Tutoring Flashcards

1
Q

innate immunity characteristics

A

rapid, acute, inflammation
some specificity
no memory

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2
Q

adaptive immunity characteristics

A

slower
highly specific
memory

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3
Q

define antigens

A

any substance that can induce an immune response

–is not always a protein

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4
Q

define epitope

A

small portion of ag that binds to ab

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5
Q

define hapten

A

very small ags/epitopes that do not initiate an immune response

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6
Q

all immunogens are ___ but not all ____ are immunogens

A

ags–ags

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7
Q

cellular immunity

A

cell components
innate – phagocytes, DCs, NKs
adaptive — abs, B cells

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8
Q

humoral immunity

A

blood components
innate — chemokines, cytokines, APPs
adaptive — abs, b cells

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9
Q

how do cells communicate

A

thru chemokines and cytokines

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10
Q

define cytokines

A

secreted proteins that regulate many activities

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11
Q

define chemokines

A

regulate cell migration and mvt via chemotaxis

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12
Q

innate immunity cells

A

phagocytes
dendritic cells
basophils/eosinophils
mast cells

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13
Q

phagocytes

A

take up/destroy

also secretory functions

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14
Q

macrophage in tissue

A

M-CSF stim production
long half life
typically stay in tissue

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15
Q

dendritic cells

A

ag presenting cells - APCs

help to stim t cells

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16
Q

basophils/eosinophils

A

associate w/ helminth rxns

parasites

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17
Q

mast cells

A

allergic rxns

release most inflammatory factors

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18
Q

specificity of AI

A

ensures that the immune response to a microbe is selective to that microbe

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19
Q

diversity of AI

A

enables the immune system to respond to a large variety of ags

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20
Q

memory of AI

A

increases the ability to combat repeat infections by the same microbe

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21
Q

clonal expansion of AI

A

increases the number of ag-specific lymphocytes to keep pace w/ microbes

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22
Q

specialization of AI

A

generates responses that are optimal for the defense against dif microbes

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23
Q

contraction and homeostasis of AI

A

allows the immune system to recover from one response so that it can effectively respond to new ag

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24
Q

nonreactivity to self of AI

A

prevents injury to the host during responses to foreign ags

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25
clonal selection
happens w/o the ag present w/o disease state will make all kinds of lymphocytes even tho there is no disease
26
occurrence of clonal expansion vs selection
expansion = ag is present selection = ag not present
27
occurrence of clonal expansion vs selection
expansion = ag is present selection = ag not present
28
active immunity
injected w/ an ag via vaccine host generates ab and saves as memory
29
passive immunity
--injecting abs from another host which will clear your infection --skips first phases of adaptive immune response --results in no memory
30
development of lymphocytes begins in fetal _____
liver
31
lymphocytes use lymph to circulate but cannot enter ?
immunoprivilaged sites eyes brain testes
32
classic DCs recognize ?
proteins
33
ags generated in the blood are delivered to ?
spleen
34
interferons are anti-_____
antiviral
35
______ are the only thing that can activate a naïve T cell
DCs
36
homing is mvt of ?
leukocytes from blood to tissue to fight in response to infection
37
recirculation is mvt of ?
leukocytes from tissue to blood in order to look for ags
38
families of cytokines that regulate mvt of leukocytes differ because ?
of the number of cystines
39
CCL2/MCP-1
monocyte recruitment
40
CCL19/MIP-3B
t cell/dc migration in LN
41
CCL21/SLC
t cell/dc migration in LN
42
CXCL8
****important | neutrophil recruitment
43
CXCL10
effector t cell recruitment
44
CXCL12
naïve b cells to LN | homing
45
CXCL13
b cell migration to follicles
46
list steps in transepithelial migration
``` infection detected activation of endothelium tethering rolling adhesion-stop transmigration ```
47
list steps in transendothelial migration
``` infection detected activation of endothelium tethering rolling adhesion-stop transmigration ```
48
post infection detection, leukocytes enter LN via ?
post capillary venules
49
what cells are the first to detect infection?
neutrophils and monocytes
50
_________ cells are the first to detect pathogens and are activated in ______ and begin to produce ?
neutrophils and monocytes in tissues IL-1 and other cytokines --used to recruit other cells
51
________ released during infection/inflammation causes ?
cytokines activation of endothelium to express selectins on surface these are not expressed in healthy states
52
in transendothelial migration what does activation of endothelium mean?
endothelium expresses selectins
53
types of selectins
P, E, L
54
p-selectins
on endo activated by --histamine, thrombin ligand -- xialyl lewis x bodies
55
e-selectins
on endo activated by ---TNF, IL-1 ligand -- xialyl lewis x bodies
56
L-selectins
on leukocytes/lymphocytes ligand -- pNAD on HEV endo
57
xialyl lewis x bodies are located on ?
on lymphocytes and leukocytes
58
tethering
selectins are present on endo bind their respective ligands on passing cells necessary to slow them down to initiate rolling
59
rolling of leukocytes is mediated by ?
integrins mediate adhesion of cells to endo found on leukocytes
60
integrins involved in rolling and their respective ligands
LFA1 --- ICAM MAC1 --- ICAM VLA4 --- VCAM1 A4B7 --- VCAM1, MadCAM1
61
integrins on leukocytes and no chemokines present, results in ?
weak affinity for endo chemokines from neutrophils/monocytes in tissue
62
inside-out signaling
when neutrophils/monocytes release chemokines in response to pathogen presence this gives integrins on leukocytes high affinity for their ligands on endo in order to migrate
63
inside-out signaling
when neutrophils/monocytes release chemokines in response to pathogen presence this gives integrins on leukocytes high affinity for their ligands on endo in order to migrate
64
naïve leukocytes/lymphocytes have no ______ receptors thus cannot tether/roll/migrate
no chemokine receptors
65
adhesion and stop ---- migration
integrins bind to ligands on endo w/ high affinity rolling stops T cells are different
66
adhesion and stop ---- migration of T cells
CD44 on endo---mediates rolling this mobilizes effector t cells CD44 binds hyaluronic acid on T cell
67
significance of CD44 binding hyaluronic acid on T cells
it upregulates the VLA-4/VCAM integrin binding
68
transmigration into tissue occurs via ______ . discuss this migration
diapedesis | cells slide thru gap junctions to enter tissue using ameboid shapes
69
once cells migrate into tissue how do they know where to go?
migrate towards sight of infection as directed by the chemokines being released by cells already at the site
70
naïve cells enter LN via ? and ____-selectins on them to bind ?
via HEV | L-selectins to bind to pNADs on HEV
71
T cell entrance to LN via HEV
CCR7 on t cell -- binds CCL19/21 on HEV which activates integrins on HEV
72
when no ag is found, b and t cells return to lymph via ________ and enter other ______ lymph organs, eventually reaching ?
``` efferent lymph vessel other 2ndary lymph organs thoracic duct ---and then returned to circulation-IVC ```
73
when an ag is found, b/t cells are activated and return to ______ where they will then undergo migration into tissue. which is the same for all _______ cells.
circulation same for all effector/memory b/t cells t cells bind CXCL10
74
when an ag is found, b/t cells are activated and return to ______ where they will then undergo migration into tissue. which is the same for all _______ cells.
circulation same for all effector/memory b/t cells t cells bind CXCL10
75
how are b and t cells separated in LN
are attracted to different chemokines present
76
chemokines for B cells in LN, and other organs
CXCR5 on b cell binds -----CXCL13 primary follicle in spleen enter in red pulp and migrate to 13 in white pulp where mature and return to circulation
77
chemokines for T cells in LN
CCR7 on t cells binds | ---- CCL21 in T cell zone
78
timeline of activated T cells exit from LN
usually stay in LN for a few days to allow for proliferation to create an army before going to war
79
TLR 2,6
peptidoglycan | gram positive bacteria
80
TLR 4
LPS gram neg bacteria endotoxin
81
TLR 5
flagella
82
TLR 9
CpG
83
TLR 3
dsRNA
84
TLR 7,8
ssRNA
85
extracellular TLRs
1,2,4,5,6
86
intracellular TLRs
3,7,8,9
87
receptor NLR
ligand = intracell proteins formation of inflammasome and caspase mediated apoptosis
88
scavenger receptor
ligand = negatively charged bacterial components not all scavengers have same extracell domain
89
lectin receptors
ligand = carbs **eukaryote - terminal sugar is galactose or sialic acid bacterial/PAMP - terminal sugar is mannose
90
lectin receptors
ligand = carbs **eukaryote - terminal sugar is galactose or sialic acid bacterial/PAMP - terminal sugar is mannose
91
HMGB1 binds to
RAGE**
92
uric acids binds to
unknown receptor
93
HSPs bind to
CD91
94
DAMPS receptors are generally on ?
dendritic cells
95
source of antimicrobial peptides
epithelial cells or granule containing leukocytes
96
defensins have direct _____ to kill ?
toxicity | to kill microbe via disruption of memb
97
cathe'licidins have direct _____ and are released by ?
toxicity | by neutrophils predominantly
98
what is the main function of antimicrobial peptides?
to kill microbes and recruitment of other cell types --- especially mast and t cells
99
discuss why NK and macrophages must be inter-dependent
NK cells can bind to pathogen and kill the cell macrophages must then clean up the waste so other cells are not infected
100
macrophages must be _____ in order to phagocytize things
activated
101
release of IL12 from ______ induces ______ . and then ?
tissue macrophage NK cell nk will release IFN-y
102
IFN-y and macrophages
is released by NK cells to activate macrophages to kill phagocytosed pathogen
103
IFN-y and macrophages
is released by NK cells to activate macrophages to kill phagocytosed pathogen
104
proteases are secreted in ____ form and then ?
secreted as inactive must be cleaved to become active
105
result of C3 convertase
cleave C3 into: C3a C3b
106
C3b becomes apart of _______ to form _______ .
C3 convertase to form | C5 convertase
107
result of C5 convertase
cleaves C5 into: C5a C5b
108
C5b is joined by _______ to form ?
C6, C7, C8, C9 to form memb attack complex MAC
109
MAC causes ____ and is the same in _____ complement pathways
lysis same for all pathways
110
what activates the alternative pathway?
C3 is spontaneously cleaved to C3b on cell surface
111
alternative pathway to form C3 convertase
1. c3 spontaneously cleaved 2. factor B binds C3b 3. factor D binds FB 4. FB cleaved = Bb, Ba 5. Bb binds C3b = C3bBb = c3 convertase
112
alternative pathway to form C3 convertase
1. c3 spontaneously cleaved 2. factor B binds C3b 3. factor D binds FB 4. FB cleaved = Bb, Ba 5. Bb binds C3b = C3bBb = c3 convertase
113
C3 convertase to end: alternative pathway
1. c3 convertase cleaves c3 2. c3b binds C3bBb = C3b3bBb = c5 convertase 3. c5 convertase cleaves c5 4. C5b joins other = MAC
114
function of Properdin
it stabilizes the interactions of the alternative pathway
115
how is the lectin pathway activated ?
mannose binding lectin | MBL binds to surface of mannose bacterial walls
116
lectin pathway: formation of C3 convertase
1. MASP2 is bound MBL 2. MASP2 cleaves C2 n C4 3. C4b+C2a = C4b2a = C3 convertase
117
lectin pathway: C3 convertase to MAC
1. C3 convertase cleaves C3 2. C3b + C4b2a = C4b3b2a = C5 convertase 3. C5 convertase cleaves C5 4. MAC formation
118
lectin pathway: C3 convertase to MAC
1. C3 convertase cleaves C3 2. C3b + C4b2a = C4b3b2a = C5 convertase 3. C5 convertase cleaves C5 4. MAC formation
119
function of C3b
opsonization via CR1 on macrophages
120
function of C5b
initiates MAC formation
121
function of C7
inserts into the cellular membrane
122
function of C9
polymerizes to form pore
123
components of the MAC complex
``` C5b C6 C7 C8 C9 ```
124
functions of C5a
strong chemoattractant and initiates killing via ROS
125
functions of C5a
strong chemoattractant and initiates killing via ROS
126
which is a greater anaphylatoxin: C5a or C3a?
C5a
127
what is an anaphylatoxin?
inflammation SM contraction increase in vascular permeability degranulation of mast cells
128
regulatory compliment proteins
DAF | CR1
129
function of DAF
blocks C2:C4 interactions | dissociates C4b2a or C3bBb classic or alter
130
function of CR1
dissociates C4b2a or C3bBb w/ FI - cleaves C4b or C3b phagocytosis when bound to C3b (all paths)
131
function of CR1
dissociates C4b2a or C3bBb w/ FI - cleaves C4b or C3b phagocytosis when bound to C3b (all paths)
132
discuss complement mediated macrophage activation
1. CR1 binds to C3b and is phagocytized 2. phagosome fuses w/ lysosome 3. IFN-y releases trigger = killing of pathogen via ROS
133
Catalase (+) ________ can survive ?
phagolysosomes by forming oxygen and water with the enzymes inside
134
inflammatory molecules
IL-1 TNF IL-6
135
purpose of inflammatory molecules
all are redundant and illicit multiple rxns | but serve a specific purpose
136
function of inflammatory molecules
IL-1 = fever inducing TNF = increase vascular dilation and permeability IL-6 = acute phase proteins - CRP, SAP (particularly CRP)
137
CRP is a clinical indication of ?
indication of immune response
138
type 1 and type 2 interferons
1 = alpha and beta 2 = gamma
139
type 1 and type 2 interferons
1 = alpha and beta 2 = gamma
140
intracellular TLR are in particular ?
viral RNA
141
response of type 1 interferons
on healthy cells create antiviral replication proteins on infected cells enhance killing via CTL (CD8 cells)
142
response of type 2 interferons
enhanced macrophage killing production of IgG abs
143
antibodies are associated w/ ______ responses
humoral
144
abs respond to ______-cell pathogens only, and abs can only circulate in ________.
extracell pathogens in blood/tissues
145
abs are produced by _____ and are apart of _______ immunity.
B cells | adaptive immunity
146
effector properties of abs
1. agglutination 2. neutralize toxins 3. activate complement 4. opsonization 5. regulatory properties
147
agglutination
bind pathogens together
148
opsonization facilitates ?
facilitates phagocytosis
149
opsonization facilitates ?
facilitates phagocytosis
150
effector regulatory properties w/ production of ?
cytokines for: T cell response inflammatory response
151
general structure of abs
4 chains total - -2 light chains --- either kappa or lambda - -2 heavy chains --- 4 dif types
152
light chain types of abs
kappa or lambda | will always be one or the other - not both
153
regions of ab chains
Fab region = binds ag - small Y limbs Fc region = carries out effector function - long Y limb
154
what connects Fab and Fc regions
connected by hinges allows binding of 2 ags at a time
155
all abs start as ?
membrane bound | IgM or IgD
156
membrane bound ab properties
has extra Ch domain No tail piece either IgM or IgD (B cell receptors)
157
abs are either _______ or _______ bound.
secretory or memb bound
158
secretory ab properties
has tail piece IgE, IgA, IgG
159
IgG can be both ?
memb bound and secretory
160
papain
cleaves abs at hinges leaves 2 separate Fabs and 1 Fc so 3 pieces total
161
where are papain and pepsin found?
papain = in papayas pepsin = digestive enzyme in humans
162
where are papain and pepsin found?
papain = in papayas pepsin = digestive enzyme in humans
163
pepsin
cleaves below hinges leaves 1 Fab and 1 Fc Fab can still bind 2 ags Fc dissociates Fab now called F(ab')2
164
what ags antibodies recognize
proteins nucleic acids polysaccharides
165
proteins that abs recognize as ags
in conformational form linear form or cut form
166
T cells can only recognize ____ ags
protein ags
167
affinity
how tight an ag binds to an ab increases w/ second exposure
168
avidity
strength of an ag-ab complex depends on affinity and valence increases as valence increases
169
valence
the number of ags that can bind to an ab typically minimum is 2
170
ag binding site for b cell receptor and TCR
binds to variable heavy and light chains binds to variable alpha and beta
171
type of ag that binds to b cell receptor and TCR
proteins, polysaccharides, lipids proteins only -- in linear form
172
binding affinity: b cell receptors and TCR
higher less than B cell binding
173
B cell receptors
IgM and IgD
174
immature B cells always produce _____ first
IgM
175
mature B cells produce membrane ____ and _____ which are ?
IgM and IgD mature B cell receptors
176
mature B cells produce membrane ____ and _____ which are ?
IgM and IgD mature B cell receptors
177
activated B cells can maintain what ? and form ?
maintain memb IgM, IgD form secretory abs (A,G,E)
178
activated B cells can form secretory abs but is dependent upon ?
on T cells and cytokines they produce
179
plasma cells have constant secretion of ?
abs | secretory abs only
180
isotype switching requires ________. | to switch causes changes in ?
cytokines change of heavy chain Fc portion Fab stays the same
181
compare structure of abs
G, E, D = normal monomers M = pentamer w/ J chain A = dimer w/ J chain + secretory section
182
location of IgG
serum highest level in serum (not body) can invade tissues
183
location of IgM
serum | naïve b cells
184
location of IgE
mast cells
185
location of IgA
mucosal areas highest in these areas of the body
186
location of IgD
naïve b cells only
187
function of IgG
phagocytosis can pass from mom to fetus can be secreted highest during 2ndary response **highest in serum
188
function of IgM
``` complement activation memb bound **always present first highest during primary response high avidity low affinity ```
189
function of IgE
allergic response can be secreted acute inflammation infections by worms
190
function of IgA
mucosal defense can be secreted can cross endo memb transferred in breast milk
191
function of IgD
only found on b cells
192
IgE is present during _____ responses via ______ cell activation.
allergic | mast cell activation
193
cytokines that stimulate each ab
``` G = IFN-y M = IL-2,4,5 E = IL-4 A = TGF-B ```
194
types of T cells
Th0 CD4 CD8
195
Th0 = ?
naïve t cell
196
CD4 T cells
T helper cells | recognize ags on MHC II on APCs
197
types of t helper cells
Th1 = intracell pathogens produce IFN-y Th2 = extracell pathogens help develop B cell to memory cells
198
Cd8 t cells
cytotoxic T cells associated w/ MHC class I fights intracell pathogens
199
describe T cell receptors (TCR)
only on t cell memb's most are made of alpha n beta chains can only bind *processed* protein ag
200
regions of TCRs
TM region w/ alpha/beta chains constant regions variable regions --- have ag binding site
201
ysigma T cells
small percentage of T cells made of y and sigma chains (instead of a/b) much wider specificity --- meaning don't have to bind proteins only
202
components of TCR complex
TCR - a n b chains CD3 zeta chain CD4 or CD8 (which bind to MHCs)
203
CD3
--found on ALL t cells --used as diagnostic tool to find t cells --sends signals into t cell = production/release of cytokines
204
zeta chain
apart of TCR complex --signaling part of complex
205
MHC class I -- loci genes
HLA-A HLA-B HLA-C
206
MHC class II -- loci genes
HLA - DQ HLA - DR HLA - DP
207
MHC loci genes
each person gets 6 HLA genes 3 from mom/3 from dad --allowing for variations
208
MHC - class I properties
1. on all nucleated cells (so not RBCs) 2. contains 1 a chain 3. **B-macroglobulin 4. intracell pathogens
209
MHC class I molecules bind to ?
short linear peptides to CD8 t cells -- binds to a chain
210
there is enhanced expression of MHC - I with ?
IFNy | IFN-a/B
211
MHC class II properties
1. expressed on prof APCs 2. two chains - a n B 3. typically extracell peptides
212
MHC class II molecules bind to ?
CD4 t cells to short linear peptides but longer than ones that MHC I binds presents to CD4 t cells -- binding to B chain
213
enhanced expression of MHC-II under ?
IFN-y
214
co-stimulation
CD40 -- macrophages/DCs/B cells CD40L -- t cells important for co-stimulation of t cell and activation of APC
215
MHC-I processing pathway
1. virus peptides tagged/destroyed 2. TAP 3. MHC-I created 4. MHC-I:Ag complex sent to golgi
216
virus peptides
tagged by ubiquinase sent to proteasome for degradation
217
TAP
this takes peptide fragments to ER
218
creation of MHC-I
in ER meets up and binds w/ virus peptides
219
MHC-I:Ag complex is sent to ?
to golgi to exocytotic vesicle to memb
220
MHC-II processing pathway
1. extracell proteins takin in 2. mhc-II made 3. mhc-II vesicle fused w/ phagolysosome 4. CLIP 5. HLA-DM 6. sent to memb
221
MHC-II processing --- extracellular proteins are taken in via _______ and fuse ?
endocytosis fuse w/ lysosome = phagolysosome
222
creation of MHC-II
made in ER processed by golgi sent via exocytotic vesicle fuses w/ phagolysosome
223
CLIP
in the vesicle this binds MHC-II so that nothing else will bind it
224
HLA-DM
removes clip stabilizes binding of peptide to MHC-II
225
define cross presentation
sometimes extracell pathogens are brought in via endocytosis and leak into cytoplasm
226
steps in cross presentation
extracell pathogens leak into cytoplasm get tagged - Ub --once tagged go thru MHC-I pathway
227
results of cross presentation
results in extracell pathogens presented on MHC-I to be bound by CD8+ T cells
228
peptide binding/recognition
LY | low yield