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SFM Quiz 2 > Innate Immunity > Flashcards

Innate Immunity Flashcards

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1
Q

barriers against disease

A

skin, mucous, lysozomes, pH, sebum, etc

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2
Q

humoral defense against disease

A

bacteriocidal substances, ROI, complement, APP, transport proteins, coagulation proteins, interferon

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3
Q

cellular defense against immunity

A 
blood cells (neutrophils, eosinophils, basophils, monocytes, NK cells) 
tissue: macrophages, dendritic cells, mast cells
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4
Q

skin and mucous membranes contain

A

sebaceous glands and sebum which inhibit microbe growth with a low pH or with antimicrobial stubastances and cilia

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5
Q

inflammation is triggered by

A

injury or invasion

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6
Q

inflammation functions to

A

protect tissues but causes damage and disease too

normally the damage is repaired, but inflammation can become chronic

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7
Q

inflammatory mediators result from vasoactice mediators such as

A

prostaglandins, leukotrienes and histamine from mast cells

bradykinin from kinin system

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8
Q

microbes/injury trigger tissue/sentinal cells

A

mast cells, macrophages, dendritic cells

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9
Q

signs/systems of inflammation and infection

A

blood supply increases, causes redness and warmth

BV are permeable, so swelling happens

immune cells are recruited and kill pathogens, causing tissue debris

WBC attack and release substances to continue inflammation

inflammatory mediators can cause pain by nerve stimulation

body reacts with chills, fever, muscle aches

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10
Q

innate responses are often sufficient to

A

prevent infection in tissues and blood, but might not be enough to overcome large numbers of microorganisms

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11
Q

fever is caused by

A

TNF, IL1, IL6 from macrophages in response to pathogens

controlled by hypothalamus

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12
Q

innate immune cells can tell

A

self from nonself using PAMPs

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13
Q

PAMPs (on the surface of the pathogen!)

A

pathogen-associated molecular patterns

unique to specific classes of pathogens-molecular patterns

cannot be altered, supressed or hidden from the surface

not structurally similar to self-antigens

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14
Q

PAMPs include

A 
porins 
lipoproteins
lipopolysacharadies
teichoic acid
mannoproteins 
b-glycan 
lipoarabinomannan
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15
Q

PRRs

A

example is mannose receptor

bacteria, fungi, and viruses need a glycan with mannose tails

no human cells have glycans with terminal mannose

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16
Q

PRRs are coded in

A

germ line

undergo non clonal distribution meaning that all cells have receptors with idenitical specificities

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17
Q

Toll like receptros

A

pair with eachother and recognize pathogens

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18
Q

Extracellular TLRs

A 
1
2
4
5
6
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19
Q

intracellular TLRs

A

3
7
8
9

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20
Q

TLRs recognize

A

PAMPs and activate inflammation

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21
Q

endosomal TLRs

A

located in endosomes into which microbes are ingested

respond only to nucleic acids

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22
Q

TLR signals activate

A

transcription factors that stimulate expression of cytokines and other mediators for inflammation

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23
Q

nuclear factro kB

A

NF-KB one of the most important TF activated by TLRs

promotes expression of various cytokines and adhesion molecules (MOST important for inflammation)

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24
Q

Interferon regualtory factors

A

another inportant Tf

stimualtes production of antiviral cytokines IFNa/b

aka type I interferons

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25
bacteria
``` TLR 1 2 4 5 9 ```
26
viruses
3 7 8 9
27
Fungi
2 | 6
28
MyD88
adaptor protein
29
TRIF
adaptor protein
30
IRF
a transcription factor
31
IRAK
kinase
32
TRAF6
adaptor protein
33
TLR4 dependent cell activation
TLR4, MD2, CD14 and LPS is assebled on pathogen surface MyD88 binds TLR4 and activates IRAK4 to p1 TRAF6 leading to activation of IKK IKKp IxB causing its degradation and release of NFkB to go to nucleus NFkB activates genes for inflammatory cytokines made in cytoplasm and secreted via ER
34
Pamps activate complexes called
inflamasomes containing NLRs
35
NLRs act as
scaffolding proteins assemble signaling platforms that trigger activation of NF-kB and MAPK
36
best NLR is
NLRP3
37
inflammasomes activate
protease caspase 2
38
main function of caspase 1 is to make
IL-1B and IL-18 which drive inflammation these are produced in the inflammasome
39
DAMPs
damage associated molecular patterns danger molecules released in damaged or dying vells
40
while PAMPs are from pathogens, DAMPs are from
cell/ecm both trigger similar types of inducers and same types of sensors leading to same mediators
41
DAMPs released a lot in ___ and little in ___
necrosis; apoptosis
42
DAMPs include
HGMB1 uric acid HSPs when these are released from a necrotic cells trigger TLR 2, 4 and NLRP 3 which trigger NFkB
43
loss of self tolerance leads to
development of autoimmune diseases DAMPs play a role in development of the loss of self-antigen recognition
44
PRR-triggered response: fMet
Fmet is part of prokaryotes but not eukaryotes fMet is typical PAMP neutrophils and macrophages see fMEt to distinguish self from nonself formyl peptide receptor PRR (GPCR) involved in chemotaxis phagocytes bind to bacterial proteins starting with fMet and use them to inititate phagocytosis
45
macrophages respond to
danger signals-DAMPs and PAMPs
46
mcarophages regulate exravasation of
blood into tissue
47
machrophages degrade by
phagocytosis and do tissue repair
48
macrophages play a role in inflammation by
``` cytokines and chemokines ROI NO prostaglandins defensins ```
49
macrophages present antigens to
effetor t cells
50
macrophages immunomodulate meaning
maintain homeostasis in tissue
51
mast cells express receptros for
many DAMPs and PAMPs
52
mast cells can amplify or supress
innate and acquired immune repsonses
53
mast cells secrete
proinflammatory antiinflammatory immunosupressive products
54
mast cells are located in areas exposed to
external environment regualte vascular permeability and recruitment of blood cells can modulate effector cells through release of mediators
55
cytokines
small proteins secreted by cells mediate inflammation, immunity, and hematopoeisis can be endocrine, paracrin and autocrine
56
cytokines in the innate immunity have two different classes
proinflammatory | antiinflammatory
57
chemokines
small protein chemoattractants important for traffickin immune cells
58
ANTIINFLAMMATORY CYTOKINES
``` IL 10 (only true antiinflammatory) TGF-B ```
59
Inflammatory cytokines
TNFa IL 1 IL6 IL8
60
activation of the complement system result in
procution of several different polypeptide cleavage fragments involved in functions of inflammation
61
all complement pathway prodcuts lead to
C3b which activates C5 which forms the MAC which puts holes in plasma membranes and kills pathogems
62
lipoppolysaccharide is the most
potent activator on macrpphages for forming inflammatory mediators
63
classic complement pathway initiation
binding of one IgM or two IgG on microbial surface
64
classic complement pathway c1 complex binds to
IgM or 2xIgG becomes activated
65
activated C1 cleaves
C2 and C4 (one activated C1 molecule can cleave many C2 and C4 molecules) makes C4b and C4b makes C2b and C2a
66
C4 covalently attaches to
microbial surfaces
67
C2a binds to the
surface attached C4b thus forming C4bC2a=C3 convertase
68
C3 convertase cleaves
Cd3 into C3a and C3b
69
C3b deposits on
surface of bacteria
70
surface bound C3b is an
opsonin and increases phagocytosis by phagocytic cells
71
C3b can form a complex with
C3 convertase to make the C5 convertase (c4bc2a3b)
72
C5 convertase cleaves C5 into
C5a and C5b
73
C5b initiates
MAC (lytic pathway)
74
C5a is teh
anaphylactoxin
75
MAC
contains C5b, C6, C7, C8 togeher with many C9 leads to cell lysis
76
APP
CRP mannose binding protien a-acid glycoprotein serum amyloid P component
77
CRP and MBP
fix complement, opsonize
78
mast cell receptors
IgE, Ag PAMPs cytokine/chemokine receptors C3a, C5a complement temperature/pressure cell to cell contact
79
mast cell effector molecules
``` histamine proteases serotinin heparin cytokines IL4,TNF ``` prostaglandins leukotriene cytokines chemokines
80
interferon gamma a and b activates
macrophages inteface between innate and adaptive macrophages express all OTHER cytokines
81
cytokines that produce fever
6, 1b, TNF-a
82
IL8
chemotactic factor, recruites cells to infection (T, basophils, neutrophils)
83
IL12
activates NK cells, induces CD4 T cells into Th1 cells
84
without IL 12, goes toward
B cell/immunigloblin
85
IL12 also acts on NK and T cells to make
IFNy which activates macrophages
86
IL6 generates
APP
87
sicknes behaviour syndrome
due to TNF-a, IL1, IL6
88
rolling
neutrophils come into contact with endothelial cells of blood capillaries and interact with surface adhesion molecules
89
TNFa, IL1, mast cells and macrophages induce activation of endothelial cells which will increase expression of
P selectins and E selectins which will bind to their ligands on neutrophils (4 steps)
90
4 steps of binding neutrophils to selectins
tethering: neutrophils slow down and roll on endotheliuam, mediated by ligand binding tight binding: integrins on neutrophils and ligands on endothelial cells diapedesis: transmigration through endothelium chemotaxis: IL8 controls migrations of neutrophols to inflammatory sites of tissues
91
LGA1 and VLA4 are the integrins on the
neutrophils and monocytes in a low affinity state while rolling, chemokine on endothelial cell can bind to receptor neutrophils this binding activates LFA1 and VLA4 to increase affinity and binding with ICAm and VCAM
92
monocyte rolling
similar in steps 1-3 as neutrophils monoyte chemoattractant protein is the most important chemokine that regualtes migration and infiltration of monocutes matureation of monocute into macrophage is controlled by cytokine microenvironemnt
93
classically activated macrophages
m1 induced by TLR and cytokines especially IFNy and are microbicidal and proinflammatory
94
alternatively activated macrophages
M2 indcued by IL4 and IL!3 important in tissue repair and fibrosis
95
oxygen dependent intracellular killing is a byproduct of teh
respiratory burst taht accompanies phagocytosis
96
events of the respiratory burst
oxygen consumption increased superoxide anion produced converted to H202 by superoxide dismutase hydrogen peroxide is broken down by catalase singlet ocygen made hydroxyl radicals made myeloperoxidase (toxic peroxidation) hypochlorite made (antimicrobial)
97
antiviral innate immune response is mediated by
type I interferons (a/B) which block viral replication in teh host cell NK cells which kill virus infected cells
98
type I IFNs induce expression of proteins that interfere with
viral replcaition to limit spread of virus inteferon regulates PKR wich blocks viral RNA translation IFNs activate nuclease ribonuclease L to degrade viral RNA activate NK cells to kill infected cells
99
NK cells recognize ligands
on infected cells or cells undergoing other types of stress NK cells kill infected/stressed cells NK cell eliminate reservoirs of infection by killing of host cells and releasing intracellular pathogens for phagocytosis
100
NK cells secrete
IFNy type II most powerful activator of macrophages to kill phagocutozed microbes
101
NK cells have activating receptors that are called
KIR (killer cell Ig like receptors) that recognize stress molecules like MICA and MICB on surface of abn. cells trigger PTKs
102
NK cells have inhibiting receptors that recognize
inhibitory receptors called class I MHC and activate PTP to inihibit activation (KIR binds to this as well to inhbit)
103
insufficient KIR-MHC I binding occurs then the NK cell will
kill the target cell
104
if KIRs bind to the MHC I suffiencently, host cells is
not killed
105
NK cells kill infected cells with
perforins to make holes granzymes to activate apoptosis macrohage to eat dying cells
106
somce cells have resistance to innate defense mechanisms like
phagocytic resistance ROS resistance complement resistance anitmicrobial peptide antibiotics resistance
107
T cells need two signals to activate
signal one: binding of antigen signal two: costimulatory molex molecues from APC extra signals from cytokines
108
innate immunity indirectly controsl
ab-mediated responses of adaptove immunity (becasue innate activates B and T's are needed for B's which make Ab)
109
linking innate and adaptive
PRRs activated and mature APC APC presented to naive T cells secreted cytokines assist in the development and maturation of T cells

SFM Quiz 2 (25 decks)

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