PRELIM LECTURE L2: INNATE IMMUNITY Flashcards
some cards can be lengthy as it also functions as notes
1
Q
which lines of defenses are under nonspecific defense mechanism
A
first line and second line of defense
2
Q
which line of defense is under specific defense mechanism
A
third line of defense
3
Q
components of first line of defense
A
physical, chemical, and biological barriers
4
Q
components of second line of defense
A
cellular (phagocytic cells) and humoral factors (APRs, complement, cytokine)
5
Q
components of third line of defense
A
lymphocytes and anitbodies
6
Q
define innate immunity
A
ability to resist infection by means of normally present body functions
7
Q
T or F:
innate immunity is not present at birth since the immune system of newborns are not fully developed
A
F
it is present at birth
8
Q
why is innate immunity considered non-adaptive or non-specific?
A
It responds the same way to all infections and does not retain memory of past encounters
9
Q
what does physical barriers do
A
block or limit access to the body
10
Q
what does humoral and cellular factors generally do
A
initiate activation of immune mechanism
11
Q
skin should always be ____ to remain protected from infections
A
intact, unbroken
12
Q
what maintain the pH of the skin, inhibiting the growth of some microorganisms
A
lactic acid in sweat
fatty acids in sebum
13
Q
pH of the skin
A
5.6
14
Q
what protein has an antibacterial effect against gram-negative bacteria (E. coli)
A
psoriasin
15
Q
which cells produce psoriasin
A
keratinocytes
16
Q
complication where keratinocytes have excessive production of psoriasin
A
psoriasis
17
Q
attacks the cell wall of microbes, especially gram positive bacteria
A
lysozyme
18
Q
what does lysozyme digest
A
Beta (1,4)-glycosidic bonds
19
Q
NAM stands for
A
N-acetylmuramic acid
20
Q
NAG stands for
A
N-acetyl glucosamine
21
Q
where is the point of digestion of lysozyme in the bacterial cell wall
A
between NAM and NAG
22
Q
mechanism of the respiratory system as first line of defense
A
repels foreign pathogen through coughing and sneezing
23
Q
components of respiratory system that aids repelling of pathogens
A
mucus, surfactants, and cilia
24
Q
mechanism of the urinary system as first line of defense
A
flushing action through urination, slight acidity
25
what substance that is found in the genital tract that destroys pathogens with its acidity + pH
lactic acid, 5
26
this inhibits the growth of bacteria and fungi in female reproductive tract
acid mantle of vagina
27
mechanism of the digestive system as first line of defense
halts microbial growth and helps eliminating pathogens with its hydrochloric acid
28
this bacteria can withstand the pH of HCl and causes peptic ulcer
Helicobacter pylori
29
mechanism of the lacrimal and salivary glands as first line of defense
lysozyme in tears defend against gram positive bacteria
30
who demonstrated the antibacterial activity of lysozymes through crystallization of tears
Alexander Flemming in 1992
31
mechanism of the auditory canal as first line of defense
has earwax that serves protection against pathogens
32
non-pathogenic organisms in some parts of the body that deter growth of pathogens
normal flora (microbiota)
33
two ways the microbiota can deter growth of pathogens
competitive exclusion
producing substances
34
define competitive exclusion
two species that compete for the same source cannot coexist; inferior species will be eliminated
35
example of competitive exclusion
vaginal normal flora competes with C. albicans
36
substance that is produced by gut bacteria that binds and penetrates to negatively charged surface of certain bacteria
colicins
37
these cells monitor the entrance of a pathogen
sentinel cells
38
cells present in the peripheral blood
neutrophil
eosinophil
basophil
monocytes
39
cells present in the tissues for primary defense
macrophages
mast cells
dendritic cells
40
primary granules of neutrophil
myeloperoxidase, lysozymes, etc.
41
secondary granules of neutrophil
lysozyme, lactoferrin, respiratory burst components, etc.
42
main function of neutrophils in the immune system
phagocytosis, antimicrobial properties
43
lysozymes are aka
muramidase
44
it is an iron-binding glycoprotein that competes with bacteria
lactoferrin
45
myeloperoxidase is important for
respiratory and oxidative burst
46
also serves as an adhering molecule of neutrophil for it to adhere to epithelial cells
lactoferrin
47
granules of basophils
histamine, small amount of heparin, eosinophil chemotactic factor-A
48
when this immunoglobulin binds to basophil or mast cell the cell will degranulate
IgE
49
what happens after basophil or mast cell degranulates
induce or maintain allergic reactions through release of inflammatory mediators such as histamine and heparin
50
mechanism of eosinophil chemotactic factor-A
calls eosinophil to the site of allergen
51
granules of eosinophils
acid phosphatase, major basic proteins
52
this eosinophil factor recognizes IgE on helminth parasites
epsilon receptor (FceR)
53
how does eosinophil degranulate during presence of helminths
when IgE binds to FecR of eosinophils, the IgE will also bind to the helminth, leading to degranulation of eosinophils and MBP will be released to digest the helminth
54
why are monocytes considered "agranulocytes"
its granules are not visible under the microscope (fine-dustlike granules)
55
the MBP is rich in what amino acid
arginine
56
this is released by eosinophils to lessen hypersensitivity reactions
amine oxidase
57
mechanism of amine oxidase in lessening hypersensitivity reactions
neutralizes histamine
58
T or F:
macrophages do not contain peroxidase
T
59
why is macrophage less efficient in phagocytosis
because of its slow mobility (because it is located in the tissue)
60
important functions of macrophage
secretion of cell mediators and antigen presentation (APC)
61
macrophage of the central nervous system
microglial cells
62
macrophage of the kidney
mesangial cells
63
macrophage of the liver
Kupffer cells
64
macrophage of the lung
alveolar macrophage (dust phagocytes)
65
macrophage of the lymph node
lymph node macrophage
66
macrophage of the spleen
splenic macrophage
67
macrophage of the synovial fluid
synovial A cells
68
macrophage of the connective tissues
histiocytes
69
macrophage in the bone marrow
promonocyte, monocyte
70
aerobic macrophage
alveolar macrophage
71
anaerobic macrophage
M1 macrophage
72
lineage of mast cells
mesenchymal lineage
73
T or F:
mast cells have longer life span than basophils
T
longer lifespan because they reside in tissues
74
granules of mast cells
ACP, ALP, proteases, histamine
75
main functions of mast cells
allergic reaction and antigen presentation
76
most potent phagocytes
dendritic cells
77
main function of dendritic cells
phagocytose antigen and present it to helper T lymphocytes
78
group of non-specific serum components that enhance the effect of antibody
complement
79
3 types of complement
classical pathway
alternative pathway
mannose-binding lectin pathway
80
enzyme with antibacterial activity found in tears saliva and other cells
lysozyme
81
major functions of complement
opsonization
chemotaxis
lysis of cells
inflammation
82
serum protein with bactericidal and viricidal effects in the presence of the third complement component of magnesium ions; stabilizes the complement
properdin
83
overall function of complement
mediation of inflammation
84
heat stable cationic substance with bactericidal activity found in the serum
betalysin
85
family of glycoproteins produced by all animal cells that exert virus-nonspecific but host-specific antiviral activity
interferon
86
how does interferon act as an antiviral agent
by interfering with viral replication
87
aside acting as antiviral agent, interferon can also act as
immunomodulators
antineoplastic agents (interferes with cancer cell multiplication)
88
what IFN is produced by leukocytes
IFN-alpha
89
what IFN is produced by fibroblasts and epithelial cells
IFN-beta
90
function of IFN-alpha and beta
antiviral
increases MHC class 1 expression
91
what IFN is produced by T cell and NK cells
IFN-gamma
92
function of IFN-gamma
major macrophage activator
induces MHC class 2 and can synergize with TNF
93
what happens to cells with no MHC class 1
attacked by NK cells (so it should be found in normal, healthy cells)
94
MHC-HLA stand for
major histocompatibility complex- human leukocyte antigen
95
MHC-HLA is used for what test
organ compatibility testing
96
this stimulates the recruitment of neutrophils and monocytes to sites of infection and activates them to eradicate microbes
tumor necrosis factor
97
TNF-alpha is knows as
cachectin
98
target cells of cachectin
macrophages, nk cells
99
prominent biological activities of cachectin
local inflammation
endothelial activation
100
TNF-beta is known as
lymphotoxin
101
target cells of lymphotoxin
t cells, b cells
102
prominent biological activities of TNF-beta
killing
endothelial activation
103
what consequence can happen when TNFs gain access to the circulation during infection
they mediate a series of reaction, induce shock and result to SEPTIC SHOCK
104
naturally occurring proteins that mediate communication between cells
interleukins
105
function of interleukins
regulate cell growth, differentiation, motility
stimulate immune responses (e.g. inflammation)
106
interleukin:
proinflammatory cytokine; induces fever
IL1
107
interleukin:
activates nk cells to become lymphokine activated killer cells (LAK)
IL2
108
formerly known as t-cell growth factor
IL2
109
interleukin:
induces hematopoiesis
IL3
110
formerly known as multi colony-stimulating factor
IL3
111
interleukin:
key regulator in humoral and adaptive immunity; induces transformation of naive helper T cell to TH2 cell
IL4
112
interleukin:
induce acute phase response of inflammation along with IL1 and TNF
IL6
113
interleukin:
principal secondary mediators of inflammation produced by several cells
IL8
114
define acute phase reactants
glycoproteins that are normal in serum but rise at different rates and levels during inflammation
115
cells that synthesize APRs
hepatocytes
116
how long do hepatocytes synthesize APRs
12-24 hours
117
what triggers hepatocytes to rapidly synthesize APRs
cytokines
118
triggers of pro-inflammatory cytokine production
IL-1 beta
IL-6
TNF-alpha
119
example physiologic trigger of APR release
strenuous exercise (due to heat production)
120
which cells produce pro-inflammatory cytokines
monocyte and macorphage
121
2 types of APRs
positive and negative
122
examples of positive APRs
CRP, mannose binding protein, serum amyloid A
123
examples of negative APRs
albumin, transferrin, antithrombin
124
actions of APRs
bind to microorganisms and promote adherence (phagocytosis)
limit destruction caused by proteolytic enzymes from WBCs
125
cause of albumin to decrease in inflammation
capillary impermeability
126
cause of transferrin to decrease in inflammation
production of CRP
127
cause of antithrombin to decrease in inflammation
since it is used in modulation of infection to promote adherence and phagocytosis
128
a primitive form of antibody (thought to be an antibody because it precipitated with C-polysaccharide of pneumococcus bacteria)
CRP
129
who discovered CRP
Tillett and Francis in 1930
130
functions of CRP
opsonization
agglutination
precipitation
complement activation (classical pathway)
131
main substrate of CRP
phosphocholine
132
T or F:
CRP binding is calcium-dependent and specific
F
non-specific
133
response time of CRP
4-6 hours
134
normal concentration of CRP
0.5 md/dL
135
times of increase of CRP
1000x
136
CRP peaks within how many hours
48 hours
137
T or F:
CRP rises faster than ESR but slower than WBC count
F
rises faster than both
138
T or F:
CRP rapidly declines even without stimulus
T
139
most widely used indicator of acute inflammation
CRP
140
physical properties of CRP
do not cross the placenta
thermo-labile
141
temperature and time CRP can be destroyed
56 C for 30 minutes
142
why it is necessary to heat CRP and destroy it in the serum in some testing
so it will not interfere with some testing for presence of antibodies
143
electrophoretic mobility of CRP
gamma region
144
apolipoprotein transported by HDL site of infection
serum amyloid A (SAA)
145
functions of SAA
helps remove cholesterol from cholesterol filled macrophages in tissue injury
helps recycle cell membrane cholesterol and phospholipids for building new cells
help clean up of injured area
146
how many hours does SAA peak
24-48 hours
147
response time of SAA
24 hours
148
normal concentration of SAA
5 md/dL
149
times increase of SAA
1000x
150
T or F:
SAA increases more in bacterial infection than viral infections
T
151
SAA can be found in what conditions
atherosclerotic lesions
152
T or F:
high levels of SAA can be toxic to the heart
T
contribute to inflammation in coronary artery disease
153
major component of alpha band in serum electrophoresis
alpha 1-antitypsin (AAT)
154
function of AAT
inhibits leukocyte proteases
regulate pro-inflammatory cytokines (inhibit WBC)
inactivate serin proteases (produced in complement cascade and fibrinolysis)
155
leukocyte protease that damages lungs during chronic inflammation
neutrophil elastase
156
deficiency of AAT can lead to what conditions
emphysema
hepatic disorders
157
what happens if lungs lack AAT
open to damage by neutrophil elastase
158
how can abnormalities in AAT cause liver damage
due to it being trapped in the liver
159
protein cleaved to make up fibrin clot
fibrinogen
160
function of fibrinogen
stimulates fibroblast proliferation and growth
161
increased levels of fibrinogen can increase the risk of
coronary artery disease
162
response time of fibrinogen
24 hours
163
normal concentration of fibrinogen
200-400
164
times increase of fibrinogen during inflammation
2-5x
165
binds to free hemoglobin released during intravascular hemolysis
haptoglobin
166
haptoglobin binding: reversible or irreversible
irreversible
167
function of haptoglobin
protect the body (esp. kidney) from oxidative damage
conserves iron
168
electrophoretic mobility of haptoglobin
a2
169
why is haptoglobin initially low in early inflammation
because of intravascular hemolysis (CC1 principle)
170
copper transporting protein
ceruloplasmin
171
ceruloplasmin deficiency
Wilson's disease
172
function of ceruloplasmin
binds to copper
convert ferric iron (toxic) to non-toxic (ferrous)
173
end-game of complement pathway is always:
cell lysis
174
response time of complement C3
48-72 hours
175
normal concentration of complement C3
60-140 mg/dl
176
times increase of complement C3
2x
177
function of complement c3
opsonization
lysis
178
response time of haptoglobin
24 hours
179
normal concentration of haptoglobin
400-290 mg/dl
180
times increase of haptoglobin
2-10x
181
response of ceruloplasmin
48-72 hours
182
normal concentration of ceruloplasmin
20-40 mg/dl
183
times increase of ceruloplasmin
2x
184
overall reaction of the body to injury or infection
inflmmation
185
1st objective of inflammation
localize and eradicate irritant and repair surrounding tissue
186
stages of inflammation
vascular response
cellular response
resolution and repair
187
5 cardinal signs
rubor
calor
tumor
dolor
functio laesa
188
T or F:
inflammation should always lead to recovery
T
189
what are the two main processes involved in the vascular response during inflammation?
vasodilation
increased capillary permeability
190
what causes vasodilation
mediators such as histamine from injured mast cells
191
purpose of vasodilation
to increase blood flow to site
192
T or F:
vasodilation is only experience by peripheral sites of the body (e.g. skin)
T
193
cardinal signs under vasodilation
rubor and calor
194
causes plasma leakage to tissues
increased capillary permeability
195
cardinal signs under increased capillary permeability
dolor and calor
196
what are the two main processes involved in the cellular response during inflammation?
neutrophil activation
migration of macrophage and other cells
197
process of migration to tissue from blood vessels
diapedesis
198
directed migration of WBCs toward infection or injury due to chemical signals (chemokines)
chemotaxis
199
diapedesis of neutrophils takes how many hours
24-48 hours
200
how long does it take for neutrophil to move
30-60 minutes
201
which attract WBCs to site of injury
chemokines
202
release chemokines that cause vasodilation and induce selectins
resident macrophages and mast cells
203
cause circulating WBCs to toll along the vascular wall
selectins
204
cause leukocytes to bind firmly to endothelial cells
chemokine-induced integrins (on WBCs)
205
purpose of integrins in diapedesis
enable leukocytes to crawl between endothelial cells
206
migration of macrophage and other cells involves:
phagocytosis= clearing
207
why macrophage and dendritic cells arrive late on the site of infection
they clean up debris released from neutrophils
"janitors"
208
two classes of chemotaxis
positive chemotaxis
negative chemotaxis
209
chemotaxis towards the stimulus
positive
210
chemotaxis away from the stimulus
negative
211
T or F:
without chemotactic factors, cell motion is random
T
212
How do opsonins enhance phagocytosis?
coat pathogens, making them more recognizable to phagocytes
213
3 ways resolution and repair can result to
1) affected area totally repaired
2) injury can lead to formation of abscess and lead to functio laesa
3) granuloma formation of cell sue to delayed hypersensitivity reactions (e.g. MTB)
214
who first described functio laesa
Rudolf Virchow in 19th century
215
two classes of phagocytosis
direct and indirect
216
direct or indirect phagocytosis:
enhanced by opsonization
indirect
217
direct or indirect phagocytosis:
do not need opsonins
direct
218
direct or indirect phagocytosis:
via primitive pattern recognition receptor (PPRP)
direct
219
direct or indirect phagocytosis:
via opsonins (Antibody, Complement, CRP)
indirect
220
direct or indirect phagocytosis:
use of toll-like receptors (TLR)
direct
221
direct or indirect phagocytosis:
use of cell surface reseptors (FcR, C'R)
indirect
222
steps of phagocytosis
1) adherence (physical contact; pseudopod formation)
2) engulfment
3) formation of phagosome
4) granule contact
5) formation of phagolysosome
6) digestion
7) cytopepsis
8) excretion
223
components in pathogens that aid in direct phagocytosis
pathogen-associated molecular patterns (PAMP)
224
PAMP of gram + bacteria
peptidoglycan
225
PAMP of gram - bacteria
lipoprotein
226
PAMP of flagellates
flagellin
227
natural receptors that detect PAMP
pathogen recognition receptors (PRRs)
228
T or F:
PAMP is always present in bacteria
T
229
how many TLRs in human
10 (TLR1-TLR10)
230
types of PPRs
TLRs
C-type lectin receptors (CLRs)
Retinoic acid-inducible gene-I-receptors (RLRs)
Nucleotide-binding oligomerization domain receptors (NOD)
231
PRR that detect mannans and beta glucans in fungi
CLRs
232
PRR that detects RNA from RNA viruses
RLRs
233
PRR that detects peptidoglycans of gram + bacteria and intracellular protozoans
NOD
234
what part of antigen does opsonin bind
epitope
235
what organism is Toll discovered
fruit fly Drosophila
236
TLR for MTB
TLR1
237
TLR for gram + bacteria
TLR2
238
TLR for gram - bacteria
TLR4
239
TLR is found highest in which cells
macrophage, monocyte, neutrophil
240
241
APR that activates macrophage and monocyte
SAA
242
TLR for motile bacteria
TLR 5
243
TLR for viral dsDNA
TLR 3
