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Immunology > Immuno CCOM 2 > Flashcards

Immuno CCOM 2 Flashcards

1
Q

Do T cells recognize intracellular or extracellular contents?

A

intracellular

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2
Q

Moelcules from the exongenous pathwar are loaded onto which HLA class? And presented to which cell?

A 
HLA class II
CD4+ T cell
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3
Q

Molecules from the endogenous pathway are loaded onto which HLA? And presented to which cell?

A 
HLA class I
CD8+ T cell
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4
Q

On which chromosome are the MHC and HLAs found?

A

short arm of chromosome 6

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5
Q

How do MHCs exhibit genetic polymorphism

A

overall structure will be the same but a.a. sequence will vary

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6
Q

Describe the structure of HLA-1

A

1 cytoplasmic tail
monomer of : a1, a2, a3
B-microglobulin (not covalent)

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7
Q

Where do processed polypeptides and CD8 cells associate with HLA-1?

A

peptides: cleft bw a1 and a2
CD8: a3 subunit

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8
Q

Describe the structure of HLA-2

A

2 cytoplasmic tails

dimer: a chain and b chain

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9
Q

Where do processed polypeptides and CD4 cells bind to HLA-2?

A

peptides: cleft bw a1 and B1
CD4: B2 subunit

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10
Q

Where is HLA-2 synthesized?

A

ER

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11
Q

What is li?

What does it do?

A

A molecular chaperone for HLA-2 molecules

  • stabilizes unbound HLA-2
  • blocks incidental binding of endogenous self antigens
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12
Q

What is peptide exchange?

A

switch bw CLIP and foreign antigenic peptides on the HLA-2

HLA-DM catalyzes this

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13
Q

On which cells are HLA-2 expressed in all conditions?

In which cells can HLA-2 expression be induced?

A

constitutively: APCs (DCs of spleen/lymph node, theymic epithelial cells, B cells)
induced: tissue macrophages, endothelial cells

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14
Q

What is ubiquitin?

A

attaches to molecules in endogenous pathway to mark for proteolysis by proteasomes

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15
Q

What are the transporter molecuels involved in the endogenous pathway?

A

TAP1 and TAP2

they transport degraded molecules through ER membrane

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16
Q

What are teh chaperones involved in the endogenous pathway? What do they do?

A

calnexin
calreticulin
-These are released after HLA1 binds antigen
-they strenghtn B2-microglubulin binding

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17
Q

How do HLA-1:peptide complexes get transported?

A

Golgi’s exocytic pathway

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18
Q

On which cells are HLA-1 expressed?

A

Constitutively on all nucleated cells

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19
Q

Describe the cross presentation pathway

A
  • APC presents exogenous peptides to CD8 via MHC 1

- prolly from escaped virus/cell debris

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20
Q

What is the molecule of interest in the cross presentation path?

A

CD1 : present lipid and glycolipid antigens to T cells

similar structure to MHC-1 but binding mechanism similar to HLA2

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21
Q

What cells can CD1 activate? Where are they found

A

activate CD4+, CD8+, NK cells

found on B cells and DCs

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22
Q

Where do T cells originally develop?

A

in bone marrow stem cells

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23
Q

When T cells exit the thymus, what differentiation level will they be?

A

mature but naive

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24
Q

What do Th1 cells influence?

A

Positively influence cellular immune repsonse

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25
Q

What do Th2 cells influence

A

up-regulate Ab response

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26
Q

What is it called when children are born without a thymus? What happens?

A

DiGeorge’s syndrome

there are no mature T cells

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27
Q

Describe how a T cell is educated in the thymus

A
  1. Acquires TCR -> specificity
  2. learns tolerance of self
  3. learns self-H:A restriction
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28
Q

What is the general a.a. length of antigen fragments involved in the exogenous and endogenous pathways?

A

exongenous: 12-17 a.a.
endogenous: 8-9 a/a/

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29
Q

How do the common lymphoid progenitors home to the thymus?

A

chenokines and

CD44 adhesion molecule

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30
Q

What makes up the TCR?

A

B chain
pre-Ta
CD3
zeta chain

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31
Q

What makes up the double positive cell?

A 
a and beta chain of TCR
(with TCR-a and TCR-b)
CD3
CD4
CD8
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32
Q

Which cells do the double positives have to pass through to under go central tolerance?

A

thymic epithelial cells

interdigitating thymic DCs

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33
Q

Which cells express both HLA-1 and HLA-2 molecules?

A

thymic epithelial cells constitutively

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34
Q

What is positive selection?

A

if biding of HLA is not right -> apoptosis
Expansion of cells that respond to self HLA plus processed antigen
HLA restricted

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35
Q

What is negative selection?

A

Weeds out self-reactive cells through interaction with interdigitatin DCs
Now are self-tolerant

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36
Q

What is the gamma/delta TCR?

A

develop independent from thymus
not HLA restricted
no CD4 nor CD8
involved in innate defense

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37
Q

When does the adaptive immune response begin?

A

When antigen-laden tissue-based DCs migrate from infected tissue to lymph node

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38
Q

What is the main function of secondary lymphoid tissue?

A

to trap antigens and concentrate them with APCs and lymphocytes

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39
Q

What happens when a naive T cell is activated? How is the activated T diff than the naive T?

A

expression of different adhesion molecules and chemokines receptors
activated T cells recirculate via spearate/distinct pattern more specific

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40
Q

Why does the immune system need both B and T cells?

A

B cells target extracellular anitgens w Abs

T cells target intracellular or cell-associated antigens via chemokines or cytotoxicity

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41
Q

Describe how a TCR is clonally distributed

A

each T cell clone bears a unique TCR

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42
Q

Describe the signaling process after presentation of the antigen to the TCR

A

conformational change of TCR
CD3 and zeta ITAM activated
signal cascade to activate T cell

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43
Q

What is the funciton of CD3

A

chaperones transport of TCR to membrane

cell signaling molecule

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44
Q

Activation of CD4 includes the transcription of which chemokine?

A

IL-2 (growth factor)

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45
Q

When are CD4 and CD8 expressed at the same time?

A

Very short period of time on immatrue T cell (double pos)

Otherwise, they are mutually exclusive

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46
Q

What are the roles of B7 and CD28? WHere are they located?

A

B7 is on APC, CD28 on T cell

critical to activation of naive T cell but not required fro activation of memory T cell

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47
Q

What is the first cytokine produced after activation of T cells?

A

IL-2

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48
Q

During what develpmental stage of T cells is central tolerance achieved?

A

double positive T cell

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49
Q

What will you see be expressed on the surface right before T cells enter the thymus

A

just chemokine receptors

50
Q

What chemokines are involved when naive T cells circulate randomly?

A

CCL21 (from HEV endothelial)

CCL18 (from DCs in nodes)

51
Q

What cytokines does Th2 produce:

A

IL4
IL5
IL10
IL13

52
Q

What cytokines do Th17 cells produce?

A

IL17
IL21
IL22

53
Q

What cytokines do Th1 cells produce?

A

IL2

IFN-gamma

54
Q

What cytoines do Treg cells produce?

A

TGF-B
IL-10
IL-4

55
Q

What diseases are RESOLVED by Type 1 immune responses?

A 
Chlamydia
HIV
Intracellular parasites
Leprosy
Tb
56
Q

What diseases are RESOLVED by Type 2 responses?

A

Pneumococcal pneumonia
Heominth-worms
Diptheria
Meningococcal disease

57
Q

What diseases are CAUSED by Type 1 responses?

A

Contact hypersensitivity
Delayed Hypersensitivity
Silicosis

58
Q

What diseases are CAUSED by Type 2 responses?

A

Lupus
Allergies
Lepromatous Leprosy
Asthmal

59
Q

What is required in order for CTL to be activated? Where does it come from?

A

IL-2

Comes from either CD4 cell secretion or from itself in autocrine fashion

60
Q

How do CTL kill target cells?

A

Via perforin- binds to membrane and polymerizes to make channels
granule release- induces apoptosis via TNF-B, TNF-a, Granzymes

61
Q

What other structure is perforin very similar to?

A

C9 complement component

also similar function in membrane attack complex

62
Q

What is fragmentin?

A

Granzyme that induces DNA fragmentation and apoptosis

63
Q

What is the minor pathway in T cell cytotoxicity?

A

Fas-FasL
FasL on CTL binds FAS on target
activates caspases that induce apoptosis

64
Q

What is the surface expression of NK cells?

A

CD56/CD16

65
Q

What is the mechanism of NK cells in killing?

A

NK cells have KIRs
When MHC binds KIR, NK is inhibited
If no MHC binds, cell is killed
SO KN recognize lack of MHC expression

66
Q

How can NK cells be upregulated?

A

IL-2

IFN-gamma

67
Q

How can macrophages be cytotoxic?

A

lysosomal content release
release TNF-a
N and O radicals

68
Q

How does ADCC work?

A

Killer cells that have Fc receptors for IgG (CD16 in NK) bind to Ab-labelled cell

69
Q

What does non-sterilizing elimination entail? example?

A

controlling replication of pathogen but not actually eliminating it
ex: Herpes virus

70
Q

How does the immune system target encapsulated bacteria?

A

Opsonization with C3b against capsule. Overcomes inability of macrophages to ingest hydrophilic substances

71
Q

What are examples of bacteria that avoid the circulatory system by colonizing mucosal surfaces w low phagocytic and complement levels?

A 
Cholera
Diptheria
Pertussis
(These orgasnisms never penetrate epithelium)
(They release toxins)
72
Q

Endo-toxins are produced by what type of bacteria? example?

A

produced by gram-negative

ex: LPS

73
Q

Which endogenous pyrogens are induced by LPS?

A

IL-1
TNF-a
IL-6

74
Q

Are endotoxins or exotoxins neutralizing to Abs? Why

A

Exotoxins

Since there is very little variance in antigenic structure, Abs can bind it

75
Q

What are superantigens and what do they do?

A

type of exotoxin
bind to HLA-II
activate T cells that posess certain TCR allele
cytokines–> toxic shock

76
Q

What does IFN-gamma do in terms of intracellular bacteria immunity?

A 
restricts protein synth
decrease membrane fluidity
NO
alters cell metabolism
Increased HLA-1
77
Q

What factors, in order of effect, increase macrophage/monocyte phagocytosis?

A

TNF-a
LPS
IFN-gamma
(LPS and INF-gamma are synergystic)

78
Q

How can obligate intracellular pathogens evade the immune response?

A
  • they result in a Th2 response that is ineffective against intracellulars
  • they become latent until immune response wanes
79
Q

How is humoral immunity inolved in viral infections?

A

Abs can block viral attachment
Abs can opsonize
Classical pathway -complement
ADCC

80
Q

What is the antiviral state?

A

decrease membrane fluidity
enzymes that destroy virals
inhibits viral protein synth
upregulates HLAs

81
Q

How can virals escape immune reponse?

A 
Block IFN pathways
Block HLA expression
Block complement activation
mutating themselves
immune suppression
82
Q

What type of immunity is directed twoards parasites?

A

Humoral (Ab and complement) befcasue it is extracellular

83
Q

What are two hallmarks of helminth parasites?

A

-High IgE levels
-esoinophelia
so you will see symptoms mimicking allergies

84
Q

What type of T cell response is induced from parasites? What cytokines are involved?

A

Th2 immune response

IL-4 and IL-5

85
Q

What can cause SIRS?

A 
LPS
gram-pos peptidoglycan or teichoic acid
f-met-phe-leu
mCPG
bacterial and viral superantigens
86
Q

Describe the presentation of SIRS

A 
circulatory collapse
DIC
hemorrhagic necrosis
multiple organ failure
spetic shock
87
Q

What disease are some people susceptible to after getting streptococcal pharyngitis?

A

rheumatic fever -
Some will develop Abs against carbs on strep bacteria that are similar to those found on heart valves. These Abs bind heart tissue

88
Q

What is herd immunity?

A

If enough members of a population are immunized, transmssion of disease is interrupted

89
Q

What is attack rate?

A

Number infected compared to number exposed

90
Q

How do scientists kill organisms for vaccines?

A

physical - heat or irradiation

chemical- formaldehyde, glutaraldehyde

91
Q

What type of immune response is generally seen after a killed/inactivated vaccine is given>

A

exogenous antigen processing pathway and Th2 response

boosters are often needed

92
Q

Describe the nature of live/attenuated vaccines and how they are safe?

A

They lose their virulence yet retain their ability to replicate within the host

93
Q

Why are live vaccines better than killed ones?

A

1) processed exogenously and endogenously so Ab and cell-mediated responses
2) sustained immune response so lesser need for booster

94
Q

What are some disadvantages of the live vaccines?

A

-less stable and can revert back to virulent form

95
Q

What are some examples of recombinant vaccines?

A

Hep B
HPV - Quad
HPV- Bi
Lyme Disease

96
Q

What are the valencies of acellular pertussis, Gardasil, and pneumococcal vaccines?

A

pertussis: 4
Gardasil: 4
pneumococcal: 23

97
Q

What are potential concerns of formaldehyde as an inactivating agent?

A

hypersensitivity -hand eczema

not carcinogenic

98
Q

What is the advantsage of FluMist?

A

intranasal adminisration of ‘cold-adapted’ virus allows growth in cool mucosa but cant spread to warmer areas in body

99
Q

Which two adjuvants are liscensed for human use? How do they work?

A

alum
AS04
-restrict Ag dispersion to form depot and slow release and granuloma forms for proonged immune response

100
Q

How does neomycin interfere w bacteria?

A

it binds to 30S subunit of bacterial ribosomes

used in vaccines to prevent contamination

101
Q

Why is 2-PE added to vaccines

A

it’s a preservative

effective against pseudomonas aeruginosa (and broad spectrum)

102
Q

What are the two main components of the preservative Thimerosal?

A

organic Hg

thiosalicylate

103
Q

What are the complications of Thimerosal?

A

allergies - periorbital dermatits possible

But generally it is ok in vaccines

104
Q

What are some contraindications of vaccines?

A
  • an immunocompromised person and live vaccines
  • allergy to vaccine products
  • pregnancy
105
Q

What are the benefits of maternal immunization w regards to the neonate?

A
  • If it is not viable, then it is safe to give in 2nd tri

- enhances passive immunity through transplacentally acquired IgG

106
Q

For how long can HISG prtect a hypogammaglobulinemic pateitn?

A

one month

107
Q

What are donors for HISG screened for

A

Screened for pathogens

Not screened for Ab titers

108
Q

What is the difference bw IGIM and IGIV?

A

IGIV - processed to prevent clumping

IGIM - may cause anaphylaxis if given i.v.

109
Q

When is IGIV used?

A

Group B streptococcal infections

Kawasakis disease

110
Q

What is SHIG? How is it different form HISG?

A

donors have high levels of specific Ab

111
Q

What must you consider when given patient serum from heterologous animal species?

A

Serum sickness

112
Q

What are contraindications for polyclonal preps?

A
  • shouldnt be given IV unless stated - anaphylaxis

- in IgA deficient pts. cuz they may have anti-IgA Abs (anaphylactic rxn through IgE production)

113
Q

What are most monoclonal Abs derived from?

A

mouse myeloma cell fused with a mouse spleen-derived plasma cell producing desired Ab

114
Q

What is the most common monoclonal Ab used for Allograft rejection prevention?

A

anti-CD3

115
Q

What type of bacteria is normal gut flora i general?

A

gram neg

116
Q

Define Sepsis

A

SIRS + infectious etiology

117
Q

Define severe sepsis

A

Sepsis + 1 organ failure

118
Q

What cytokines are released from macrophages in toxic shock syndrome?

A

IL1
IL6
TNFa

119
Q

What cytokines are released from T cells in toxic shock syndrome?

A

IL2

IFN gamma

120
Q

How much Ab is produced from exotoxins?

A

usually very little so they may be susceptible to similar disease

121
Q

Why would a PPD show up negative when someone has AIDS?

A

normally: assess cellular immune response by seeing delayed hypersensitivity
AIDS: no CD4 , so no CMI, so no rxn

122
Q

How does decreased CD4 in AIDS effect other immune cell populations?

A

very low levels of cytokines will yeld ineffective immune repsonses

Immunology (7 decks)

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