Immunology Flashcards
(155 cards)
1
Q
2 examples of self-reactivity in the immune system
A
- cancer
2. autoimmune diseases
2
Q
what types of immune cells are located in the blood?
A
leukocytes, WBC
3
Q
what types of immune cells are present in the lymphatic tissue?
A
lymphocytes
4
Q
lymphocytes are a type of __
A
leukocytes
5
Q
there is as much lymphatic tissue in the ___ as in the rest of the body combined
A
GI tract
6
Q
what structures are involved in the immune system? (4)
A
- lymph drainage
- lymph nodes
- spleen
- distributed lymphatic tissue
7
Q
the innate immune system acts ___ (before/after) the adaptive immune system
A
before
8
Q
what is unique about the adaptive immune system?
A
it is specific to a pathogen / infection
9
Q
in the innate immune system, a cut in the skin results in a neurological response, causing stimulation of ___
A
neuropeptides
10
Q
neuropeptides stimulate __
A
mast cells
11
Q
mast cells are often found near ___ and always near ___
A
nerves; blood vessels
12
Q
mast cells that have been stimulated by neuropeptides release___ into blood vessels
A
mediators
13
Q
in the innate immune response, once mediators have been released into BV, what are released and what is their effect?
A
clotting factors and platelets; direct effect on bloodstream
14
Q
clotting factors can cleave the ____
A
complement
15
Q
what is the “complement”? What does it break down into?
A
group of proteins in the blood; C3A and C3B
16
Q
which part of the complement has an effect on mast cells?
A
C3A
17
Q
which part of the complement has an effect on the macrophages?
A
C3B
18
Q
what is the receptor for C3A protein?
A
C3aR
19
Q
what is the receptor for C3B protein?
A
C3R
20
Q
the complement is a cascade of ___
A
serum proteins
21
Q
how many proteins made up the complement cascade?
A
9 (C1-C9)
22
Q
what are the 4 most important proteins in the complement cascade?
A
- C1
- C3 (a + b)
- C5 ( a + b)
- C5b–C9
23
Q
C5b–C9 are involved in __
A
complement destruction
24
Q
the lipopolysaccharide is used largely for __
A
protection
25
what happens to LPS to cause an immune response?
being shed off surface
26
what are CPG motifs and in whom are the common?
runs of cytosine and guanine in DNA; common in bacteria (not humans)
27
CPG motifs stimulate ___
inflammatory response
28
what are DAMPs?
Damage Associated Molecular Patterns
29
LPS and CPG motifs make ___
Pathogen associated molecular patterns (PAMPs)
30
DAMPs are ___ proteins with ___ fragments
heat shock; hyalouronic
31
DAMPs stimulate __
inflammatory response
32
TLR (Toll-Like Receptors) are receptors for __ (3)
LPS, CPG, DAMPs
33
TLR are a type of ___ recognition receptor
pattern
34
TLR recognize molecular patterns associated with __
infection / inflammation
35
T/F TLR recognize specific antigens
false
36
presence of LPS/CPG may indicate a ___ infection
bacterial
37
structure of mast cell
very large, contains many different granules
38
mast cells are found only in the __
tissues
39
precursors to mast cells are found in the __
blood
40
mast cell precursors are tissue basophiles (T/F)
false
41
mast cells are involved in the ___ response
allergic
42
mast cells have a lot of ___ and ___ and the ____ cause it to stain purple
nucleus and cytoplasm; granules
43
structure of monocytes/macrophages
curved nucleus, plenty of cytoplasm but not a lot of granules
44
monocytes / macrophages are important early responders to infection because they are ___
phagocytic
45
monocytes/macrophages are involved in acute and chronic __
inflammation
46
monocytes are found only in the __
blood
47
macrophages are found only in the
tissue
48
when stimulated, monocytes/macrophages release ___
histamine (prostaglandins)
49
histamines are released ___ because they are produced in what way?
immediately; pre-formed by mediators
50
prostaglandins are released ___ because they are produced in what way?
later; continually produced
51
which has longer-lasting effects, histamines or prostaglandins?
prostaglandins
52
release of histamines/prostaglandins causes increase in ___ and ___ that is localized to the area
vascodilation and vascular permeability
53
what are the 4 hallmarks of acute inflammation?
swelling, pain, redness, heat
54
vascodilation is responsible for which of the 4 hallmarks of acute inflammation?
swelling and pain
55
vascular permeability is responsible for which of the 4 hallmarks of acute inflammation?
redness and heat
56
swelling in acute inflammation is caused by increased __
plasma to intersitial fluid
57
increased plasma that causes swelling in inflammation carries ___ and ___ that are meant to kill the bacteria
antibody and complement
58
the antibody is useful in killing the infection if __
the bug has been seen before
59
the complement is useful in killing the infection if ___
always, because it can kill the bug all by itself
60
what are the 3 ways to activate the complement?
1. classical
2. alternate
3. lectin
61
what is the classical way to activate the complement?
involves antibody (bug has been seen before)
62
what is the alternate way to activate the complement?
spontaneous cleavage of C3 protein ( C3b binds to bug and pokes holes in it)
63
what is the lectin way to activate the complement?
lectin directly activates C
64
what are the 4 functions of the complement?
1. target lysis
2. target neutralization
3. enhance phagocytosis
4. inflammation
65
what is the role of target neutralization by the complement?
prevents infectivity
66
how does the complement enhance phagocytosis?
C3b bound to a bacteria makes macrophages bind to C3b by their receptors and then phagocytize
67
inflammation is mostly caused by which part of the complement?
C3A
68
C3A is known as the ___ factor for other immune cells
chemotactic activating
69
(T/F) The complement will bind directly to the bug regardless of if it has been seen before or not
true
70
only if the bug has been seen before, ___ will bind and activate a number of killing pathways
antibody
71
what 2 pathways are activated by the antibody?
1. antibody-mediated complement pathways
| 2. antibody-mediated phagocytic pathways
72
what makes macrophages different from mast cells?
they phagocytize bacteria
73
what is the benefit of macrophages phagocytizing bacteria?
helps in activation
74
what are 2 phagocytic enhancers?
1. antibody
| 2. complement
75
why do antibodies enhance phagocytosis?
macrophages have Fc receptors for antibodies and the antibodies act like a "candy coating"
76
why does the complement enhance phagocytosis?
macrophages have receptors for C3, so if C3b is on the bacteria it makes the macrophage more likely to bind
77
what is the first thing to happen once a bacteria has been phagocytized?
vesicle acidification
78
what are 2 benefits of vesicle acidification?
1. harder for bacteria to survive
| 2. some enzymes work better at lower pH, so they will only harm the pathogen, not the host
79
a lysosome merges with the phagosome and secretes ___
digestive enzymes
80
bacteria get broken down in the __
phagolysosome
81
what is done with the bits of bacteria that are not digested in the phagolysosome?
removed and recycled, and then the message is taken to the lymphocytes
82
what are the 4 reactive oxygen intermediates?
1. superoxide (O2-)
2. hydroxyl radicle (OH-)
3. hydrogen peroxide (h2O2)
4. hyperchlorite anion (ClO-)
83
what are the 2 reactive nitrogen intermediates?
1. nitric oxide (NO)
| 2. nitrous acid (HNO2)
84
nitrogen intermediates require ___ (which is made by Tcells)
IFNy
85
why do nitrogen intermediates require control by IFNy?
they are very potent and can damage tissues
86
what 3 things are involved in phagocytic effector cell function?
1. reactive oxygen intermediates
2. reactive nitrogen intermediates
3. lysosomal enzymes
87
macrophages contribute to local immune/inflammatory response by producing ____ and ___
cytokines and chemokines
88
what cytokines are produced by macrophages?
IL-1 and TNF
89
what chemokines are produced by macrophages?
IL-8
90
what are cytokines?
produced by one cell and have an effect on another (way immune system communicates)
91
what are interleukins?
a particular type of cytokine with a particular molecular structure
92
what does TNF stand for?
tumour necrosis factor
93
what are the effects of TNF? (3)
1. kills tumours
2. potentially inflammatory
3. effect on vascular system
94
what is interleukin 8?
a chemokine that activates neutrophils
95
neutrophils are involved in __
fighting bacterial infection
96
Interleukin 8 causes changes in ___ that cause neutrophils to be ___
CAMs; attracted
97
what does CAM stand for?
cell adhesion molecules
98
____ change, allowing neutrophils to leave vasculature and get to macrophage
CAMs of vasculature
99
neutrophils are also known as ___
polymorphic nuclear cells
100
what is the most common type of WBC?
neutrophils
101
___ are an important first responder to bacterial infection
neutrophils
102
neutrophils are highly ___ in tissues
phagocytic
103
neutrophils are involved in tissue ___
remodelling
104
what is trans-endothelial migration?
neutrophils come into tissue from blood due to attraction to CAM
105
____ of neutrophils bind to CAM to cause rolling
selectins
106
what is the purpose of selectins binding to the neutrophil?
the rolling slows down the neutrophil
107
once the neutrophil has rolled, it releases ___ and produces ___ that will bind to another ___
selectin; integrin; another selectin
108
neutropils binding to the endothelial cell, leading to ___ and ___
adhesion and diapedesis
109
what is diapedesis?
neutrophil forcing its way out of the blood vessel into tissue
110
what are NETs?
extracellular structure made of chromatin and specific proteins released by neutrophils after death
111
what is a happens during necrosis of neutrophil?
large, sticky strands of DNA (that can stick to bacteria) are released into the local environment
112
cellular proteins associate with NETs to __
damage bacteria
113
T/F: neutrophils expel more "garbage" than macrophages
true
114
neutrophils "putting out the garbage" is extremely important to __
activation of dendritic cells
115
dendritic cells are the bridge between ___ and ___
innate and adaptive immune response
116
at the site of infection, dendritic cells have high __ and low __ . Why?
uptake; movement. More garbage to uptake
117
further from site of infection, dendritic cells have high __ and low __. Why?
movement; uptake. Less garbage to uptake
118
dendritic cells carry "garbage" from ____ site to ___
infection; local draining node
119
all lymphatic drainage moves from __ to __
periphery to core
120
lymphatic drainage is carried out by a series of ___ that are controlled by ___ contraction
one-way valves; muscular
121
what 2 veins have a large role in lymphatic drainage?
2 subclavian veins
122
describe how dendritic cells take up garbage and present it to the lymph nodes (adaptive immunity)
```
dendritic arm picks up garbage and takes it in.
lysozyme then merges to form phagolysosome and breaks garbage into peptides that can be placed into vessicle class 2 MHC and brought to surface of dendritic cell to present to Tcells
```
123
what is class 2 MHC made of ?
alpha and beta chains
124
class 2 MHC is found on the surface of ___
dendritic cells
125
class 2 MHC binds with a __ that is presented to the T cells
peptide
126
can class 2 MHC present its antigen (peptide) to any T cell?
no, the T cell must recognize the antigen
127
____ T cell binds directly to a class 2 MHC
CD4
128
the dendritic cells produces ___ to activate the CD4 T cell
interleukin 12
129
interleukin 12 signals that it is likely a ____ infection type
bacterial
130
B7 on ___ binds to CD28 on __
dendritic cell; CD4 Tcell
131
the binding of CD4 with the class 2 MHC and the B7 with CD28 results in ___
co-stimulation
132
the signal sent from B7 on the dendritic cell to the CD28 on the T cell promotes the T cell to ___ to respond to the peptide and infection
proliferate
133
activating T cells to proliferate is done by activating t-cell ___ factor (interleukin __)
growth; IL-2
134
do resting t cells have the receptor for IL-2?
no
135
inorder for a tcell to be activated by the IL-2 it is making to proliferate, it must also make __
IL-2 receptor and bring it to its surface
136
by resting tcells not having the receptor for IL-2, it creates ___ in activation of t cells
specificity
137
IL-2 binding to its receptor results in __ replication of T cells
clonal
138
what are the 2 fates of clonal t cells?
1. memory cells
| 2. effector cells
139
what is the role of effector t cells? (2)
1. the orchestra leaders of the immune response
| 2. help b cells make antibodies (because t cells cant make them)
140
can b cells make antibodies without the help of t cells?
no
141
what surface antibody is found on b cells?
IgM
142
what must happen for a b cell to activate?
specific antigen must bind to the antibody
143
b cells do not see the peptide in MHC, what do they see?
soluble protein
144
once the soluble protein binds to the antibody on b cell, what happens to it?
it is taken in by receptor-mediated endocytosis
145
once the protein has been endocytized by b cell, the lysosome forms an endolysosome with the vesicle containing __ and brings ___ to the surface, stuffed in a groove
MHC; peptide
146
how do the effector t and b cells interact?
if effector t cells see the peptide on the surface of the b cells, it will interact
147
are there naive t cells present in the b cell area?
no
148
CD4 t cells produce b cell growth factor (interleukin __
IL4
149
T/F: when a b cell clones itself, all the surface antibodies will be the same
true
150
what are the 2 fates of cloned b cells?
1. memory cells
| 2. plasma cells (majority)
151
structure and role of b plasma cells
lots of ER, produce and secrete lots of antibodies
152
t cells release ___ that tell b cells what antibody to secrete
cytokines
153
in the beginning, most b cells are producing Igm, but t cells what them to produce __. To do this, they must undergo a class __
IgG; class switch
154
to perform a class switch, a t cell produces ___ (switch factor)
IFN-y
155
antibody is produced in the __ and gets into blood and to site of infection due to increased __
vascular permeability
