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Immuno > Immunology week 4 > Flashcards

Immunology week 4 Flashcards

1
Q

What is the complement system?

A

Inert proteins(like 30 of them) that are activated by pathogens
○ They have to be cleaved to become activated
○ If they aren’t activated they aren’t useful!
○ Basically a domino effect

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2
Q

What is the complement system?
Inert proteins(like 30 of them) that are activated by pathogens
what is required to become activated?
Is activation necessary?

A

What is the complement system?
● Inert proteins(like 30 of them) that are activated by pathogens
○ They have to be cleaved to become activated
○ If they aren’t activated they aren’t useful!
○ Basically a domino effect

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3
Q

What is the complement system?

what are they important for?

A

Extremely important for inflammation

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4
Q

What is the complement system?

where are they commonly activated?

A

Commonly activated on the surface of pathogens

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5
Q

What is the complement system?

How many pathways? what result?

A

There are 3 different pathways that will result in the same end function.

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6
Q

What is the complement system?
what 2 functions?

A

Has INNATE & ADAPTIVE functions!!!

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7
Q

What is the complement system?
What are the names of the 3 different pathways

A

classical pathway: antigen:antibody complexes
Lectin Pathway:
Lectin binding to pathogen surface
Alternative Pathway:
Pathogen surface

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8
Q

What is the complement system?
what are the end
results of these pathways?

A

Recruitment of inflammatory and immunocompetent cells
Opsonization of pathodens
Killing of pathogens

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9
Q

Complement system
What are 3 Ways of protection:

A

Ways of protection:
1. Some components act as

chemoattractants-
a. Recruit phagocytic cells to sites of

comp.Activation (low-> high conc)
2. Complement proteins that bind
covalently to the pathogens
opsonizing them for
phagocytosis
3. MAC!
a. Creating pores in the pathogens
membrane & destroying it

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10
Q

Complement system
Adaptive immunity functions
what does opsonizarion all allow for?
enhancement of what response to do what?

A

Adaptive immunity functions
● Opsonization also allows for the uptake
of microbes by APC like DC
● Enhancement of B cell response to
complement coated microbes

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11
Q

Rules of the complement :)
Name is based on order of what?

A

● Named based on order of discovery
C1-C9

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12
Q

Rules of the complement :)
Smaller fragment =?
Larger fragment=?

Except when?

A

● Smaller fragment= a
● Larger fragment= b
● Exception for C2 the lg fragment is
C2a!!!!!
○ Please know this!

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13
Q

Rules of the complement
what are alternative pathway components called?

A

● Alternative pathway components are
called factors!
○ Large fragment=b and small= a

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14
Q

Rules of the complement
what does each system result in?

A

Each system results in a C3 convertase
bound to the pathogen

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15
Q

Rules of the complement
what does C3 cleave?
what result?
explain?

A

C3 cleaves C4
○ Results in C5 convertase
○ C3b= VERY NB EFFECTOR MOLECULE
(opsonin molecule)
C3a= mediator of inflammation

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16
Q

Rules of the complement
when C5 Cleaved, what result?

A

C5 is cleaved
○ C5a= inflammatory peptide
○ C5b= results in the formation of MAC

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17
Q

The classical pathway
what are they IgM and IgG?
what happens?

A

IgM and IgG= activators
○ 1 IgM molecule of several IgG molecules
bind to an AG and the Fc portion of the
AB binds to the C1 molecule

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18
Q

The classical pathway
C1 has __?_ segments

A

C1 has 1q,r,s segments

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19
Q

The classical pathway
C1 is activated when what?

A

C1 is activated when 2 globular heads of
the C1q bind to the Fc region of the AB
that is bound to the AG.

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20
Q

The classical pathway
C1q activation causes what?
this results in what?

A

C1q activation activates C1r which
cleaves itself then cleaves C1s

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21
Q

The classical pathway
Activates Cls cleaves to what?

A

Activates Cls cleaves C4

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22
Q

Classical pathway
C4b attaches to the surface of what and/or what?

A

C4b attaches to the surface of the
microbe or and AG-AB complex

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23
Q

Classical pathway
C1s cleaves what?

A

C1s cleaves C2

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24
Q

Classical pathway
C2a binds to C4b and makes what?

A

C2a binds to C4b(C4b2a complex)

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25
Q

Classical pathway
C4b2a is the classical pathway of what?

A

C4b2a is the classical pathway of C3
convertase

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26
Q

Classical pathway
C3 contratase cleaves C3

true or false

A

true
C3 convertase cleaves C3 (obvi)

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27
Q

Classical pathway
C2b binds to what?

A

C2b binds to c3 convertase

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28
Q

Classical pathway
C4b2a3b = what?

A

C4b2a3b= c5 convertase

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29
Q

Classical pathway
C5 convertase cleaves what?

A

C5 convertase cleaves C5

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30
Q

Classical pathway
when C5 convertase cleaves C5
C5b remains what/what result?

A

C5 convertase cleaves C5
○ C5b remains associated with the
C4b2a3b complex which is NB for MAC

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31
Q

Classical pathway

Fill in the blanks
C1 binds to IgM or several IgG–>
C1q cleaving ___?__–>
C1r cleaves Cls—>
Cls cleaves ___?_

this leades to either:
Cb4 attaching to the surface of _?____
or
Cls cleaving C2 –>
C4b2a= ___?___
(this aids in the opsoniisation 1 goal of comp) —>
C3 contravers=cleaves C3—>
C4b2a3b=____?___ –>
C5b=remains associated with the C5 convertase complex=aids in MAC FORMATION

(see slide 8 for diagram)

A

C1q cleaves C1r

C1s cleaves C4

C4b2a=C3convertase
C4b2a3b=C5 convertase

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32
Q

The lectin pathway :)
What kind of IR?
what does it bind to?

A

Independent innate IR!
○ Binds to carbohydrate residues of
paths

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33
Q

The lectin pathway
MBL (sim to C1q) & Ficolins can do what?

A

MBL (sim to C1q) & Ficolins can
recognize microbial specific carbs on the
surface of microbes

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34
Q

The lectin pathway
MBL = binds to what?
what change occurs?
this promotes what?

A

MBL= binds to the microbe cell wall and
an conformational change occurs which
promotes activation of MBL-associated
serine proteases (MASPs)

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35
Q

The lectin pathway
MASP’s cleave what and what?

A

MASPs cleaves C4, and C2.

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36
Q

The lectin pathway
C4b2a=

A

C4b2a= C3 convertase cleaves C3

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37
Q

The lectin pathway
C4b2a3b=
initiates what?

A

C4b2a3b= C5 convertase
○ Initiates MAC

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38
Q

The lectin pathway
fill in the blank:
MBL binds to __?___
–>
MASPS= ____?___
—>
C4b2a3b= __?______
—>
this aids in ______?____

A

MBL binds to the cell wall
MASP’s = activated and cleaves C4 and C2
C4b2a=C3 conertase
C4b2a3b=C5 convertase
this aids in MAC Formation

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39
Q

The Alternative Pathway
Utilized the nonspecific (this is called what?)
which does what? to C3

A

Utilized the nonspecific (spontaneous
cleavage) low level hydrolysis of C3

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40
Q

The Alternative Pathway
If C3b binds to a healthy cell mem what happens?
Are these found on microbial membranes and cell walls?
Residues on the membrance promote what?

A

If C3b binds to a healthy cell mem it is
rapidly degraded due to sialic acid
(which aren’t found on microbial
membranes and cell walls) residues on
the membranes which promote binding
of C3b to factor H

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41
Q

The Alternative Pathway
what is going on with Factor H and Factor I?

A

Factor H and Factor I inactive and
degrade the inappropriately bound
C3b
○ “HI”PLS DON”T KILL ME*

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42
Q

The Alternative Pathway
where is this occurring?

A

On the Microbes surface

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43
Q

The Alternative Pathway
C3b binds to Factor B= ?

A

C3b binds to Factor B= C3bB

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44
Q

The Alternative Pathway
C3bB=cleaved by factor D=?

A

C3bB= cleaved by factor D= C3bBb

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45
Q

The Alternative Pathway
C3bBb=C3 convertase (cleabes C3)
stabilized by what?

A

C3bBb= C3 convertase (cleaves C3)
○ Stabilized by factor P

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46
Q

The Alternative Pathway
C3bBb3B= ?

A

C3bBb3B= C5 convertase

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47
Q

The Alternative Pathway
Cleaves C5= what?

A

Cleaves C5= aids in the MAC formation

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48
Q

The Alternative Pathway
The alternative pathway on a host cell
Fill in the blanks
C3 spontaneously cleaved
—> ___?__ binds to cell surface
—> binds to __?__ factor
—> factor __?___
—> “hi” please don’t kill me
—-> degrades __?____

A

C3–> spontaneously cleaved
—>C3b binds to cell surface
—->binds to Factor H
—-> Factor l
—-> “hi” please don’t kill me
—-> degrades to C3b

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49
Q

The Alternative Pathway
On a microbe membrane
fill in the blank
C3b—>
binds to Factor __?__
—> C3bB complex
—> cleaved by Factor ____?
—> C3bBb= ______?__
–> stabilized by Factor P (Properdin)
—-> C3bBb3B= ___?____
MAC

A

On a microbe mem
c3B—>binds to Factor B
—>C3bB complex
—->cleaved by Factor D
—->C3bBb=C3 convertase
—>stabilized by Factor P (Properdin)
—> C3bBb3b=C5 convertase
—> MAC

* check this C3bBb3b—on the previous slide it was C3bB3B Idk which one is correct.

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50
Q

What is MAC?!?!?!-> Membrane attack pathway

A

Constructs a protein complex that makes a hole in the target membrane
and kills the microbe

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51
Q

What is MAC?!?!?!-> Membrane attack pathway
C5 convertase initiates the formation of ?
Classical and lectin=?
alternative =?

A

C5 convertase initiates the formation of MAC
○ Classical and lectin= C4b2a3b/ alternative= C3bBb3b

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52
Q

What is MAC?!?!?!-> Membrane attack pathway

C5b= recruits what to make what
then C8 binds

A

C5b= recruits c6 and C7= C5b67 then C8 binds

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53
Q

What is MAC?!?!?!-> Membrane attack pathway

what does it result in?

A

Results in a hydrophobic region

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54
Q

What is MAC?!?!?!-> Membrane attack pathway
10-16 copies of C9= ?

A

10-16 copies of C9= make a pore

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55
Q

What is MAC?!?!?!-> Membrane attack pathway
?= make a pore

A

10-16 copies of C9= make a pore

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56
Q

What is MAC?!?!?!-> Membrane attack pathway
MAC then allows H2O to enter the cell= ?

A

MAC then allows H2O to enter the cell= osmotic lysis

57
Q

What is MAC?!?!?!-> Membrane attack pathway

___= osmotic lysis

A

MAC then allows H2O to enter the cell= osmotic lysis

58
Q

MAC
Membrane Attack Complex

Fill in the blank

C5b recreuits C6 and C7 to the target membrane, forming the complex _____?__
—>
C8 binds to the complex C5b67 complex, unflolding a hydroponic region that wedges into the target membrane
—>
recuit and inserts 10-16 copies of C9 into the membrane to create a ______?___
—->MAC breaches the cell membrane of the microbes allowing___?__ to rush into the cell
—->
_________?_ of the microbe by sufficient numbers of MAC on the membrane.

A

C5b67
cylindrical pore
water
osmotic lysis

59
Q

Regulation of the complement system:
explain
How?

A

Control proteins prevent the complement from acting on inappropriate targets
and acting in perpetuity
○ They inhibit the protease activities or facilitate the degradation of activated complement
complexes

60
Q

Regulation of the complement system:
where is the C1 inhibitor and what does it do?

A

C1 inhibitor- found in plasma/ serum inactivates C1r, C1s, & MASPs

61
Q

Regulation of the complement system:
Factor H and I
whre is it and what does it do?

A

Factor H and I- found in the plasma/ serum binds to C3b and accelerates decay

62
Q

Regulation of the complement system:
Decay- accelerating Factor (CD55)
where is it and what does it do?

A

Decay- accelerating Factor (CD55)- found on cell mem of RBC, neu.,
lymphocytes, monos, PLT, and endo cells regulates the alternative pathway &
accelerates decay of C3 convertase

63
Q

Regulation of the complement system:
Protectin CD59
where is it expressed
what does it do
what does it prevent

A

Protectin CD59- expressed on cell mem of RBC, leukocytes, and vascular endo.
Aids in MAC binds to C5b678 and prevents C9 recruitment and MAC formation
○ CD59= C9

64
Q

Clinical correlations:
How does cobra venom work?

A

● Cobra venom contains a c3b analogue which will bind to factor Bb and
Factor P to make C3 convertase stable.
● As a result Factors H&I will not destroy C3b and it will continually
hydrolyse which leads to local tissue damage

65
Q

Outcomes of the complement activation

If the outcome is
Direct target lysis

and the complement products are
MAC

What was the action?

A

Osmodyregulation and lysis of target cells

66
Q

Outcomes of the complement activation

If the outcome is
Tissue inflammation

and the complement products are
C3a and C5a

What was the action?

A

Activation of mast-cell degranulation leading to release of vasoactive amines (histamine and serotonin)

67
Q

Outcomes of the complement activation

If the outcome is
Endothelial activation

and the complement products are
C3a and C5a

What was the action?

A

increased expression of adhesion molecules

68
Q

Outcomes of the complement activation

If the outcome is
chemotaxis

and the complement products are
C3a and C5a

What was the action?

A

promotes migration of neutrophils, eosinophils, and mactophages toward site of complement activation

69
Q

Outcomes of the complement activation

If the outcome is
Opsonization

and the complement products are
C3b and iC3b

What was the action?

A

Enhancement of particle phagocytosis by macrophages and neutrophils

70
Q

Outcomes of the complement activation

If the outcome is
immune complex clearance

and the complement products are
C3b (and iC3b)

What was the action?

A

blocking of growth and facilitation of dissociation of immune complexes; immobilisation and clearance of immune complexes through interaction with CR1 on erythrocytes

71
Q

Antigens=

A

ANTIGEN= ANTIbody GENerator

72
Q

ANTIGEN= ANTIbody GENerator
what are they?
what do they bind to?

A

Molecules that induce an IR when introduced into the body
○ They bind to either AB, MHC molecules, or lymphocytes receptors (TCR-BCR)

73
Q

ANTIGEN= ANTIbody GENerator
2 subtypes and what do they do?

A

**● 2 subtypes
○ Immunogens- induce an IR
○ Haptens- by themselves cannot stimulate an IR but can when complexed with a larger
molecule (ex: host protein)

74
Q

ANTIGEN= ANTIbody GENerator
2 features
what are they
what do they do

A

2 features:
○ Immunogenicity- capability of inducing an IR
○ Antigenicity- capability to bind to products of the IR they induce

75
Q

ANTIGEN= ANTIbody GENerator
what is an epitope?
what does it do?

A

Epitope- antigenic determinant part of an AG that is actually responsible
for inducing the IR and binding to the products of the IR

76
Q

Sources of AG
2
examples?

A

Sources of AG
● Infectious agents
○ bacT, viruses, parasites, fungi
● Altered self
○ Tumors

See slide 19 for diagrams wk 4 or slide 13 wk 5

77
Q

Factors Affecting Immunogenicity of AG
9
what are they?

A

Foreignness-
size-
Chemical composition-
Physical properties
Degradability-
Genetic factors-
Age-
Chemical nature of AG
Route of admin

78
Q

Factors Affecting Immunogenicity of AG
explain foreignness

A

Foreignness- IS distinguishes between self and nonself only nonself
substances- immunogenicand induce IR (so the more foreign the greater the response)

79
Q

Factors Affecting Immunogenicity of AG
explain size

A

size- the larger the AG the more immunogenic typically

80
Q

Factors Affecting Immunogenicity of AG
explain chemical composition

A

Chemical composition- complex molecules are usually immunogenic

81
Q

Factors Affecting Immunogenicity of AG
explain physical properties
hint: particulate AG, Denatured AG

A

● Physical properties
○ Particulate AG are more immunogenic than soluble AG
○ Denatured AG are more immunogenic that native forms (bc their AG determinants are
exposed)

82
Q

Factors Affecting Immunogenicity of AG
explain degradability

A

Degradability- AG easily degraded are highly immunogenic

83
Q

Factors Affecting Immunogenicity of AG
explain genetic factors

A

Genetic factors- some AG are more immunogenic for a given spp.
○ Due to genetic variations in genes encoding for AG receptors on T & B cells

84
Q

Factors Affecting Immunogenicity of AG
explain age

A

Age- young/old people have less capability to mount an IR
babies & grannies= more sus.
○ Have less capability to mount an IR compares to middle aged people

85
Q

Factors Affecting Immunogenicity of AG
explain chemical nature of AG
specifically proteins
polysaccharides
nucleic acids
lipids

A

● Chemical nature of AG
○ Proteins- largest group of AG & highly immunogenic
○ Polysaccharides- good immunogens
○ Nucleic acids- weak AG but can become highly immunogenic when conjugated to proteins
○ Lipids- not immunogenic but some are haptens
■ What is a hapten???

86
Q

Factors Affecting Immunogenicity of AG
explain route of admin

A

● Route of admin
○ Per os
○ Intranasal
○ Intramuscular
○ Intravenous
○ Intradermal
○ Subcutaneous
○ Adjuvant- a substance that enhances the body’s IR to an AG

87
Q

Types of AG
7 what are they?

A

T- independent AG
T-dependent AG
SuperAG
Haptens
Autoantigens
Exogenous AG
Endogenous AG

88
Q

Types of AG
T- independent AG
explain
what do they stimulate
what is the structure
what can they activate
relationship to degradation
example

A

T- independent AG
○ Directly stimulate B cells to produce AB w/o the need of helper t cells
○ They have a polymeric structure so the same AG determinant repeats several times
○ They can activate lymphocytes polyclonality
○ They are resistant to degradation (so they can stimulate b cells & hang longer)
○ Ex: lipopolysaccharides

89
Q

Types of AG
T-dependent AG
explain
what do they stimulate
what do they contain
example

A

○ Indirectly stimulate B cells to produce AB via a helper t cell
○ They contain a few copies each of various AG determinants
○ Ex: most proteins= t dependent

90
Q

Types of AG
SuperAG
explain
what can they activate
from where
what do they bind to

A

SuperAG
○ Can activate a large number of lymphocytes at one time nonspecifically(not good)
○ Mainly from bacT and viruses
○ They bind to the variable domain B(vb) chain in the TCR of CD4 cells and the alpha chain of the MHC 2
molecule on APC
○ Induces a very strong signal
○ Polyclonal activation leads to excessive
production of IL1,2,3,TNFa, MIPa and B.=
systemic toxicity
*see slide 23 for diagram wk 4 or slide 17 wk 5

91
Q

Types of AG
Haptens
explain
what are they
how do they work
complete or incomplete AG

A

Haptens
○ Small non-immunogenic substances
○ On their own cannot induce an IR but can if they become bound to a carrier
○ So they are incomplete AG
**see slide 23 for diagram wk 4 or slide 17 wk 5

92
Q

Types of AG
Autoantigens
explain
what are they
example

A

Autoantigens- natural constituents of the body as opposed to foreign AG
○ autoimmunity - rxn of IS against host AG

93
Q

Types of AG
Exogenous AG
what is it?

A

Exogenous AG- AG that have entered the body from outside

94
Q

Types of AG
Endogenous AG
what is it?
how?

A

Endogenous AG- Generated within cells as a result of normal cell
metabolism or because of viral/ intracellular bacT infection

95
Q

MCH1
Part 1

Clinical correlation
Caprine arthritis encephalitis virus (CAEV)
what is it?
what are the outcome from infection
genetics

A

Clinical correlation

● Caprine arthritis encephalitis virus (CAEV)
○ What do you think it causes??? Caprine Arthritis Encephalitis
○ Progressive dz
○ Leukoencephalomyelitis and ascending paralysis
● Outcomes from infection
○ Remain healthy
○ Untx debilitating polyarthritis and kids develop encephalomyelitis
● GENETICS
○ Goats w/ severe CS carry 1 or 2 of the MHC alleles Be1 Be14
■ So the MCH gene may play a role in the severity of the DZ

96
Q

MCH1
Part 1

Clinical correlation
Caprine arthritis encephalitis virus (CAEV)
what is it?
what are the outcome from infection
genetics

A

Clinical correlation

● Caprine arthritis encephalitis virus (CAEV)
○ What do you think it causes??? Caprine Arthritis Encephalitis
○ Progressive dz
○ Leukoencephalomyelitis and ascending paralysis
● Outcomes from infection
○ Remain healthy
○ Untx debilitating polyarthritis and kids develop encephalomyelitis
● GENETICS
○ Goats w/ severe CS carry 1 or 2 of the MHC alleles Be1 Be14
■ So the MCH gene may play a role in the severity of the DZ

97
Q

Activation of T cells & MHC
T CELL ACTIVATION
what is T cell function
what is T cell activation
what is internxn
what is presentation to T cells

A

● T cell function: protect the body against
intracellular pathogens but they must be
activated first.
● T cell activation: interxn of t cells with
APC (DC,mac,B cells)
● Interxn: receptors on T cells and
proteins of APC
● Presentation to T cells: MHC molecules
on APC

98
Q

Activation of T cells & MHC
MHC INFO
how discovered
relationship to graft rejection
do all animals have MHC
how many classes in a MCH cluster
How are MHC genes passed
How are they expressed

A

MHC INFO
● Discovered due to graft rejection
○ Self vs nonself
○ The region of the gene that controlled
graft rejection: Major histocompatibility
complex MHC

● All animals have MHC each MHC cluster
has at least 3 classes
● MHC genes are passed down from mom
and dad (50/50)
● They are codominantly expressed

99
Q

MHC molecule Classes
how many?

A

3

100
Q

MHC molecule Classes
MHC 1
where are they expressed?
loci=?
are all loci functional?

A

MHC 1
● Expressed on ALL nucleated cells
● Loci= highly polymorphic (Class 1a,
1b,1c)
○ class 1d= outside of the MHC
● Not all of the loci are functional

101
Q

MHC molecule Classes
MHC 2
found where?
how many paired loci?

A

MHC 2
● Found only on APC
● Has 3 paired loci

102
Q

MHC molecule Classes
MHC 3
explain loci code
what does it aid in?

A

MHC 3
Loci code for various proteins and aids in the
innate IS

103
Q

MHC molecule Classes
Summary of important points to know for life :)
what are the main APC molecules?

A

● MHC 1 and 2 are the main APC molecules

104
Q

MHC molecule Classes
Summary of important points to know for life :)
MHC 1=?
so that means they are not on?

A

● MHC 1= on all nucleated cells & present to CD8 T cells
○ So they’re not on RBC, gametes, neurons, or trophoblast

105
Q

MHC molecule Classes
Summary of important points to know for life :)
MHC2=?
they are on? and they present to?

A

● MHC 2= on APC(DC, macs,B cells) & they present to CD4 T cells

106
Q

MHC molecule Classes
Summary of important points to know for life :)
MHC3=
what does it not do?

A

● MHC 3= does not participate in AG presentation

107
Q

MHC 1 structure
what kind of chain is it?
comprised of what?

A

● MHC 1
○ Heterodimer w/ an a (1,2,3) chain and a
B2-microglobulin chain

108
Q

MHC 1 structure

● MHC 1
what does the stable expression of the MHC1 require?

A

○ Stable expression of the MHC 1 requires
the peptide binding cleft, B2
microglobulin, transmembrane region,
and a cytoplasmic domain

109
Q

MHC 1 structure

MHC 1
Peptide binding =?
what part of the molecule is this?

A

○ Peptide binding= between a1 and a2
(most variable part of the molecule)

110
Q

MHC 1 structure
T cell co receptor what does it do, where?

A

T cell co receptor CD8 binds to the
non-variable region of a3
**see diagram slide 29 wk 4 or slide 7 wk 5

111
Q

MHC 2 structure
what are the chains?

A

● a1 , a2 & B1, B2 chains

112
Q

MHC 2 structure
Where is the peptide binding groove?

A

Peptide binding groove: a1, b1

113
Q

MHC 2 structure
what does stable expression require.

A

Stable expression requires the 2 chains
and a bound peptide
*see slide 30 for diagram

114
Q

MHC molecules
Can MHC molecules bind to many peptides at once? are they specificic?

A

MHC molecules can only bind to 1
peptide at a time but they have a broad
specificity for peptide binding (not
specific like t cells)

115
Q

MHC molecules
when does MHC expression increase?

A

MHC expression increases during
immune responses

116
Q

MHC molecules
IFNa,b,y=?

A

IFNa,b,y= increase expression of MHC 1

117
Q

MHC molecules
IFN y=?

A

IFN y= increases MHC 2 on macs and DC

118
Q

MHC molecules
how are pathogens recogized?

A

Recognition of pathogens by DC through
TLR increased MHC 2

119
Q

MHC molecules
Cytokines
secreted by what, resulting in what?

A

Cytokines secreted by CD4 increase
MHC 2

120
Q

MHC molecules
what result with a foreign AG peptide that does not fit the MHC molecule?

A

Foreign AG peptide that does not fit the
MHC molecule will not stimulate an IR
(broad not universal)

121
Q

MHC molecules
AThe greater the diversity–> what?

A

The greater the diversity-> the more AG
they can respond to

122
Q

MHC molecules
Heterozygous=What? what result with binding?

A

Heterozygous= more alleles, &can bind
to more AG peptides

123
Q

MHC molecules
Homozygous= what result?

A

Homozygous= less variety

124
Q

It’s a balance
explain African cheetas
vs
florida anthers
what is the optimal # of MHC genes?

A

● EX: african cheetahs= homogeneous can
cannot fight off infectious peritonitis
● EX: Florida panthers= all come from a
single female so they introduced new
pumas to increase the genetic diversity
● The optimal # of MHC genes is a
balance btwn the need to respond to
AG and the ability to avoid
autoimmunity

125
Q

You’re at shipwreck trying to enjoy a limecolada whenever
your annoying immuno TA comes up to you and starts
asking you immunology questions. What were the two
cardinal features of an antigen???

Short response

A

You’re at shipwreck trying to enjoy a limecolada
whenever your annoying immuno TA comes up to you
and starts asking you immunology questions. What
were the two cardinal features of an antigen???

immunogenicity - ability to induce an IR
Antigenicity- ability to bind to products of the IR they induce

126
Q

Limecoladas are your immuno TA’s favorite drink so she
decided she would sit with you and continue to talk to
you about immuno. What is the antigenic determinant of
an AG?
A. Bilirubin
B. Immunogenic site
C. Hapten
D. Epitope
E. IDK GO AWAY ANGEL

A

D

127
Q

Which of the following factors affecting immunogenicity
of an AG is correct?
A. The smaller the AG the more immunogenic
B. AG that are hard to be degraded are more immunogenic
C. AG that are more like self are typically more immunogenic
D. Lipids are highly immunogenic
E. Proteins are the largest group of AG and highly immunogenic
F. All of the above
G. None of the above

A

E

128
Q

You see your immuno TA walking on the golfcourse and
even though you try to avoid her 24/7 she has Lilo with
her and you really want to pet the cutest island scruff so
you walk up to her. She says you can only pet her if you
can tell her what a superantigen is.

Short answer

A

You see your immuno TA walking on the golfcourse and
even though you try to avoid her 24/7 she has Lilo with
her and you really want to pet the cutest island scruff so
you walk up to her. She says you can only pet her if you
can tell her what a superantigen is.
A superAG can activate a large number of lymphocytes at one time
nonspecifically. It is mainly from bacT and viruses. They bind to the variable
domain in the TCR of CD4 cells and the alpha chain of the MHC 2 molecule on
the APC

129
Q

After your anatomy practical you and your friends went to Monkey bar to
celebrate. But while you’re there you decide to quiz each other on immuno
for your block next week. Which of the following is not something you would
say about the complement system?
A. There are 3 different systems and they all result in the formation of MAC.
B. Factor H and Factor I inhibit C3b forming in the alternative pathway.
C. C3 convertase for the classical and lectin pathway is C4a2b.
D. The proteins in the complement system have to be activated.

A

C

130
Q

While you are at strip you see your favorite immuno prof. They come up to
you and ask you to explain the MAC formation to them. What do you tell
them?

A. C5b recruits c6 and c7 to the target membrane.
B. C8 binds to the complex and created a hydrophobic region in the
membrane.
C. 10-16 copies of c9 create a pore.
D. Water rushes in the cell and causes osmotic lysis.
E. All of the above
F. You say nothing and run

A

E

131
Q

Which of the following regulators of the complement
system are paired correctly?
A. Factor H and I bind to C4a and accelerates decay on self cells
B. Protectin CD59 prevents C9 recruitment and MAC formation
C. C2 inhibitor inactivates C2r, C2s, and MASPs
D. All of the above are correct
E. Angel, stop lying there aren’t any regulators of the complement system.

A

B

132
Q

You can’t catch a break and now your favorite immuno TA is quizzing you.
She asks you to walk her through the classical pathway. Which order is
correct?
A. C1q cleaves C1r, C1r cleaves C1s, C1s cleaves C4, Cls, cleaves C2, C4bC2a
cleaves C3, C4b2a3b cleaves C5.
B. MASPS cleaves C4 and C2, C4b2a cleaves C3, C4b2a3b cleaves C5.
C. C3b binds to factor B, C2bB, factor D, C3bBb, Factor P, C3bBb3b.
D. C1z cleaves C1x, C1r cleaves C1x, C1e cleaves C4, Clz, cleaves C2, C4zC2e
cleaves C3, C4z2e3x cleaves C5.

A

A

133
Q

You’re now at home but you can’t sleep so you are still thinking about
immunology. Which of the following is NOT correct about the alternative
pathway?
A. It utilizes the spontaneous cleavage of C3
B. If C3b binds to a self cell it is rapidly degenerated by Factors H and P.
C. C3 convertase is C3bBb
D. C5 convertase is C3bBb3b

A

B

134
Q

All of this talk about immuno is making you hungry so you decide to go
and make you some popcorn at 4:55 am. You are too lazy to turn on your
light though and you hit your toe. For some reason this makes you think
about the signs of inflammation. What are the signs of inflammation?
A. Redness
B. Heat
C. Swelling
D. Loss of function
E. Pain

A

ALL OF THE ABOVE

135
Q

Your friend is sick but even though you have hung out with her everyday
for the past 10 days you are showing no symptoms. You remember
learning about MHC complexes in immuno last week. Which of the
following explain why she is sick but you aren’t.
A. You have homozygous alleles therefore you are able to fight off more
illnesses than she is.
B. You have more MHC complexes
C. You get the majority of your MHC complexes from your dad and he is
never sick so you just have better genetics.
D. You have heterozygous alleles and your friend has more homozygous
alleles.

A

D

136
Q

You are watching the NEW hocus Pocus and the 3 sanderson sisters make
you think about the 3 MHC classes. Which of the following are correct?
A. MHC 1 is expressed on all nucleated cells including RBC.
B. MHC 2 is expressed on APC and binds to CD8 t cells
C. MHC3 is important for AG presentation
D. The MHC 1 binding cleft is made of a1 and a2.
E. The MHC 2 binding cleft made of a1 and b1
F. A and B are correct
G. D and E are correct

A

G

137
Q

True or False: MHC molecules can only bind to 1 Antigen
at a time but they have a broad specificity for peptide
binding so they can bind to any AG.

A. True
B. False

A

B

138
Q

True or false: The complement system is commonly
activated on the surface of a pathogen or the AG-AB
complex.
A. True
B. False

A

A

139
Q

You are currently a baby DOGtor, fresh out of clinics. Your first patient of
the day is thackery binx. You’re fangirling pretty hard and want to flex
your second semester immunology on him. What is something you might
would say?

A. MHC genes are passed down from your parents but the majority of them
come from your moms mitochondrial DNA.
B. MHC 3 is important for protein activation.
C. There are 3 complement systems lectin, jazz, soul.
D. The complements only goal is to recruit inflammatory cells

A

B

Immuno (13 decks)

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