Exam I Flashcards

(132 cards)

1
Q

majority of Ab in circulation, unique ability to cross mammalian placenta (passive immunity)

A

IgG

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2
Q

expressed on surface of naive B cells, only Ab made when see infection for primary immune response

A

IgM

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3
Q

Ab in allergic reactions and parasitic infections

A

IgE

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4
Q

less common than IgM

A

IgD

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5
Q

found in mucosal areas, most produced per day in adult

A

IgA

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6
Q

antigen that elicits immune response

A

immunogen

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7
Q

Ag that induces immunological tolerance or immune non-responsiveness

A

tolerogen

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8
Q

Ag that causes immediate hypersensitivity reaction

A

allergen

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9
Q

cross-reactivity

A

between Ab and Ag generated against a diff but similar Ag

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10
Q

differences between gram negative and positive cell envelopes

A
\+ = thick PDG, teichoic acid, small periplasmic space, no outer membrane or LPS
- = thin PDG, no teichoic acid, outer membrane, LPS
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11
Q

transporters that move iron across outer membrane

A

TonB recepter (gram - only)- transfers iron siderophore complex

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12
Q

transporters that move iron across plasma/inner membrane

A

ABC transporters

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13
Q

gram positive cell wall

A

thick, lots PDG and teichoic acids

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14
Q

gram negative cell wall

A

thin, little PDG, b/t PM and OM in periplasmic space

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15
Q

hair like filaments ached to PM, function to attach to surfaces

A

pili (fimbriae)

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16
Q

types of specialized pili

A

F-pilus = sex pilus, exchange DNA b/t G- via conjugation

Type IV pilus = produced by pathogenic bacteria, adhere to host cell and inject virulence effector molecules

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17
Q

categories of metabolic reactions

A

fueling - generate energy, reducing agents and precursor metabolites
biosynthetic - use precursor metabolites to form macromolecules
polymerization - macromolecule synthesis
assembly - localization of macromolecules into cellular compartments

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18
Q

3 fueling reaction pathways

A

glycolytic, pentose phosphate, krebs

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19
Q

terminal e- acceptors of anaerobic respiration

A

Fe3+, SO42-, NO3-

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20
Q

types of mobile genetic elements

A

transposons, IS elements, plasmids

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21
Q

extrachromosomal, circular, self replicating DNA fragments

A

plasmids

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22
Q

mediate own transfer from cell to cell or species to species

- responsible for spread of antibiotic resistance

A

conjugative plasmid

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23
Q

What do plasmids and conjugative plasmids always have in structure

A

O of R, antibiotic resistance gene, restriction enzyme recognition site

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24
Q

What do plasmids sometimes have in structure

A

origin of transfer, other genes

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25
advantages of plasmid
selective advantage, pathogenic ability
26
What are transposable elements
excise themselves from chromosome or plasmid and insert into another chromosome or plasmid
27
IS element structure
transposes gene flanked by inverted repeats
28
Non composite transposon structure
transposes + accessory genes; flanked by in repeats
29
composite transposon structure
accessory genes, flanked by 2 IS elements
30
advantages of transposition | disadvantages
- selective advantage and pathogenic virulence | - can knockout imp/essential/virulence genes
31
one way transfer of genetic material between bacterial cells through sex pilus
conjugation
32
what does TRA genes encode?
sex pilus proteins, proteins that fuse to membrane and surface exclusion proteins to prevent mating
33
direct uptake of naked DNA from environment by competent cells
transformation
34
What makes cell competent?
ability of bacterium to take up DNA directly from environment (induced by DNA damaging stress)
35
advantages of transformation | disadvantages
- DNA damage repair, selective advantage, pathogenic virulence - possible gene activation or loss
36
transfer of DNA between bacterial cells by phage
transduction
37
options for linear DNA once acquired by bacterium (homologous recombination)
naked DNA -> transformation | transduced DNA -> incorporated into chromosome or plasmid
38
requirement for homologous recombination
large area, Rec A protein
39
Fur regulation (negative repressible operon)
iron = co-repressor fur = repressor High iron -> iron binds fur -> fur binds fur-box -> blocks transcription Low iron -> promotor site free -> transcription -> express siderophore
40
alternative sigma factors
allow bacteria to alter gene expression in response to extracellular stress signals
41
components of 2 component regulatory system
component 1 = sensory histidine kinase - detects signal -> autophosphorylates in response to signal -> transfers phosphoryl group to component 2 component 2 = response regulator - gets phosphorylated -> activates or represses transcription
42
roles of normal human microbiota
exclude pathogens, prime immune system, aid in nutrition
43
skin defenses
skin lipids and fatty acids, conjunctiva/eye mucous membrane secretes lysozyme, digest cell wall
44
where are the highest bacterial levels in skin
moist areas, staphylococci, propionibacterium all over skin
45
mouth bacteria
streptococci
46
throat bacteria, stomach, small intestine, colon
neisseria, H.pylori, streptococci E.coli and clostridium, E coli
47
nostrils bacteria, nasopharynx, lower respiratory tract
S aureus, S pneumo N meningitidis Haemophilus, transient bacteria due to cilia
48
vagina bacteria, puberty, menopause, bladder
staphylococci, lactobacilli, lactobacilli, sterile except lower 1 cm
49
Where are virulence genes found in a cell?
pathogenicity islands, plasmid encoded (virulence plasmids), transposon, prophage
50
quorum sensing
system of cell to cell communication where bacteria monitor density of population to synchronize behavior to accomplish task
51
signaling molecule in gram - QS
acyl homoserine lactone (produced by LuxI)
52
receptor/response regulator in gram - QS
Lux R -detects AHL -> turns on expression of virulence genes
53
signaling molecule in gram + QS
oligopeptide - transported out of cell
54
receptor and response regulator in gram + QS
``` receptor = on cell surface regulator = transcription activator ```
55
How do non phagocytic bacteria survive once invade host?
lyse and escape vacuole -> replicate and infect adj cells
56
how do phagocytic cells survive once invade host?
lyse phagosome -> escape into cytosol -> replicate OR | remain in phagosome -> replicate -> prevent lysosome binding and block oxidative bursts
57
Types of immune evasion by bacteria
hide, cell envelope modification, effector molecule, mimicry
58
What is a biofilm?
organized multicellular community of bacteria
59
biofilm formation
planktonic bacteria in fluid environment -> attach to living or inert surface -> multiply -> reach particular density and secrete exopolysaccharide -> grow to mushroom shape
60
Active dispersal of biofilm
enzymatic degradation of polysaccharide matrix
61
passive dispersal of biofilm
sloughing off or breaking off
62
Advantages of biofilm
resistant to antimicrobials, host defenses, and mechanical removal, pool nutritional resources and traps addition nutrients from fluid
63
How is intracellular iron bound?
by ferritin or Hemoglobin
64
how is extracellular iron bound?
by transferrin
65
What does iron bind after RBC lysis?
haptoglobin and hemopexin
66
What does iron bind during infection
lactoferrin extracellularly
67
Sources of iron for bacteria
receptors already mentioned, siderophores, and hemophores
68
How has host cell adapted to bacterial siderophores? | Bacterial response?
``` produce siderocalin (Sn) -> binds to siderophore receptors so iron can't bind - bacteria produce stealth siderophores that prevent Sn binding ```
69
Severe systemic response, interaction of bacterial components with macrophages, characterized by hemodynamic derangement and multiple organ failure
sepsis
70
Most often cause of sepsis
endogenous infections of peritoneum, urinary tract and upper respiratory tract
71
features of hemodynamic derangement
decrease BP, increased cardiac output, low organ movement
72
modes of inhibiting cell wall synthesis
ALL bactericidal - inhibit PDG synthesis - disrupt translocation of PDG to cell wall - district PDG cross links
73
Modes of inhibiting nucleic acid synthesis
ALL bactericidal - inhibit DNA gyrase or topoisomerase - produce cytotoxic int to damage DNA - bind RNAP, prevent transcription
74
Mode of inhibiting protein synthesis
- irreversibly bind 30S ribosomal unit (bactericidal) - block tRNA binding to 30S (bacteriostatic) - bind peptide transferase component of 50S, blocking peptide elongation (bacteriostatic) - bind 50S preventing ribosome movement (bacteriostatic)
75
Modes of inhibiting essential folate synthesis
ALL bacteriostatic - inhibit dihydrofolate reductase preventing folic acid synthesis - compete for incorporations into folic acid synthesis reaction
76
Modes of damaging cell membrane
ALL bactericidal | - cationic detergent like activity, permeabilize cells, contents leak out
77
3 types of antibiotic resistance
modifications of antibiotic, preventing antibiotic from reaching target, modification of target
78
When does somatic recombination (VDJ) occur and where?
in bone marrow during maturation
79
When does central tolerance occur?
maturation - checks to see if B cells are recognizing self antigens
80
When does somatic hypermutation occur and where?
lymph in differentiation
81
When does affinity maturation, peripheral tolerance and isotope witching occur?
differentiation
82
3 signal model of Td B cell activation
recognize antigen -> internalize and present on MHC -> B-T conjugate, linked recognition and CD40 costimulatory molecule interaction -> cytokine stimulation -> B cell differentiation
83
linked recognition
reduces likelihood that autoreactive B cell will be activated - B and T cell epitopes must be present on same macromolecular structure or in same pathogen
84
lymphoid follicle vs germinal center
follicles are present in context of lymph nodes -> follicular dendritic cells trap ag on cell surface to stimulate B cell differentiation -> 1˚ follicle converted to 2˚/ germinal center
85
somatic hypermutation
random point mutation that occur in V region of Ab
86
Function of plasma cells
secrete Ab, neutralization and opsonization, APC to T cells
87
Which Ab is active in the primary immune response? secondary?
IgM | IgG
88
4 effector functions of AB
neutralization classical complement activation - Fc region exposed from binding C1q and MAC opsonization - Ab enhance recognition by phagocytic cells Ab-dependent cell mediated cytotoxicity - destroy large pathogens, release granulocytes to destroy (NK cells and esosinophils)
89
Which effector functions of Ab are FcR mediated and isotope dependent?
classical complement activation is isotope dependent | opsonization and Ab-dependent cell-mediated cytotoxicity are both FcR mediated and isotope dependent
90
components of BCR
non-covalent assoc between membrane bound Ig and transmembrane Iga/IgB heterodimer = BCR
91
Somatic recombination
gene rearrangement, NOT Ag driven, occurs during B cell development in bone marrow - H chain = VDJ while L chain is only VJ
92
Junctional diversity
imprecise joining of gene segments | - deletion of nucleotides, add P/N nucleotides during VDJ rearrangement
93
What are CDRs?
located on V regions of H/L chains, shortenings stretched of 5-7 aa separated by "framework" regions - provide diversity for Ig to recognize molecules
94
Linear vs conformation epitope
``` linear = recognized by linear sequence aa conformational = 3D shape (most Ab recognize) ```
95
strength of non covalent assoc b/t one Ag binding site and antigenic epitope
affinity
96
overall strength of binding b/t multivalent Ab and Ag
avidity
97
results when 1 epitope shared by 2 Ag or 2 epitopes on separate Ag are similar in structure
cross-reactivity
98
2 examines of extracellular bacteria
strep. pneumonia and aeruginose and staphylococcus aureus
99
Endotoxin vs Exotoxin
``` endotoxin = lipid portions of LPS molecules within gram - cell wall, release when bacterial cell damaged, activate macrophages and induce cytokine production exotoxin = toxic proteins secreted by gram + or - ```
100
types of phagocytosis
type I = use PRR to bind PAMPs | type II = use opsonic receptors, more efficient
101
2 types intracellular bacteria
mycobacterium tuberculosis and listeria monocytogenes
102
Which type of immune mechanism is predominant in extracellular killing of bacteria?
cell mediated rather than Ab
103
Good effects of inflammation
dilution of toxins, entry of Ab, fibrin formation, delivery of nutrients and O2, stimulation of immune response
104
Harmful effects of inflammation
persistant cytokne release, destruction of normal tissues, swelling, inappropriate inflammatory response
105
prostaglandins and nitric oxide
vasodilation
106
histamine, bradykinin, complement leukotrienes, prostaglandins, O2 free radicals
increase vascular permeability
107
IL, leukotriene, complement
chemotaxis
108
complement, IL, platelet activating factor
lysosomal granule release
109
complement
phagocytosis
110
IL, TNF-a, prostaglandins
fever
111
prostaglandins, bradykinin, histamine
pain
112
lysosomal enzymes, O2 free radical, nitric oxides
tissue damage
113
granulomatous inflammation
distinctive pattern of chronic inflammation with focal collection of macrophages
114
2 types of outcomes after inflammation
resolution and fibrosis
115
variables affecting repair after inflammation
infection, nutrition, anti-inflammatory drugs, mechanical variables, vascular disease, tissue type, degree of exudate removal, regulation of cell proliferation
116
4 steps of leukocyte migration
1) tethering rolling: slow LC down 2) integrin activation: chemokine act on rolling LC increasing integrin affinity 3) adherence: cytoskeleton rearrangement 4) migration through endothelium
117
2 types of adhesins
``` chemokine = expressed on LC integrin = expressed on endothelial cells ```
118
MALT type I mucosa
simple columnar or pseudo stratified columnar, organized lymphoid structures (lungs, gut, uterus, urethra)
119
MALT type II mucosa
stratified squamous epithelial cells , lack organization (mouth, vagina, nose, middle ear)
120
inductive vs effector sites
``` inductive = encounter Ag 1st effector = dispatch LC ```
121
2 major sections of GALT
epithelium and lamina propria (lymphoid follicles in LP)
122
What is the main IG present in mucosal sites?
SIgA
123
3 components of SALT
epidermis, dermis, hypodermis
124
dendritic cells of skin
langerhan's cells (APC)
125
What do TLR recognize?
LPS, not found in host cell | - TLR tells nucleus to make Type I interferons
126
What do Type I interferons do? TNF a/b?
prevent infection from occurring, TNF a/b are two classes of type I interferons that inhibit viral replication and protein synthesis
127
Receptors on phagocytes?
N-foryml-methionyl, mannose and scavenger
128
What happens when have DAMPS
phagocytosis increases
129
What do all TLR result in the production of?
inflammatory cytokines
130
What do intracellular TLR produce?
Type I IFN
131
What do cytokines induce formation of?
reactive endothelium
132
What are the 3 parts of LPS?
lipid A: anchors substrate, toxic O-antigen: Ab target, outermost region core polysaccharide: short chain uncommon sugars, highly conserved