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D2 - FALL - Par 2 > Micro - Things IDK yet... > Flashcards

Micro - Things IDK yet... Flashcards

1
Q

What is the red complex, and what bacteria does it include?

A
  • related strikingly to clinical measures of periodontal disease
  • particularly pocket depth & BOP
  • includes Poryphormonas gingivalis, Tannarella forsythia, Treponema denticola.
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2
Q

What is the orange complex, and what bacteria does it include?

A
  • also related to pocket depth
  • this relationship & the relationship to other clinical parameters is less striking than the red complex
  • includes P. intermedia, C. rectus, C. showae, E. nodatum, F. nucelatum, P. micros, P. nigrescens
  • need orange complex for red complex to come in and flourish
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3
Q

What is a common trait of Red complex? And what does it do?

A

the expression of trypsin-like proteases; Trypsin-like proteases interact w/ host cell protease-activated receptor PAR-2

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4
Q

Pg gingipains have been shown to stimulate the secretion of cytokines via activation of…?

A

PAR-2

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5
Q

What pathogens share the ability to penetrate the gingival epithelium (invasive)? And why?

A

Aa, Pg, Tf, Td; due to their ability to produce toxic proteases (ex. endotoxins)

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6
Q

What bacteria are useful indicators of progressive periodontitis (in aggressive & chronic disease)?

A

Aa, Pg, Pi, Td, Tf

  • one or more of these species occur in 99% of progressive lesions
  • collectively, these species avoid/compromise host defenses and induce tissue dmg
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7
Q

what is one of the first stages of initiation of gingivitis?

A

bacterial exotoxins (i.e. Hyaluronidase) destroying intercellular connections betw epithelial cells lining the gingival sulcus.

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8
Q

Pg is commonly found in large numbers in gingivitis patients. Why is this?

A

WRONG! FALSE! NOOOOO! Pg is RARELY found in gingivitis patients and also remember, it is ABSENT from edentulous.

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9
Q

Gingipains are what and do what?

A

Gingipains are trypsin-like /cysteine proteases that degrade collagen, fibrinogen, fibronectin, complement components C3 & C5a, IgG & IgA.
*also have 2 arginine-specific and 1 lysine-specific

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10
Q

What does Arg-gingipain do?

A

It agglutinates and lyses the erythrocytes providing heme-a growth factor for Pg

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11
Q

What does gingipain cleave and what is the resulting consequence?

A

Gingipains cleave monocyte CD14, contributing to hyporesponsiveness to LPS and other bacterial triggers of mac activation.

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12
Q

______ and ______ promote adherence to host cells, contributing to the invasive capacity of Pg.

A

Pg fimbriae & Arg-gingipain

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13
Q

How does Pg persist in the plaque biofilm on tooth surfaces?

A

It attaches to Streptococcus gordonii via the major fimbrial subunit protein (FimA)

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14
Q

What is special about Pg’s LPS?

A

It has hemin-dependent alteration in its structure of Lipid A that may reduce the host’s ability to mount an innate immune response.

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15
Q

How is Aa invasive?

A
  1. enter epithelial cells
  2. escape phagocytic vacuoles
  3. multiplies in cytoplasm
  4. spread to adjacent epithelial cells via protrusions
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16
Q

How does Aa affect PMNs and mac’s?

A

It produces a leukotoxin that can destroy PMNs and mac’s by forming cation-selective pores that lead to the osmotic lysis of these cells.

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17
Q

What are the major Td virulence determinants?

A
  1. Dentilisin
  2. Major outer sheath protein (Msp)
  3. Sip protein
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18
Q

What is dentilisin?

A

a major Td virulence determinant that is a serine protease that degrades matrix prot & host cell junctional prot
- also activates host MMPs to degrade matrix

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19
Q

What is the Major outer sheath protein (Msp)?

A

a major Td virulence determinant that is a porin, causing membrane depolarization in some cells–cytotoxic to others
- alters fibroblast cytoskeleton reorganization, diminishing the cell migration, which prolongs tissue remodeling and wound healing

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20
Q

What is the Sip protein?

A

a major Td virulence determinant that induces arrest of T-cells in G1 and subsequent apoptosis, suppressing T-lymphocyte proliferation in response to mitogens (substances that induce mitosis)

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21
Q

In order for Td to be present, what else must be present?

A

Pg! They coaggregate not only w/ F. nucleatum but also with each other.

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22
Q

What is a major virulence determinant for Tannarella forsythia (Tf)?

A

BspA protein = binds to fibronectin & fibrinogen and stimulates neutrophil recruitment, inflammation, and bone resorption.

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23
Q

What type of patients would you find Prevotella intermedia (Pi)?

A

gingivitis, healthy, and edentulous patients

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24
Q

Pi expresses proteases and resists killing by phagocytes, but it lacks what…?

A

antiphagocytic capsule & collagenase production

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25
Q

Pi often dominates the subgingival flora in what type of gingivitis?

A

NUG = necrotizing ulcerative gingivitis

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26
Q

Predisposition to more severe chronic periodontitis occurs with…?

A

certain genetic polymorphisms (i.e. IL-1 genes)

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27
Q

What opportunistic pathogens/bacteria can infect a patient with a suppressed immune response due to periodontal disease?

A

cytomegalovirus, Epstein-Barr virus, and herpesvirus co-infections

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28
Q

Peripheral blood monocytes from PD pts release 2-3x more …?

A

IL-1B (osteoclast activating factor)–this increase due to monocytes stimulated by LPS

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29
Q

What is wrong with treating oral infections w/ systemic antimicrobial agents? And why?

A

It risks side effects and gives varied results.

  • Bc it is difficult to maintain adequate drug levels for a sufficient time at site of action
  • Also bc of reduced susceptibility of bact in biofilm compared to planktonic bacteria on which AB MIC (minimum inhibitory conc) values determine
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30
Q

What is the solution for local delivery of antimicrobial agents for PD disease?

A

deliver an antimicrobial agent directly to the PD pocket by use of drug-containing gels or films

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31
Q

Examples of local delivery of antimicrobial agents?

A
  1. metronidazole - gel or cellulose strip
  2. chlorhexidine - chip; can kill most of red complex
  3. tetracycline - fiber
  4. doxycycline - gel
  5. minocyclone - gel or powder
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32
Q

What is Actisite?

A

first ex of localized antimicrobial therapy; ethylene vinyl acetate copolymer (EVA) fiber containing 25% tetracycline

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33
Q

What is the amt/yield for normal delivery of tetracyclines in both serum & gingival crevicular fluid?

A

~10 ug/ml

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34
Q

What are afimbrial adhesins?

A

outer-memb or surface-exposed proteins that can bind to host cell surface-exposed proteins/carbs or can bind host proteins that then bind to the cell.
- they are made on the surface of the bact

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35
Q

What are coagulases?

A

enzymes that accelerate the formation of a fibrin clot around the organism which protects against phagocytosis by neutrophils & mac’s

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36
Q

What do Immunoglobulin A proteases allow?

A

They digest IgA, allowing colonization of mucous membranes.

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37
Q

How does Chlamydia survive inside a host’s cell?

A

It grows within a phagosome (inclusion) and does not fuse w/ the lysosome; it is obligate intracellular

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38
Q

How does Listeria survive inside a hist’s cell?

A

It enters the cell in a phagosome, and then escapes the phagosome by digestion of the memb; it is facultative intracellular; motile in cytoplasm bc of actin tails

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39
Q

What are enterotoxins?

A

exotoxins that result in watery diarrhea and tend to increase cellular lvls of cAMP (release of water & electrolytes > diarrhea)

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40
Q

What produces endotoxins?

A

ONLY G(-) bacteria; not secreted by exotoxins–released when cell lyses.

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41
Q

At high levels, what can LPS cause?

A

lethal toxicity, hypotension, septic shock, death

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42
Q

What recognizes LPS?

A

TLR4 & associated proteins

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43
Q

What is the toxic part of LPS?

A

Lipid A

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44
Q

Why is LPS not an effective vaccine target?

A

weakly immunogenic; does not result in an adaptive immune response w/ “memory”

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45
Q

What are the traits of exotoxins? (8 pts)

A
  1. secreted from living cell
  2. produced by G(+) & G(-)
  3. heat-labile
  4. highly immunogenic; can be converted to toxoids
  5. antisera neutralizes toxin
  6. highly toxic
  7. doesn’t usu cause fever
  8. frequently encoded on extrachromosomal elements (plasmids & phage)
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46
Q

What are the traits of endotoxins?

A
  1. produced by G(-) only
  2. heat-stable
  3. weakly immunogenic (cannot be converted to toxoids)
  4. antisera does not neutralize toxicity
  5. moderately toxic
  6. induce inflamm, fever, and septic shock
  7. encoded by chromosomal genes
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47
Q

Antisera can neutralize endotoxins, but not exotoxins?

A

WRONG, They can neutralize extotoxins, NOT endotoxins.

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48
Q

What mechanisms do microbial pathogens use to

adhere to host cells?

A

pili or fimbriae, and afimbrial adhesins!

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49
Q

What are the effects of base-pair substitutions?

A
  1. none (no AA change)
  2. missense (AA change)
  3. nonsense (stop codon created)
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50
Q

What is the difference between forward and reverse genetics?

A

Forward genetics is an approach used to identify genes (or set of genes) responsible for a particular phenotype of an organism.
Reverse genetics analyzes the phenotype of an organism following the disruption of a known gene.

***simplified: reverse genetics- force a mutation in DNA and look for change in phenotype. forward- see a change and then map the DNA

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51
Q

What are the types of mutations?

A
  1. base-pair substitutions
  2. addition/deletion
  3. DNA rearrangements
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52
Q

What is an example of a chemical mutagen?

A

base analogs - chemicals that mimic bases & get incorporated in DNA; usu results in improper base pairings (ex. intercalating agents, modifying agents)

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53
Q

What is an example of physical mutagens?

A

ionizing radiation, ultraviolet light (they result in distortion of DNA molecule itself

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54
Q

What does ionizing radiation do to cause mutations?

A

double and single-stranded DNA breaks

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55
Q

What does ultraviolet light do to cause mutations?

A

produce pyrimidine dimers on the same strand

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56
Q

What are the causes of mutations?

A
  1. chemical mutagens
  2. physical mutagens
  3. replication errors
  4. DNA insertions
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57
Q

What is a cistron? Operon? Regulon?

A
  • cistron: DNA encoding a prot
  • operon: DNA encoding > 1 prot (usu linked together)
  • regulon: group of genes that co-regulate (don’t have to be directly next to each other)
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58
Q

The binding of certain promoters is directed by what?

A

sigma-factors (that form part of the RNA polymerase)

- sigma factors directs polymerase to promotor–process = promoter recognition

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59
Q

What does a repressor protein do?

A

Binds near a promoter and blocks transcription (negative control)

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60
Q

What are examples of positive control?

A
  • activator protein binding near promoter and enabling transcription
  • molecule binding to repressor protein causing its release
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61
Q

What does the operon consist of?

A

promoter (P), operator )O) sites, & structural genes which code for protein.

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62
Q

The operon is regulated by what?

A

the product of the regulatory gene (I)

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63
Q

Where does the repressor protein generally bind?

A

to the operator sequence, which is downstream of the promoter and upstream of the structural gene(s).

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64
Q

What is a direct repressor? Co-repressor?

A
  • Direct repressor - controls expression of operon

- Co-repressor - requires binding of a 2nd molecule before binding the operator sequence

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65
Q

What is the role of tryptophan in the Trp biosynthetic operon?

A
  • When Trp (co-repressor) is present, it binds to Repressor protein, which then binds to the operator–results in no expression of operon!
  • However, when Trp is absent, no binding of the repressor protein, and there will be expression of genes to synthesize Trp
  • Trp = repressor! (oppos of Lactose)
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66
Q

What do inducers do?

A

They inactivate repressor proteins by binding to them, thus preventing them from binding to the operator sequence.

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67
Q

Enzymes encoded by ____ are required for lactose catabolism.

A

lacZYA

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68
Q

What happens when lactose (allolactose) is absent? What happens when it is present?

A
  • absent: LacI repressor binds to operator, no expression
  • present: LacI repressor binds to allolactose, is inactivated & released from operator
  • allolactose = inducer!! (oppos of Trp)
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69
Q

What is signal transduction a response to?

A

an environmental condition

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70
Q

What is the role of a sensor? Role of transducer?

A

Both are part of the 2 component system of Signal Transduction

  • Sensor: on outer surf of bact will phosphorylate the intracellular transducer when a signal is detected
  • Transducer: activated by the phosphorylation will bind to upstream region of genes & activates transcription (basically turns expression on)
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71
Q

What is the PhoP/PhoQ System?

A
  • system that pathogens have evolved to determine the inside/outside of cells
  • PhoQ = sensory of extracytoplasmic Mg2+ (which is in high conc outside of a cell, and low conc in cytoplasm of mammalian cells)
  • PhoP = is phosphorylated by PhoQ and controls expression of a large number of genes under low Mg2+ conc by binding a direct hexanucleotide repeat
  • PhoP controls a system that activates a second 2 component sys that controls biosynthesis of LPS
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72
Q

What is the autoinducer?

A

Molecule that controls quorum sensing system; produced by bacteria

  • acylhomoserine lactones in G(-)
  • peptides in G(+)
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73
Q

What is “Quorum Quenching”?

A

use of autoinducer analogs to control expression of bacterial virulence factors

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74
Q

What are the 3 primary mechanisms of horizontal transfer of DNA? Briefly elaborate on the 3 mechanisms.

A
  1. Conjugation: direct cell-to-cell transfer of plasmid DNA (highly efficient)
  2. Transduction: viral transfer of DNA (smal chromosomal pieces, low freq event)
  3. Transformation: transfer of free DNA (inefficient process, but some bact are “naturally competent” & have high transformation rates”
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75
Q

What is f-factor movement?

A

plasmid transfer via sex pilus results in conversion of F- cell to F+ cell

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76
Q

What is HFR formation?

A

HFR = high frequency recombination

- following plasmid transfer, the plasmid is integrated into recipient cell’s chromosome

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77
Q

What is resistance transfer factors (RTF)?

A

conjugative plasmids that contain 1 or more transposons that carry AB resistance markers; spread rapidly in bacterial pop.

78
Q

What occurs in phage transduction?

A

Bacteriophages (virus-like bact) during lytic cycle degrade host chromosomal DNA

  • small fragments incorporated in newly formed phage particle
  • transferred to a new host & can be incorporated by recombination–slow process
79
Q

What is the lytic pathway?

A

“living phase”

  • DNA circularizes after entry & rapid replication and synthesis of new virions occurs.
  • Bact cell lyses, new virions released
80
Q

What is the prophage pathway?

A

DNA recombines in chromosome

  • induction: excision of prophage & lytic cycle will start then
  • waiting for the right moment to enter lytic cycle again! usu when host cell is immunocompromised
81
Q

How is naked DNA taken by by the bacterial cell in transformation? (2 ways)

A
  1. natural bacterial systems (bacterial competence)

2. physical means (electroporation)

82
Q

What is the difference between transformation with plasmids and with DNA fragments?

A

plasmids can replicate independently, but chromosomal DNA fragments must be incorporated into bacterial chromosome by DNA recombination before replicating.

83
Q

3 types of DNA recombination?

A
  1. homologous (generalized) recombination
  2. site-specific recombination
  3. transposition
84
Q

Tell me briefly about homologous (generalized) recombination.

A
  • requires extensive sequence homology
  • involves host recombination pathways
  • major mechanism for DNA repair
85
Q

Tell me briefly about site-specific recombination.

A
  • requires small regions of homology

- specific integrases (DNA-joining enzymes)

86
Q

Tell me briefly about transposition.

A
  • involves simple or complex transposable elements
  • transposase = enzyme for movt for specific element
  • movt = nonspecific or target DNA sequences
87
Q

what is the process called when there is replacement of 1 strand of DNA w/ a very similar strand to correct errors and to move genes?

A

homologous recombination

88
Q

What does homologous recombination require in most bact?

A
  1. introduction of a ssDNA nick
  2. strand invasion directed by recombination enzymes
  3. resolution of the exchange point
89
Q

What is lambda integrase?

A

DNA joining enzyme that is involved in site-specific recombination
- will add lambda DNA into bacterial cell chromosome, making a prophage (bacterial stress will cause induction & lytic cycle of Lambda)

90
Q

What is a transposase?

A

Transposase ‐ an enzyme that recognizes the inverted repeats of transposons and catalyzes their insertion (including the intervening DNA) into a new DNA site - with no sequence homology requirement

91
Q

What is an insertion sequence (IS)?

A

minimal transposons that contain only sequences necessary for their own transposition; can even lack transposase gene

92
Q

What is a complex transposons?

A

have one to several genes in addition to genes for transposition (often are antibiotic resistance genes)

93
Q

Transposition mechanism?

A 
“Cut and Paste” transposition:
1. Transposase binds
inverted repeat to form Synaptic Complex
2. Cleavage of the transposon
3. Re-integration at a new site (certain transposons may have target recognition sequences)
*can be random or specific
94
Q

Pathogens appear to have evolved from nonpathogens largely by the _____ rather than by the adaptive evolution of preexisting genes.

A

acquisition of pathogenicity islands

95
Q

Enteropathogenic E.coli (EPEC) and cause attachment-effacement
(A/E) lesions on intestinal epithelial cells. What does attachment refer to? Effacement?

A
  • Attachment: bacteria intimately attached to a cuplike pedestal structure, the result of extensive rearrangement of the host cell cytoskeleton.
  • Effacement: loss of microvilli on enterocytes adjacent to the bacteria
96
Q

LEE pathogenicity island (PI) of E. coli does what to an infected cell? What secretion system does it use?

A

forces the infected cell to cooperate in its own infection; incorporates a Type 3 secretion system (syringe-like mechanism)

*Background info: “Enteropathogenic Escherichia coli (EPEC) produce attaching and effacing lesions. The genes responsible for this lesion are clustered on the chromosome forming a pathogenesis island called LEE.”

97
Q
  • One injected protein, the LEE-encoded ____, is modified by the host cell then inserted into the host cell plasma membrane, becoming a high-affinity receptor for LEE-encoded ____, an EPEC outer-membrane protein
A

Tir; Initimin

98
Q
  • The ______ triggers host cell accumulation of actin polymers beneath the adherent bacteria, resulting in ‘pedestal’ formation
A

Tir:Intimin interaction (intimate adherence)

99
Q

How is site specific recombination different from homologous (generalized) recombination?

A

SSR:

  1. only short stretches of homologous sequence required
  2. breakage & union occur only at specific sites
  3. alters the arrangement of chromosomal sequences
100
Q

What do these 3 enzymes do?

  1. NADPH oxidase
  2. Superoxide dismutase
  3. Myeloperoxidase
A
  • NADPH oxidase makes superoxide radicals
  • superoxide dismutase turns the superoxide radicals into H2O2
  • myeloperoxidase converts H2O2 & Cl- into hypochlorite (bleach)–used to kill bacteria
101
Q

Which TLR binds to lipopeptides?

A

TLR1:TLR2; can form a heterodimer

102
Q

Which TLR binds (viral) dsRNA?

A

TLR3

103
Q

What is NF-kB’s functions?

A

once in nucleus, it regulates transcription of hundreds of genes w/ important functions in inflamm & infection
- stimulates the release of TNFa, IL1, & IL6.

104
Q

When signalling with TLRs, what is the order of proteins and factors that is involved? Or what is the pathway of the signalling?

A

receptors (TLRs) > Adaptors (MyD88) > Kinases > Transcription factors (NF-kB) > Effectors (cytokines, chemokines, etc)

105
Q

What is the role of TNF-a?

A

activates vascular endothelium & increases vascular permeability, which leads to inc’d entry of complement & cells to tissues & inc’d fluid drainage from lymph nodes

106
Q

What is the role of IL-1B?

A

activates vascular endothelium and lymphocytes.

- local tissue destruction increases access of effector cells

107
Q

What is the role of CXCL8?

A

chemotactic factor that recruits neutrophils & basophils to site of infection using cytokines

108
Q

What are the ways/mechanisms our body uses to protect itself?
- basically asking for effects of IL-1/IL6/TNF4?

A
  1. in liver: acute phase proteins (C-reactive prot, mannose-binding lectin)
    - activates complement opsinization.
  2. in bone marrow, Neutrophil mobilization > phagocytosis
  3. hypothlamus: inc body temp; dec viral/bacterial replication
  4. fat, muscle: protein & energy mobilization to generate increased body temp
109
Q

What are the 3 complement pathways (in order)?

A
  1. Alternative = pathogen surface creates local environ conductive activation; 1st to act
  2. Lectin pathway = mannose-binding lectin binds to pathogen surface
    - 2nd to act
    classical pathway = even more creepy; C-reactive protein or AB binds to specfic AG on pathogen surface
110
Q

Sequential insertion of complement proteins into pathogen membrane results in ____.

A

“Membrane Attack Complex” (MAC).

111
Q

What is the diff between C3a & C2b?

A

C3b is covalently found on the surface of components of pathogens

112
Q

What are the 4 outward signs of inflamm?

A

redness (rubor), heat (calor), swelling (tumor), pain (dolor)

113
Q

What recognition mechanism are used by innate pathogen receptors?

A
  1. TLRs
  2. LPS receptors (CD14)
  3. mannose receptors
  4. glucan receptors
  5. scavenger receptors
  6. complement receptors (CR3)
114
Q

Where do neutrophils come from and how do they reach site of infection?

A

bone marrow; chemotaxis/diapedesis

115
Q

What events precede and follow the act of phagocytosis?

A

Precede: recognition mechanisms

  • sensing of bact
  • mov’t twd them

Phagocytosis: binding, uptake, degradation

Follow: activation of adaptive IR
- remains of bact are used to further signals to other cells

116
Q

What are the characteristics of innate immunity?

A
  1. rapid response
  2. invariant receptors
  3. limited # of specificities
  4. limited expansion during response
117
Q

What are the characteristics of acquired immunity?

A
  1. slow response
  2. variable receptors
  3. numerous highly selective specificities
  4. improves during response & has memory
118
Q

Antibodies activate what pathway of complement activation?

A

C-c-classical!

119
Q

What gives rise to lymphocytes? And what are the effector cells it can change in to?

A

lymphoid progenitor

  1. B-cells (into plasma cells)
  2. T-cells (into cytotoxic or helper T-cells)
  3. NK cell
    * all cells from this progenitor are part of adaptive immunity except NK cell
120
Q

What is a mechanism to prevent “self-reactivity” in B & T cells?

A

clonal selection

121
Q

Difference betw how B-cell & T-cell receptors recognize Ag?

A

B-cells can bind to native antigen (at epitope).

T-cells only bind to processed antigen (peptide:MHC complexes).

122
Q

What are MHC molecules in humans called?

A

Human Leukocyte Antigens (HLA)

123
Q

What cells are MHC Class I in? MHC Class II?

A

MHC Class I = infected cell; bact cleaved in ER; CD8

MHC Class II = phagocytes; bact cleave in lysosome; CD4

124
Q

How do cytotoxic T-cells fight infection?

A

recognizes complex of viral peptide w/ MHC class I and kills infected cell

125
Q

How do Helper T cells help fight infection?

A

TH1 recognizes complex of peptide Ag w/ MHC class II & activates mac’s or B cells

126
Q

What cells arise from the myeloid progenitor?

A

Blood: basophil, eosinophil, neutrophil, monocyte

Tissues: dendritic cell, mast cell, macrophage

127
Q

Which WBC is best to kill multicellular parasites? And what Ig’s do they bind to?

A

eosinophil; have receptors to bind to IgE antibody

*OR basophils bc they function like eosinophils

128
Q

What is the least abundant immune cell?

A

granulocytes

129
Q

Mast cells have a high affinity for what Ig?

A

IgE

130
Q

What substance do the granules of mast cells contain?

A

histamines & other inflamm mediators

131
Q

What are examples of bridges between innate & acquired immune systems?

A
  1. macrophages

2. dendritic cells

132
Q

What receptors do mac’s have?

A
  • Fc receptors that help it bind & destroy Ab-opsonized microbes
  • has PRR receptors (pattern recognition receptors)
  • it also have both MHC I & II
133
Q

Why are NK cells not considered lymphocytes?

A

they bear NO Ag-specific receptors.

134
Q

What is a central/primary lymphoid organ? Examples?

A
  • tissue where lymphocytes develop & mature

- ex. bone marrow, thymus

135
Q

What is a peripheral/secondary lymphoid organ? Examples?

A
  • tissues at which IR are initiated (APCs & lymphocytes interact!
  • ex. spleen, lymph nodes (i.e. tonsils), GALT, MALT/BALT, lymphatic vessels
136
Q

In the lymph node, which lymphocytes are closer to the center/core, and which ones are closer to the periphery?

A

B-cells on the outside. T-cells near the inside.

137
Q

How does a lymphocyte enter through a lymph node? Which lymphocyte would they encounter first?

A

through high endothelial venule (HEV); encounter T-cell first, then B-cell.

138
Q

What makes ABs stable?

A

disulfide bonds

139
Q

what happens to IgM’s structure once it has encountered an Ag?

A

it goes from a monomeric structure to a pentameric design

140
Q

IgA is pumped out into the mucosal layers of the body. What is the process it goes through to be released out onto the apical face of epithelial cells?

A

transcytosis

141
Q

What is the difference betw when Ab (IgM or IgG) activates

A

IgM - pentameric; C1 binds to a signle IgM molecule
IgG - monomeric; C1q binds to 2 or more IgG molecules
*both activate classical pathway–recall that Ab’s are involved with classical pathway

142
Q

Importance of IgA, IgE, IgG, IgM.

A

IgA - present in mucous membrane—transport across epith
IgE - important in triggering Mast cell degranulation—sensitization of mast cell (degranulation)
IgG - all of the IgGs can be transported across the placenta (mainly IgG1)—also does opsonization & diffusion into extravascular sites
• Allows baby to be born with some antibodies
IgM - activation of complement system

143
Q

there are two antibody isotypes that incorporate the J chain. Which ones?

A

IgA (dimeric) & IgM (pentameric)

144
Q

Histamine is released from what?

A

platelets during clotting and from mast cells

145
Q

kinins are released from?

A

clotting and granulocytes

146
Q

What is CD14?

A

a LPS receptor that is involved in a complex with MD2 & TLR4 as well. They all bind to LPS bound to LBP.

147
Q

what cytokines does NFkB code for?

A

TNF-a, IL1, IL6

148
Q

______ act locally to increase capillary blood flow and permeability. ____ also activates endothelium and increases adhesion of white blood cells.

A

Tumor necrosis factor (TNF) and IL-1 ; IL-1

*TNF induces the synthesis of IL-1 which in turn induces IL-6 and CXCL8. TNF and IL-1 act systemically to induce the fever response.

149
Q

_____ is an important chemotactic factor, acting to induce the migration of leukocytes into the site of infection.

A

CXCL8 (older name IL-8)

150
Q

IL-6 is an important cytokine that acts systemically. In the liver, IL-6 along with TNF-α and IL-1 induce the synthesis of _____.

A

acute phase proteins

  • These include C-reactive protein (CRP), serum amyloid A, fibrinogen, and mannose-binding lectin (MBL).
151
Q

Cleavage of C3 (3rd component of complement) generates the cleavage products C3a and C3b. ____ is covalently bound to the surface of a bacterium where it assists in macrophage binding and phagocytosis of the bacteria. The other, ___, acts to recruit more phagocytes to the site. This mechanism of complement activation received the name of _____.

A

C3b, C3a, “Alternative Pathway”

152
Q

Antigen receptors are assembled by ______ that randomly recombine their DNA sequences in order to generate the complete coding regions for the antigen-binding portions (the variable domains) of the (B and T) lymphocyte receptor.

A

association between gene segments

153
Q

BINDING TO ANTIGEN ALONE IS NOT ENOUGH TO ACTIVATE B AND T CELLS

Activation of B cells and T cells requires two separate stimuli (“signals”): __2__.

A

one requires binding to the surface antigen-receptor, the other is stimulation of a second cell surface receptor.

  • B-cell: Once the B cell receptor binds to its specific antigen (1st signal of activation), the B cell ingests the antigen, breaks it into pieces (peptides), and presents the peptides to an antigen-specific T helper cell. The T helper cell supplies a 2nd signal of activation to the B cell.
  • T-cell: binding of cognate antigen (1st signal of activation) must be accompanied by co-stimulation (2nd signal of activation) provided by T cell binding to a counter- receptor on the antigen presenting cell.
154
Q

Spleen’s white pulp is divided into areas that contain primarily _____, and adjacent areas containing primarily _____.

A

T cells; B cells

155
Q

Examples of MALT?

A

larynx, tonsils, bronchus, nose, some along intestinal wall, peyer’s patch

156
Q

Remember that all immunoglobulins produced by a B cell have what…?

A

the same antigen-specificity

157
Q

Both C and V domains are a roughly barrel-shaped and are formed by_____ that are stabilized by a disulfide bond.

A

two sheets of antiparallel β-strands

158
Q

When the sequences of many variable domains are compared, the greatest sequence variability is observed in 3 “hypervariable” regions of the heavy and light chain variable domains. These hypervariable regions make up the combining site. What are these regions called?

A

complementarity-determining regions

159
Q

less variable regions betw CDRs are known as framework regions ______.

A

framework regions

160
Q

two isotypes of light chains of antibodies?

A

kappa (κ) and lambda (λ)

*Approx. 60% of human IgG contain kappa light chains, the rest contain lambda chains

161
Q

what is a hapten?

A

an Ag too small to induce an IR

162
Q

Why is T-independent Ag-elicted responses limited?

A

T-independent antigen-elicited responses are usually limited to production of IgM antibody and do not elicit B cell memory.

163
Q

Which route of Ag administration elicits a potent IR? Which one induces non-responsiveness/tolerance? How about ingestion of an Ag–what happens? Respiratory tract?

A

subcutaneous administration; intravenous administration; systemic tolerance; results in allergic rxns

164
Q

Antigens delivered to the respiratory or gastrointestinal tracts can also induce antigen-specific ______ responses.

A

secretory IgA Ab (sIgA)

165
Q

What is an adjuvant?

A

any substance that enhances immunogenicity of an Ag

- they usu inc length of exposure of immune sys to Ag

166
Q

Cytoplasmic sensors of the presence of bacteria belong to the family of ___ that form an ______.

A

NOD proteins; inflammasome

167
Q

benefits and limitations of precipitation and agglutination?

A
  • Benefits: No specific treatment of antibodies required, direct method.
  • Limitations: Not particularly sensitive, relatively large amounts of antigen required.
168
Q

benefits and limitations of Western blot?

A
  • Benefits: purified antigen or antibody are not needed; highly sensitive.
  • Limitations: non-quantitative
169
Q

benefits and limitations of ELISA?

A
  • Benefits: very sensitive, quantitative.

- Limitations: must have specialized reagents and a 96-plate spectrophotometer.

170
Q

Steps in ELISA procedure?

A

Steps in the Procedure:
• Wells are coated with purified antigen.
• Dilutions of Ab sample (primary Ab) are added to wells and incubated for binding.
• Unbound Ab are washed out of the wells.
• Bound antibodies are detected with anti-immunoglobulin antiserum conjugated to enzyme (secondary antibody).
• Substrate is added to each well and incubated until color change is observed.
• Color development is read quantified in an ELISA reader (spectrophotometrically).
• Benefits: very sensitive, quantitative.
• Limitations: must have specialized reagents and a 96-plate spectrophotometer.

171
Q

_____ is a method to use fluorescence and laser light excitation to perform single cell analysis. In an adaptation, this method is capable of separating (“sorting”) positive cells.

A

Flow cytometry

172
Q

What are the benefits and limitations of flow cytometry?

A
  • Benefits: very sensitive; quantitative

- Limitations: costly; requires sophisticated software

173
Q

Ab’s are covalently bound to Ag. T/F?

A

FALSE! The Ab/Ag binding is a reversible thermodynamic equilibrium.

174
Q

What is the diff between affinity & avidity?

A

Affinity: measure of strength of a single Ab binding to a single site on an Ag
Avidity: sum of the strength of Ab binding to Ag in multivalent fashion

175
Q

What are monoclonal antibodies? And how do they usually occur?

A

MAbs are Ab’s tjat are produced by a cloned (immortalized) B-cell line, a pop. of Ab-secreting cells that all descended from a single B-cell.
- occur naturally as a myeloma or generated by fusing a B cell to a myeloma cell

176
Q

The production of which Ig does not require T cell help?

A

IgM

177
Q

What are the 2 stages of B cell maturation?

A
  1. Ag-independent

2. Ag-dependent

178
Q

What is the order of the segment joining in the construction of an Ig heavy chain variable-region exon?

A

joining of a D-region gene segment w/ a J-region gene segment, then joining of a V-region gene segment w/ the combined DJ sequence

179
Q

what occurs in clonal deletion? in anergy?

A

Clonal deletion: immature b cells that interact w/ “self”-Ag’s undergo apoptosis
Anergy: immature B cells that interact w/ soluble Ag in bone marrow are signaled to down-regulate cell surface expression of IgM and become anergic (or unable to respond to specific Ag)

180
Q

_____ is a costimulatory protein found on antigen presenting cells and is required for their activation.

A

CD40

181
Q

Tell me about light chain gene construction.

A
  1. random joining of a single V gene segment w/ a single J gene segment
  2. C gene segment does not move and joins VJ after transcription and splicing of the non-coding (intronic) RNA
  3. transcription
182
Q

Tell me about heavy chain gene construction.

A
  1. random joining of a D gene segment w/ a J gene segment
  2. random rearrangement of single V to DJ to form DNA sequence coding for complete variable domain of heavy chain (VDJ)
  3. RNA transcription followed by processing of introns and splicing of exons, brings VDJ closer to C
    * as in the light chain, C gene segment is “downstream” of the J segment but is separated from the VDJ junction by non-coding introns
183
Q

What are the proteins that catalyze DNA recombination?

A

recombinase activating genes 1 & 2 (RAG 1 & 2)

184
Q

Joining of gene segments is imprecise. What is the consequence of this?

A

Some of the VJ and VDJ joints are out-of-frame (they do not follow the triplet codon reading frame and cannot be translated into a full-size protein).

185
Q

When does rearrangement stop?

A

when the functional V region coding sequences have been formed

186
Q

All progeny of a single B cell will express the same V region genes. T/F?

A

true

187
Q

What are the 4 mechanisms that generate diversity in B-cells?

A
  1. different combinations of V, D, J
  2. imprecise joining of gene segments during somatic recombination process
  3. pairing of many possible light chains and many possible heavy chains
  4. somatic hypermutation
188
Q

How does the same gene encode a membrane-bound Ig receptor and a secreted Ab?

A

alternative RNA splicing

189
Q

Switching between isotypes of Ab’s occurs through a specialized DNA recombination mechanism that is guided by _______. As switching occurs, the recombination event loops out and removes the DNA between the original and the newly accessed constant regions.

A

switch recombination sequence

190
Q 
The Fc portion of Ab molecules can interact w/ which of these components?
A) complement proteins
B) other Fc domains
C) Fc receptors on mac's & cells
D) A & C
E) all of the above
A

E) all of the above

D2 - FALL - Par 2 (7 decks)

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