG

62
Q

can enter extracellular spaces

A

IgG

63
Q

selectively transported onto mucus membrane

A

IgA (and is in a high abundance)

64
Q

Antibody In breast milk and decreases rates of Gi tract and Resporitory diseases

A

IgA

mother’s antibody found in baby to protect baby

65
Q

no phagocytic receptors for this antibody for the Fc region

A

IgM

66
Q

excellent activator of complement

A

IgM

67
Q

requires C3b deposition on antibody prior to phagocytic uptake to occur

A

IgM

68
Q

First class of antibody to be made during a primary reaction

A

IgM

69
Q

Too large to enter extracellular spaces easily

A

IgM

70
Q

Related to allergic reactions

A

IgE

71
Q

important in parasitic defense

A

IgE

72
Q

Binds to mast cells sensitizing them to antigens

A

IgE (causes allergic reactions)

73
Q

important as a developmental marker for B cells as as it is present on naive circulating B cells

A

IgD

IgM too but not freely floating instead membrane bound

74
Q

Mechanism by which Ab combats infection

A

specific antibody-> bacterial toxins or bacteria in extracellular space->either neutralizes bacterial toxins or opsinzation by binding and marking bacterial cells-> the neutralized bacterial toxin or bacterial cell is then ingested and destroyed by phagocyte

75
Q

quality of antibody __________ during the course of an Immune response

A

Improves

76
Q

inital Dominant class of antibody in Immune Response

A

IgM

77
Q

aspects of antibodies change as IR proceeds due to _____,_______

A

somatic hypermutation

isotype switching

78
Q

IgM somatic hypermutation to IgG

A
  1. IgM is the first antibody made against infecting pathogen
  2. Somatic hypermutation selects for antibodies that bind more tightly to the pathogen
  3. Switching antibody isotype to IgGallows delivery of the pathogen to phagocytes
79
Q

Somatic hypermutation

A

addition or subtraction of nucleotides in variable of Heavy and Light chains

80
Q

purpose for somatic hypermutation

A

creates/transforms ig into “new” Ig which bind to pathogen better
B cells that do this and are successful become plasma cells
the “new” Ig that bind poorly war B cells that are not chosen to be plasma cells

81
Q

another name for Isotype Switching

A

class switch recombination)

82
Q

isotype Switching

A 
genes for another class are chosen to be transcribed 
example gamma heavy chain gene is selected instead of Mu heavy chain (this doesnt alter Variable region)
83
Q

anther name for Variable region

A

Antigen binding region

84
Q

isotype Switching ________ alter the variable region

A

does not!

85
Q

Isotype switching within Lymph node and spleen(blood)

A

from IgM to IgG

86
Q

isotype switching within the peyer’s patches(gut)

A

IgM to IgA

87
Q

isotype switching in parasitic infections

A

IgM to IgE (the Fc region of IgE can be bound by mast cells basophils and esionphils this is a pathogen specific response)

88
Q

Fc region of IgE can bind to

A

mast cells
basophils
eosinophils

89
Q

Results of somatic hypermutation

A

Better antibodies (secreted Antibodies bind to pathogen more tightly)

90
Q

Class switching

A

antibody that can be delivered to site of infection due to properties of its class

91
Q

Immunological memory

A

clonal expansion not only provides B and T effector cells it also creates memory cells

92
Q

Memory cells

A

long lived and allow for rapid secondary response if same pathogen should attack person againThey are activated more quickly then naive cells

93
Q

What advantage in preventing infection do memory cells have in second encounter with pathogen?

A

There is now an abundance of memory cells specific to pathogen as compared with time of first attack when only some naive cells were specific to pathogen

94
Q

Memory T cells

A

patrol non-lypmphoid tissues so they can detect infections at an earlier time. unlike naive T lymphocytes

95
Q

memory B cells

A

make higher affinity antibody then newly activated B cells since memory cells are a result of somatic hypermutation and class switching

96
Q

activation of naive lyphocytes is shut down when______ is resent

A

memory cells

97
Q

Cost to achieve diversity in producing theoreticall one B or T cell specific for every Antigen

A

there is a possibility of generating self-reactive receptors by this random process
thus we must have a selection process that will eliminate these self reactive cells before they cause self harm
Clonal selection/deletion is a method of preventing these self reactive cells from succeeding

98
Q

Clonal Deletion

A

result of selection due to self reactive change in antibody that causes the orignal to be deleted

99
Q

Immune tolerance

A

is usually achieved in most people

100
Q

Self Immune Tolerance

A

is inpart achieved during lymphocyte development in the thymus where immature developing T cells undergo positive or negitive selection

101
Q

Immuno intolerance

A

when one reacts to won immune sysem and own immune system attacks self

102
Q

Negitive selection for immunotolerance

A

IDs T cells that are binding too strongly to self-MHC and are thus eliminated by inducing apoptosis(they are self reactive) this is autoimmunit

103
Q

positive selection for Immunotolerance

A

Selects T Cells with TCR’s that interact with host MHC molecules on epithelial cells in the thymus cortex. these are given survival signals. is not signaled survival then cell dies via communication with immune cells

104
Q

_________ Selection occurs in Cortex of the thymus

A

Positive

105
Q

how many types of different MHC types do most people have out of the 1000 possible variations

A

20
thus many cells die
this is a result of Positive selection via self restricting group T cells

106
Q

_________ selection occurs in the medula of the thymus

A

negative

107
Q

What % of cells survive negative selection process

A

< 1%

108
Q

Result of negative selection

A

self-tolerant pool of circulating T cells that are non reactive aka autoimmune

109
Q

Where does positive and negative selection of immature developing B cells occur

A

Bone marrow

110
Q

What to B cells require to become activated?

A

B cells require help from a self-reactive T cell to activate a self reactive B cell.

111
Q

Selection for B cells

A

similar process to positive and negative selection in T cells but occurs in bone marrow

112
Q

Apoptosis

A

Cell suicide aka programmed cell death
mechanism by which auto reactive lymphocytes are eliminated
non mess way to die and doesnt harm neighboring cells (unlike necrosis)

113
Q

necrosis

A

messy cell death in which cell contents are spilled on and damage neighboring cells

114
Q

Central tolerance

A

a way to fix auto-reactivity

occcurring in primary lymphoid tissues of bone marrow and thymus

115
Q

Peripheral tolerance

A

a way to fix auto reactivity which occurs in secondary lymphoid tissue
an example of this involves regulator T cells which suppress auto-rxn in periphery

116
Q

Autoimmune disease

A

a by product of protection against a pathogen cross self rxn . in which an effective antibody against an antigen that was encountered at a young age is produced to fight infection but this specific antibody also reacts/binds to MHC on self cells thus killing them as well. mistake when regulation of IR is not controlled

117
Q

Hypersensitivity

A

allergy in which harmless substances (pollen) are attacked. often involves IgE and mast cells
this is immunologically abnormal.mistake when regulation of IR is not controlled

118
Q

hygiene Hypothesis

A

and increase in hypersenstitivity diseases and autoimmune diseases in richer countries as compared to poorer countires could this be do to hygiene vaccines and antibiotices since IgE are not being used find other antigens to react with?

Immunology (4 decks)

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