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RES Biweekly 3 > Barrington- Lung Immunity > Flashcards

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
Q

transcytosed across epithelial cells, neutralizes toxins, viruses, bacteria

A

secretory IgA

26
Q

major site for IgA production in mucosa of GI and Res. tracts

A

mucosal lymphoid tissue in lamina propria

27
Q

______receptor binds dimeric IgA and transports it to lumenal surface; where the IgA is released by proteolytic cleavage

A

Poly-Ig

28
Q

predominate defense mechanism is neutralizing pathogens

A

IgA

29
Q

____cells have PRRs (TLRs) so can mount an inflammatory response

A

epithelial

30
Q

chemokine produced that recruit neutrophils to site of infection

A

CXCL8

31
Q

blood-derived cell of mucosa

A

Dendritic cells
lymphocytes (during an infection)
eosinophils, mast cells, basophils

32
Q

immune defense in alveolar space

A

alveolar macrophages
lymphocytes
type I and II pneumocytes (surfactant)
neutrophils
IgG and opsonins

33
Q

not seen in the lungs usually unless there is an infection

A

neutrophils and lymphocytes

34
Q

immunoglobin predominant in the lungs in general

A

IgA

35
Q

immunoglobin most abundant in alveoli

A

IgG

36
Q

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)

A

tissue macrophages

37
Q

produced by the liver but can find it in lung in case of infection (a good opsonin)

A

CRP

38
Q

key soluble PRRs in alveolar spaces

A

surfactants

39
Q

less _____, macrophages less able to provide defenses against foreign threat

A

surfactant

40
Q

surfactant in steady state

A

inhibits inflammatory response

41
Q

surfactant interacting with PAMP and CD91

A

stimulates inflammatory response

42
Q

____ leads to activation of alveolar macrophage (either directly or with CD91 interaction)

A

PAMPs

43
Q

____ activation produces pro-inflammatory cytokines and recruits neutrophils to site of infection

A

NF-kB

44
Q

when activated, can ingest a large number of microbes
destroy them with oxygen independent mechanisms
produce ROS and proteases that lead to tissue damage

A

neutrophils

45
Q

professional phagocytes

A

neutrophils

46
Q

release chromatin rich material, it is sticky and will bind microbes and prevent them from disseminating and facilitate phagocytosis

A

neutrophils releasing NETs

47
Q

adaptive immune response in the lung is initiated in _______

A

draining lymph nodes

48
Q

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)

A

afferent lymphatics into lymph node

49
Q

CD4 cells can differentiate into what

A

Th1, Th2, Th17

50
Q

kill virally infected cells

A

CD8 (cytotoxic) T cells

51
Q

depends on this cytokine for clonal expansion of T cells

A

IL-2

52
Q

produces IFNgamma (can also lead to macrophage activation) CD40 ligand and bind to CD40 on macrophages and activate them really good phagocytes

A

Th1

53
Q

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

A

Th2 and Th17

54
Q

T cell receptor peptide and MHC interaction as well as costimulatory molecule

A

2 signals for T cell activation

55
Q

needs 2 signals to become activated, but once activated, just needs 1 signal to kill

A

CD8 T cells

56
Q

similar structure as lymph node w/out afferent lymph
found at bifurcations in bronchus

A

bronchus-associated lymphoid tissue (BALT)

57
Q

microbes and antigens can pass through (endocytosis or phagocytosis) into the associated lymphoid tissue

A

through M cells

58
Q

large # of microbes
PRRs stimulated and innate immune system activated and steers response towards pro-inflammation; leads to clearance of microbes and tissue damage

A

infection

59
Q

seasonal infection that can lead to pneumonia

A

viral influenza

60
Q
  1. virus-induced damage to pulmonary epithelium
  2. influenza neuraminidase and upregulation of platelet-activating factor receptor expression
  3. cytokines (e.g. interferons)
A

increase susceptibility to secondary bacterial infection after influenza virus

61
Q

engagement of alveolar macrophages -production of pro-inflammatory cytokines and recruitment of neutrophils to site of infection
get rid of microbe

A

normal lung exposed to pneumonia

62
Q

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

A

patient with pre-existing viral infection exposed to pneumonia

RES Biweekly 3 (11 decks)

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