Barrington- Lung Immunity Flashcards

1
Q

____ and ____ airways together are largest exposed epithelial surface to inorganic and organic compounds, and microbes

A

upper and lower airways

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2
Q

different ways microbes can get into lungs

A

commensal microbes
microbes in the inhaled air

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3
Q

occurs within 12 hours of exposure to antigen

A

innate immunity

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4
Q

occurs within days of being exposed to antigen

A

adaptive immunity

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5
Q

_____ particles bind to dendritic cells and instruct immune response to become tolerant to those molecules
important for the airways (inflammation will impair gas exchange—-don’t want to invoke an immune response against just anything)

A

inert

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6
Q

upper airway immune defense

A

epithelial layer (cilia and mucus); immune cells

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7
Q

lower airway immune defense

A

surfactant and alveolar macrophages

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8
Q

PRRs on innate immune cells recognize _____ on pathogens, and migrate to regional lymph nodes where they can activate cell-mediated response

A

PAMPs

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9
Q

_____ triggers a cascade of events that result in activation of transcription factors (NFkB and IRF) which will go to nucleus and activate expression of different genes (inflammatory)

A

PRRs recognizing and binding to PAMPs

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10
Q

important in chemoattracting neutrophils

A

IL-8, CXCL8, MCP1

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11
Q

intracellular TLRs recognize what

A

nucleic acids

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12
Q

TLR4 recognizes what

A

LPS on gram - bacteria

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13
Q

antibody response directed by B cells is what immunity

A

humoral immunity

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14
Q

microbe has been phagocytosed and recognized by PRRs; presents to helper T cells and activates them
further activate macrophage—making it a better clearing cell of invading microbe
(is what immunity)

A

cell-mediated immunity

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15
Q

: taken up by APCs like dendritic cells and macrophages can present antigen to cytotoxic T cells leading to their activation and need 2 signals
signal 1: antigen peptide MHC and costimulatory signal (signal 2)
once activated CD8 T cell can go to infection site and start killing infected cells (what immunity)

A

cell-mediated immunity

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16
Q

2 major lung defenses

A

airways and their mucosa
alveolar spaces

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17
Q

prevents entry of larger particulates from traveling further in the lung

A

anatomical barriers

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18
Q

a way to get material out of lungs

A

cough

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19
Q

used to transport material from bronchi to trachea

A

mucociliary transport

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20
Q

____ in mucus combat bacteria

A

anti-microbials

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21
Q

can degrade bacterial cell walls

A

lysozyme

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22
Q

chelates iron

A

lactoferrin

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23
Q

produces ROS which can be lethal to bacteria

A

peroxidase

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24
Q

forms a pore in bacteria and kills through osmotic lysis

A

defensins

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25
transcytosed across epithelial cells, neutralizes toxins, viruses, bacteria
secretory IgA
26
major site for IgA production in mucosa of GI and Res. tracts
mucosal lymphoid tissue in lamina propria
27
______receptor binds dimeric IgA and transports it to lumenal surface; where the IgA is released by proteolytic cleavage
Poly-Ig
28
predominate defense mechanism is neutralizing pathogens
IgA
29
____cells have PRRs (TLRs) so can mount an inflammatory response
epithelial
30
chemokine produced that recruit neutrophils to site of infection
CXCL8
31
blood-derived cell of mucosa
Dendritic cells lymphocytes (during an infection) eosinophils, mast cells, basophils
32
immune defense in alveolar space
alveolar macrophages lymphocytes type I and II pneumocytes (surfactant) neutrophils IgG and opsonins
33
not seen in the lungs usually unless there is an infection
neutrophils and lymphocytes
34
immunoglobin predominant in the lungs in general
IgA
35
immunoglobin most abundant in alveoli
IgG
36
C3b produced by _________ and lead to complement activation (microbe that has activated complement, get C3b on that microbe and that allows C3b to be recognized by receptors on macrophages and that will induce phagocytosis of microbe)
tissue macrophages
37
produced by the liver but can find it in lung in case of infection (a good opsonin)
CRP
38
key soluble PRRs in alveolar spaces
surfactants
39
less _____, macrophages less able to provide defenses against foreign threat
surfactant
40
surfactant in steady state
inhibits inflammatory response
41
surfactant interacting with PAMP and CD91
stimulates inflammatory response
42
____ leads to activation of alveolar macrophage (either directly or with CD91 interaction)
PAMPs
43
____ activation produces pro-inflammatory cytokines and recruits neutrophils to site of infection
NF-kB
44
when activated, can ingest a large number of microbes destroy them with oxygen independent mechanisms produce ROS and proteases that lead to tissue damage
neutrophils
45
professional phagocytes
neutrophils
46
release chromatin rich material, it is sticky and will bind microbes and prevent them from disseminating and facilitate phagocytosis
neutrophils releasing NETs
47
adaptive immune response in the lung is initiated in _______
draining lymph nodes
48
cells enter through ________ and inside there are B cell zones and T cell ones B cell zones have germinal centers (where B cells undergo class switch recombination) differentiate into plasma cells (start making antibodies)
afferent lymphatics into lymph node
49
CD4 cells can differentiate into what
Th1, Th2, Th17
50
kill virally infected cells
CD8 (cytotoxic) T cells
51
depends on this cytokine for clonal expansion of T cells
IL-2
52
produces IFNgamma (can also lead to macrophage activation) CD40 ligand and bind to CD40 on macrophages and activate them really good phagocytes
Th1
53
more important in driving antibody responses interact with B cells produce cytokines that will instruct B cell to differentiate and class switch into IgG or IgA
Th2 and Th17
54
T cell receptor peptide and MHC interaction as well as costimulatory molecule
2 signals for T cell activation
55
needs 2 signals to become activated, but once activated, just needs 1 signal to kill
CD8 T cells
56
similar structure as lymph node w/out afferent lymph found at bifurcations in bronchus
bronchus-associated lymphoid tissue (BALT)
57
microbes and antigens can pass through (endocytosis or phagocytosis) into the associated lymphoid tissue
through M cells
58
large # of microbes PRRs stimulated and innate immune system activated and steers response towards pro-inflammation; leads to clearance of microbes and tissue damage
infection
59
seasonal infection that can lead to pneumonia
viral influenza
60
1. virus-induced damage to pulmonary epithelium 2. influenza neuraminidase and upregulation of platelet-activating factor receptor expression 3. cytokines (e.g. interferons)
increase susceptibility to secondary bacterial infection after influenza virus
61
engagement of alveolar macrophages -production of pro-inflammatory cytokines and recruitment of neutrophils to site of infection get rid of microbe
normal lung exposed to pneumonia
62
some of the innate immune cells and alveolar macrophages are not able to recognize some of the bacteria during an active viral infection, turn on adaptive immunity and get IFNgamma produced IFN gamma can lead to down regulation of PRRs on alveolar macrophage
patient with pre-existing viral infection exposed to pneumonia