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Block 6: Immuno > Week 1 > Flashcards

Week 1 Flashcards

1
Q

bacterial LPS is recognized by what 3 things

A

TLR4, MD2, and CD14

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2
Q

which domain does CD8 bind to

A

α3 of MHC I

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3
Q

which domain does CD4 bind to

A

β2 of MHC II

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4
Q

positive thymic selection vs negative

A

positive: T cells need to be able to recognize self
negative: T cells can’t be TOO reactive to self; occurs by dendritic cells/macrophages

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5
Q

epitope

A

where the Ab binds to the Ag (aka antigenic determinant)

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6
Q

papain

A

cleaves Ab into Fab (contains variable region for Ag binding) and Fc regions (class switching occurs here)

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7
Q

Abs can fight infections by 3 ways. What are they?

A
  1. neutralization: binds directly to toxin/ inhibits it from binding to pt
  2. opsonization: Abs coat bacterium then a macrophage eats it
  3. complement activation
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8
Q

what Igs do complement?

A

IgG and IgM

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9
Q

what Ig is for sensitization of mast cells?

A

IgE

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10
Q

What Ig is for sensitization for killing by NK cells?

A

IgG

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11
Q

what Ig does opsonization?

A

IgG

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12
Q

what Ig is for transport across epithelium?

A

IgA

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13
Q

What Ig can cross placenta?

A

IgG

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14
Q

what part of an Ab determines the isotype?

A

Fc

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15
Q

ADCC (antibody dependent cell cytotoxicity)

A

Ab binds to Ag on target cells

Fc receptor on NK cells recognizes the bound Ab

Cross linking of Fc R tells NK cell to kill target cell → apoptosis

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16
Q

bias definition

A

any systemic error in design, conduct, or analysis of study that results in mistaken estimate of exposure on risk of disease

can occur at any stage of study and in all studies (more often in retro

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17
Q

selection bias

A

error due to differences in those who are selected/participate in a study and those that don’t

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18
Q

information bias

A

flaw in measuring exposure/outcome that may result in differential accuracy of info. between comparison groups

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19
Q

selection bias non response

A

rates of refusal to participate differ in those with disease who are exposed vs those without disease who are exposed

*to combat: keep recogrds of non-responders/analyze data

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20
Q

info. bias: diagnostic

A

validity of diagnosis altered by knowledge of exposure

ex. OC and DVT

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21
Q

nondifferential misclassification of exposure

A

amount/direction of misclassification is similar b/t cases and controls

always results in underestimating OR - can result in false negatives

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22
Q

differential misclassification of exposure

A

amount of misclassification differs b/t cases and controls - having outcome alters exposire history/recall

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23
Q

confounding

A

estimate of exposure distorted because mixed with extraneous factor; is the factor on which the exposed and unexposed differ

must be a risk factor in the unexposed group/associated with the exposure

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24
Q

opsonization process

A
  1. Ab binds to bacterium
  2. Ab coated bacterium binds to Fc receptors on cell surface (MACROPHAGES AND NEUTROPHILS, IgG NOT IgM)
  3. macrophage endocytoses bacterium coated
  4. lysosomes fuse with phagosome creating phagolysosome
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25
Q

Humira and Embrel are MoAb to what

A

TNFα

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26
Q

hapten

A

has 1 epitope

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27
Q

affinity vs. avidity

A

affinity: strength of single Ag combining site of an Ab and a single epitope of an Ag

avidity: strength of binding of an Ab for an Ag (ex. IgM has greater avidity than IgG because it has more binding sites)

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28
Q

toxoid

A

altered protein toxin used in tetanus vaccine; good becasuse it is a cross reacting Ag that induces an immune response that protects

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29
Q

when does maximum precipitation occur?

A

at equivalence with with molar ratio of Ag to Ab is in slight Ag excess giving maximal crosslinks

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30
Q

agglutination

what Ab is best at that?

A

combination of an Ab with a particulate Ag (RBC, latex particle, bacteria). Works with insoluble (particulate) Ag - see visible clumps in minutes

IgM>IgG because more binding sites

more sensitive than precipitation

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31
Q

titer

A

1/highest dilution of anti-serum that still gives a positive agglutination reaction

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32
Q

precipitation

A

soluble antigen, only precipitates at optimal AgAb ratios. IgG best at this.

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33
Q

radioimmunoassay RIA

A

an inhibition assay - radioative Ag gets displaced by unlabeled and then measure that

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34
Q

ELISA

A

coat plates with Ag, add serum. if Ab is present it will bind and then give second Ab linked to enzyme that gives color

can quantitate by testing dilutions - the last dilution that still gives measurable color is the titer

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35
Q

direct vs. indirect fluoresence

A

direct: Fl labeled Ab to T cell marker (CD3), then T cells with it will fluoresce

indirect: looking for Ab in patients serum: incubate serum with test tissue; if Ab present, will bind (invisible) then add Fl labeled anti-Ig

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36
Q

how many loci are there for Ig genes

A

3: 2 light chain (kappa and lambda, chromosomes 2 and 22)

1 heavy chain (chromosome 14)

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37
Q

VDJ recombinase

A

lymphocyte specific enzymes RAG1 and RAG2 recognize and cleave unique recombination signal sequences that flank Ig gene segments - same for B and T cells

defect = SCID

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38
Q

TdT (terminal deoxynucleotidal transferase)

A

adds extra nucleotides when joining of Ig gene segments is imprecise

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39
Q

allelic exclusion

A

normal B cell has single functional heavy chain rearrangement and single functional light chain rearrangement - means 1 B cells makes a single tupe of Ab with single Ag specificity

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40
Q

what is class switching controlled by? what enzyme is used?

A

T cells and Ag; rearrangements occur @ DNA level without RAG1/2

AID = enzyme for class swtich

occurs in germinal centers of 2° lymphoid organs

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41
Q

affinity maturation

A

during course of immune response, random mutations occur within rearranged variable regions; if they result in inc. affinity for the Ag, the b cells will be positively selected and expanded

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42
Q

structural proteins in virus

non-structural proteins in virus

A

structural: capsid, nucleocapsid (NA and capsid), matrix

non-structural: polymerase, TFs

43
Q

capsid

A

protein shell surrounding nucleic acid genome in viruses

44
Q

nucleocapsid

A

“core” of virus

nucleic acid/protein assembly packaged in virion

45
Q

tegument

A

regulatory proteins in the virion located between the nucleocapsid and envelope

46
Q

are enveloped or non-enveloped viruses more sensitive to heat, drying, detergents?

A

enveloped are more sensitive!

transmitted by direct contact (blood/sex) and transmitted via respiratory

non-enveloped are tougher droplets (influenza, measles, rubella, VZV); can be fecal-oral route

47
Q

structure of the following virses:

HSV (HSV1 and 2, EBV, CMV), HBV, smallpox

A

DNA enveloped

48
Q

structure of the following virses:

adenovirus, papillomaviruses, parvovirus

A

DNA nucleocapsid virus

49
Q

structure of the following virses:

influenza, RSV, measles, mumps, rabis, HTLV, HIV, HCV

A

RNA enveloped viruses

50
Q

structure of the following virses:

enteroviruses (polio, coxsackie, echovirus, HAV), rhinovirus, rotavirus, norovirus, HEV

A

RNA nucleocapsid viruses

51
Q

segmented RNA genoma

A

influenza virus made of 8 segments of viral RNA that carry the info needed to make virus particles; each segment can make at least 1 protein

52
Q

what does influenza recognize and on what types of cells

A

sialic acid on epithelial cells; mediates entry and delivery of virus

53
Q

what does HIV recognize and on what types of cells

A

recognizes CD4/CXCR4 on T cells

54
Q

replication of DNA viruses:

  1. where?
  2. what polymerase does it use?
  3. examples
A

nucleus

uses host DdRp to make viral mRNA

ex. parvovirus, papillomavirus, adenovirus, HSV (poxvirus is weird and replicates in cytoplasm by carrying its own polymerase)

55
Q

replicaton of (+)ssRNA viruses

  1. where?
  2. what polymerase does it use?
  3. examples
A
  1. cytoplasm
  2. can be used directly as mRNA but carries RdRp for making more virions
  3. poliovirus
56
Q

replication of (-)ssRNA viruses

  1. where?
  2. what polymerase does it use?
  3. examples
A
  1. cytoplasm
  2. RdRp using the negative strand as template
  3. influenza, measles, rabies
57
Q

replication of dsRNA virses

  1. where?
  2. what polymerase does it use?
  3. examples
A
  1. cytoplasm
  2. RdRp uses - strand as template; can unwind dsRNA
  3. rotavirus
58
Q

replication of retroviruses (HIV)

A

reverse transcriptase (RdDp) → DNA unwinding then hydrolysis of RNA in RNA-DNA hybrid by RNAse H

DNA viral copy is transcribed into viral mRNA by host RNA pol

59
Q

infectious nucleic acid

A

purified viral DNA or RNA without protein that can carry out entire viral growth cycle → production of complete virus particles

only in virses that don’t require polymerase

60
Q

can RdRp proofread?

A

no! leads to diversity in RNA viruses

61
Q

what type of viruses do budding vs lysis?

A

budding = enveloped; take from host cell membrane

lysis = non-enveloped; break membrane

62
Q

virulence factors

A

allow invasion from other sites

63
Q

capsule

A

discrete layer of polypeptide/polysaccharide that masks PAMPs like LPS and peptidoglycan that allow bacteria to avoid the innsane immune system/complement deposition

64
Q

pili

A

example of antigenic variation; expressed from pilin gene - there are silent genes and can be recombined to escape immune recognition

65
Q

gene slippage

A

phase variation = turning genes on and off

genes have many repeats in nucleotides early in sequence

66
Q

gene inversion

A

flagellin encoded by fimA which is recognized by TLR4; recombinase mediates gene inversion at promtor

67
Q

T3SS

type 3 secretion system

A
  • responsible for direct injection of protein into eukarotyotic cells
  • proteins are effectors that kill/disable/adapt eukaryotic cells for intracellular bacterial growth
  • only in gram negative bacteria
68
Q

T4SS

type 4 secretion system

A
  • secretion system responsible for transfer of DNA during conjugation
  • can also secrete proteins/complexes
  • in gram negative and gram positive
69
Q

T5SS and T7SS

A
  • uses Tat and Sec to secrete toxins, receptor binding proteins, pili
  • T7SS new virulence factor ID’d
  • only in gram negative
70
Q

siderophores

A

iron binding proteins secreted by bacteria; can outcompete human proteins for Fe (needed for rapid bacterial growth)

71
Q

neutrophils

A
  • polylobulate nuclei
  • primary (azurophilic) and secondary (specific) granules
  • stored in BM and released when need to fight infection
72
Q

C3b and opsonization

A

enhances phagocytosis (opsonization)

CR1 on macrophage/neutrophil binds C3b on bacterium (from complement deposition) → endocytosis of bacterium by macrophage → phagosome → phagolysosome

73
Q

metabolic consequences of phagocytosis

A
  1. inc. in glycolysis by hexose monophosphate shunt
  2. increase in uptake of O2
  3. increase in production of peroxide
  4. pH of phagolysosome acidifies to 4.7
74
Q

neutrophil microbicidal substances

A
  • bleach (hypochlorite)
  • cationic proteins (punch holes in membranes)
  • defensins (antibiotic properties)
  • lysozyme (breaks down microbial peptidoglycan)
75
Q

chronic granulomatous disease

A

defects in cytochrome b gene/NADPH oxidase - can’t make peroxide and superoxide. staph/e.coli/candida susceptible

76
Q

CRP

A

APRP in liver; binds phosphocholine on pneumococci and triggers complement; an opsonin

77
Q

mannose binding lectin

A

APRP made in liver

binds mannose motifs on bacteria, triggers complement

78
Q

lipopolysaccharide binding protein LBP

A

APRP made in liver

binds LPS from gram neg and helps it bind CD14 receptors on macrophages which triggers TLR4

79
Q

serum amyloid P

A

binds to several bacteria

80
Q

TLR2 target

A

gram positive bacteria, mycobacteria, yeasts and other fungi (recognizes peptidocglycans, GPI-linked proteins, lipoproteins, zymosan)

81
Q

TLR4 target and downstream effects

A

gram negative bacteria, RSV (recognizes LPS and F-protein)

downstream:

  • TRIF pathway: type I IFNs
  • Myd88 pathway: TNFα thru NFKB
82
Q

cytokine storm of septic shock

A

macrophages releases tons of TNFα, IL-1, IL-6, and IL-12

83
Q

IL-8

A

secreted by macrophages; chemoattractant to neutrophils

84
Q

IL-6

A

induces acute phase liver proteins

85
Q

what is the classical complement pathway initiated by

A

AgAb complex or CRP

86
Q

C1qrs

A

in classical pathway of complement;

C1r and s are serine proteases that are activated when C1q binds to AgAb complex (binds 2 IgG molecules or 1 IgM)

C1q only binds to Fc tail of IgG or IgM if they are bound to Ag!

87
Q

does complement get activated when IgM or IgG are soluble?

A

no!!! 1 IgM or 2 IgG need to be antigen bound thru Fc tail

88
Q

MAC

A

membrane attack complex

C5b6789m binds sequentially to form complex on cell surface that creates a pore to disrupt cell membrane

89
Q

3 distinct sites of classical complement anchoring

A
  1. C1qrs
  2. C4b2a3b
  3. C5b6789n (MAC)
90
Q

alternate pathway of complement is triggered by what?

what enzyme/protein complex is on surface?

A

microbe

C3 convertase → C3bBb then C3b amplification

C3 convertase is stabilized by properdin

C5 convertase splits C5

91
Q

lectin pathway of complement

A

triggered by MBL (protein with 6 helices) part of innate IS that recognizes microbes in absence of Ig

activates mannose binding lectin assoc. serine proteases (MASPs) to initiate complement

92
Q

C3a

A

chemotactic for neutrophils, causes mast cells to release histamine

93
Q

C3b

A

major opsonin, leads to inc. phagocytosis

94
Q

Factors H and I

A

inhibit alternate pathway of complement

95
Q

carboxypeptidase

A

degrade C3a and C5a

96
Q

C1 esterase inhibitor

absence?

A

blocks C1r and C1s

absence = hereditary angioneurotic edema

97
Q

decay accelerating factor

A

breaks down C4b2a and C3bBb

98
Q

membrane co-factor protein MCP

A

dissociates C4b2 and C3bBb and fcailitates C4b and C3b degradation by Factor I

99
Q

homologous restriction factor/CD59

defect?

A

block MAC by interfering with C9 attachment/polymerization

defect = paroxysmal nocturnal hemoglobulinuria

100
Q

C4 and C2 deficiency

A

autoimmunity

101
Q

C5-8 deficiency

A

susceptibility to gram negative infections

102
Q

C3 deficiency

A

recurrent life threatening infections

103
Q

factor I deficiency

A

uncontrolled activation of alternate pathway and depletion of C3

Block 6: Immuno (3 decks)

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