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Immunology Exam 1 > Tutoring > Flashcards

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
Q

clonal selection

A

happens w/o the ag present
w/o disease state

will make all kinds of lymphocytes even tho there is no disease

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26
Q

occurrence of clonal expansion vs selection

A

expansion = ag is present

selection = ag not present

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27
Q

occurrence of clonal expansion vs selection

A

expansion = ag is present

selection = ag not present

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28
Q

active immunity

A

injected w/ an ag via vaccine

host generates ab and saves as memory

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29
Q

passive immunity

A

–injecting abs from another host which will clear your infection

–skips first phases of adaptive immune response

–results in no memory

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30
Q

development of lymphocytes begins in fetal _____

A

liver

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31
Q

lymphocytes use lymph to circulate but cannot enter ?

A

immunoprivilaged sites
eyes
brain
testes

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32
Q

classic DCs recognize ?

A

proteins

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33
Q

ags generated in the blood are delivered to ?

A

spleen

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34
Q

interferons are anti-_____

A

antiviral

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35
Q

______ are the only thing that can activate a naïve T cell

A

DCs

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36
Q

homing is mvt of ?

A

leukocytes from blood to tissue

to fight in response to infection

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37
Q

recirculation is mvt of ?

A

leukocytes from tissue to blood

in order to look for ags

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38
Q

families of cytokines that regulate mvt of leukocytes differ because ?

A

of the number of cystines

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39
Q

CCL2/MCP-1

A

monocyte recruitment

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40
Q

CCL19/MIP-3B

A

t cell/dc migration in LN

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41
Q

CCL21/SLC

A

t cell/dc migration in LN

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42
Q

CXCL8

A

**important

neutrophil recruitment

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43
Q

CXCL10

A

effector t cell recruitment

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44
Q

CXCL12

A

naïve b cells to LN

homing

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45
Q

CXCL13

A

b cell migration to follicles

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46
Q

list steps in transepithelial migration

A 
infection detected
activation of endothelium
tethering
rolling
adhesion-stop
transmigration
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47
Q

list steps in transendothelial migration

A 
infection detected
activation of endothelium
tethering
rolling
adhesion-stop
transmigration
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48
Q

post infection detection, leukocytes enter LN via ?

A

post capillary venules

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49
Q

what cells are the first to detect infection?

A

neutrophils and monocytes

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50
Q

_________ cells are the first to detect pathogens and are activated in ______ and begin to produce ?

A

neutrophils and monocytes
in tissues

IL-1 and other cytokines
–used to recruit other cells

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51
Q

________ released during infection/inflammation causes ?

A

cytokines
activation of endothelium to express selectins on surface

these are not expressed in healthy states

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52
Q

in transendothelial migration what does activation of endothelium mean?

A

endothelium expresses selectins

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53
Q

types of selectins

A

P, E, L

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54
Q

p-selectins

A

on endo
activated by
–histamine, thrombin

ligand – xialyl lewis x bodies

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55
Q

e-selectins

A

on endo
activated by
—TNF, IL-1

ligand – xialyl lewis x bodies

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56
Q

L-selectins

A

on leukocytes/lymphocytes

ligand – pNAD on HEV endo

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57
Q

xialyl lewis x bodies are located on ?

A

on lymphocytes and leukocytes

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58
Q

tethering

A

selectins are present on endo

bind their respective ligands on passing cells

necessary to slow them down to initiate rolling

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59
Q

rolling of leukocytes is mediated by ?

A

integrins

mediate adhesion of cells to endo

found on leukocytes

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60
Q

integrins involved in rolling and their respective ligands

A

LFA1 — ICAM
MAC1 — ICAM
VLA4 — VCAM1
A4B7 — VCAM1, MadCAM1

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61
Q

integrins on leukocytes and no chemokines present, results in ?

A

weak affinity for endo

chemokines from neutrophils/monocytes in tissue

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62
Q

inside-out signaling

A

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

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63
Q

inside-out signaling

A

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

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64
Q

naïve leukocytes/lymphocytes have no ______ receptors thus cannot tether/roll/migrate

A

no chemokine receptors

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65
Q

adhesion and stop —- migration

A

integrins bind to ligands on endo w/ high affinity
rolling stops

T cells are different

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66
Q

adhesion and stop —- migration of T cells

A

CD44 on endo—mediates rolling
this mobilizes effector t cells

CD44 binds hyaluronic acid on T cell

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67
Q

significance of CD44 binding hyaluronic acid on T cells

A

it upregulates the VLA-4/VCAM integrin binding

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68
Q

transmigration into tissue occurs via ______ . discuss this migration

A

diapedesis

cells slide thru gap junctions to enter tissue using ameboid shapes

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69
Q

once cells migrate into tissue how do they know where to go?

A

migrate towards sight of infection as directed by the chemokines being released by cells already at the site

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70
Q

naïve cells enter LN via ? and ____-selectins on them to bind ?

A

via HEV

L-selectins to bind to pNADs on HEV

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71
Q

T cell entrance to LN via HEV

A

CCR7 on t cell – binds CCL19/21 on HEV

which activates integrins on HEV

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72
Q

when no ag is found, b and t cells return to lymph via ________ and enter other ______ lymph organs, eventually reaching ?

A 
efferent lymph vessel
other 2ndary lymph organs
thoracic duct
---and then
returned to circulation-IVC
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73
Q

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.

A

circulation
same for all effector/memory b/t cells

t cells bind CXCL10

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74
Q

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.

A

circulation
same for all effector/memory b/t cells

t cells bind CXCL10

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75
Q

how are b and t cells separated in LN

A

are attracted to different chemokines present

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76
Q

chemokines for B cells in LN, and other organs

A

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

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77
Q

chemokines for T cells in LN

A

CCR7 on t cells binds

—- CCL21 in T cell zone

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78
Q

timeline of activated T cells exit from LN

A

usually stay in LN for a few days to allow for proliferation

to create an army before going to war

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79
Q

TLR 2,6

A

peptidoglycan

gram positive bacteria

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80
Q

TLR 4

A

LPS
gram neg bacteria
endotoxin

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81
Q

TLR 5

A

flagella

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82
Q

TLR 9

A

CpG

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83
Q

TLR 3

A

dsRNA

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84
Q

TLR 7,8

A

ssRNA

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85
Q

extracellular TLRs

A

1,2,4,5,6

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86
Q

intracellular TLRs

A

3,7,8,9

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87
Q

receptor NLR

A

ligand = intracell proteins

formation of inflammasome and caspase mediated apoptosis

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88
Q

scavenger receptor

A

ligand = negatively charged bacterial components

not all scavengers have same extracell domain

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89
Q

lectin receptors

A

ligand = carbs

**eukaryote - terminal sugar is galactose or sialic acid

bacterial/PAMP - terminal sugar is mannose

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90
Q

lectin receptors

A

ligand = carbs

**eukaryote - terminal sugar is galactose or sialic acid

bacterial/PAMP - terminal sugar is mannose

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91
Q

HMGB1 binds to

A

RAGE**

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92
Q

uric acids binds to

A

unknown receptor

93
Q

HSPs bind to

A

CD91

94
Q

DAMPS receptors are generally on ?

A

dendritic cells

95
Q

source of antimicrobial peptides

A

epithelial cells or granule containing leukocytes

96
Q

defensins have direct _____ to kill ?

A

toxicity

to kill microbe via disruption of memb

97
Q

cathe’licidins have direct _____ and are released by ?

A

toxicity

by neutrophils predominantly

98
Q

what is the main function of antimicrobial peptides?

A

to kill microbes
and
recruitment of other cell types — especially mast and t cells

99
Q

discuss why NK and macrophages must be inter-dependent

A

NK cells can bind to pathogen and kill the cell

macrophages must then clean up the waste so other cells are not infected

100
Q

macrophages must be _____ in order to phagocytize things

A

activated

101
Q

release of IL12 from ______ induces ______ . and then ?

A

tissue macrophage

NK cell
nk will release IFN-y

102
Q

IFN-y and macrophages

A

is released by NK cells to activate macrophages

to kill phagocytosed pathogen

103
Q

IFN-y and macrophages

A

is released by NK cells to activate macrophages

to kill phagocytosed pathogen

104
Q

proteases are secreted in ____ form and then ?

A

secreted as inactive

must be cleaved to become active

105
Q

result of C3 convertase

A

cleave C3 into:
C3a
C3b

106
Q

C3b becomes apart of _______ to form _______ .

A

C3 convertase to form

C5 convertase

107
Q

result of C5 convertase

A

cleaves C5 into:
C5a
C5b

108
Q

C5b is joined by _______ to form ?

A

C6, C7, C8, C9

to form memb attack complex MAC

109
Q

MAC causes ____ and is the same in _____ complement pathways

A

lysis

same for all pathways

110
Q

what activates the alternative pathway?

A

C3 is spontaneously cleaved to C3b on cell surface

111
Q

alternative pathway to form C3 convertase

A
  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
Q

alternative pathway to form C3 convertase

A
  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
Q

C3 convertase to end: alternative pathway

A
  1. c3 convertase cleaves c3
  2. c3b binds C3bBb = C3b3bBb = c5 convertase
  3. c5 convertase cleaves c5
  4. C5b joins other = MAC
114
Q

function of Properdin

A

it stabilizes the interactions of the alternative pathway

115
Q

how is the lectin pathway activated ?

A

mannose binding lectin

MBL binds to surface of mannose bacterial walls

116
Q

lectin pathway: formation of C3 convertase

A
  1. MASP2 is bound MBL
  2. MASP2 cleaves C2 n C4
  3. C4b+C2a = C4b2a = C3 convertase
117
Q

lectin pathway: C3 convertase to MAC

A
  1. C3 convertase cleaves C3
  2. C3b + C4b2a = C4b3b2a = C5 convertase
  3. C5 convertase cleaves C5
  4. MAC formation
118
Q

lectin pathway: C3 convertase to MAC

A
  1. C3 convertase cleaves C3
  2. C3b + C4b2a = C4b3b2a = C5 convertase
  3. C5 convertase cleaves C5
  4. MAC formation
119
Q

function of C3b

A

opsonization via CR1 on macrophages

120
Q

function of C5b

A

initiates MAC formation

121
Q

function of C7

A

inserts into the cellular membrane

122
Q

function of C9

A

polymerizes to form pore

123
Q

components of the MAC complex

A 
C5b
C6
C7
C8
C9
124
Q

functions of C5a

A

strong chemoattractant and initiates killing via ROS

125
Q

functions of C5a

A

strong chemoattractant and initiates killing via ROS

126
Q

which is a greater anaphylatoxin: C5a or C3a?

A

C5a

127
Q

what is an anaphylatoxin?

A

inflammation
SM contraction
increase in vascular permeability
degranulation of mast cells

128
Q

regulatory compliment proteins

A

DAF

CR1

129
Q

function of DAF

A

blocks C2:C4 interactions

dissociates C4b2a or C3bBb
classic or alter

130
Q

function of CR1

A

dissociates C4b2a or C3bBb

w/ FI - cleaves C4b or C3b

phagocytosis when bound to C3b (all paths)

131
Q

function of CR1

A

dissociates C4b2a or C3bBb

w/ FI - cleaves C4b or C3b

phagocytosis when bound to C3b (all paths)

132
Q

discuss complement mediated macrophage activation

A
  1. CR1 binds to C3b and is phagocytized
  2. phagosome fuses w/ lysosome
  3. IFN-y releases trigger = killing of pathogen via ROS
133
Q

Catalase (+) ________ can survive ?

A

phagolysosomes

by forming oxygen and water with the enzymes inside

134
Q

inflammatory molecules

A

IL-1
TNF
IL-6

135
Q

purpose of inflammatory molecules

A

all are redundant and illicit multiple rxns

but serve a specific purpose

136
Q

function of inflammatory molecules

A

IL-1 = fever inducing

TNF = increase vascular dilation and permeability

IL-6 = acute phase proteins - CRP, SAP (particularly CRP)

137
Q

CRP is a clinical indication of ?

A

indication of immune response

138
Q

type 1 and type 2 interferons

A

1 = alpha and beta

2 = gamma

139
Q

type 1 and type 2 interferons

A

1 = alpha and beta

2 = gamma

140
Q

intracellular TLR are in particular ?

A

viral RNA

141
Q

response of type 1 interferons

A

on healthy cells create antiviral replication proteins

on infected cells enhance killing via CTL (CD8 cells)

142
Q

response of type 2 interferons

A

enhanced macrophage killing

production of IgG abs

143
Q

antibodies are associated w/ ______ responses

A

humoral

144
Q

abs respond to ______-cell pathogens only, and abs can only circulate in ________.

A

extracell pathogens

in blood/tissues

145
Q

abs are produced by _____ and are apart of _______ immunity.

A

B cells

adaptive immunity

146
Q

effector properties of abs

A
  1. agglutination
  2. neutralize toxins
  3. activate complement
  4. opsonization
  5. regulatory properties
147
Q

agglutination

A

bind pathogens together

148
Q

opsonization facilitates ?

A

facilitates phagocytosis

149
Q

opsonization facilitates ?

A

facilitates phagocytosis

150
Q

effector regulatory properties w/ production of ?

A

cytokines for:
T cell response
inflammatory response

151
Q

general structure of abs

A

4 chains total

  • -2 light chains — either kappa or lambda
  • -2 heavy chains — 4 dif types
152
Q

light chain types of abs

A

kappa or lambda

will always be one or the other - not both

153
Q

regions of ab chains

A

Fab region = binds ag - small Y limbs

Fc region = carries out effector function - long Y limb

154
Q

what connects Fab and Fc regions

A

connected by hinges

allows binding of 2 ags at a time

155
Q

all abs start as ?

A

membrane bound

IgM or IgD

156
Q

membrane bound ab properties

A

has extra Ch domain
No tail piece
either IgM or IgD (B cell receptors)

157
Q

abs are either _______ or _______ bound.

A

secretory or memb bound

158
Q

secretory ab properties

A

has tail piece

IgE, IgA, IgG

159
Q

IgG can be both ?

A

memb bound and secretory

160
Q

papain

A

cleaves abs at hinges
leaves 2 separate Fabs and 1 Fc

so 3 pieces total

161
Q

where are papain and pepsin found?

A

papain = in papayas

pepsin = digestive enzyme in humans

162
Q

where are papain and pepsin found?

A

papain = in papayas

pepsin = digestive enzyme in humans

163
Q

pepsin

A

cleaves below hinges
leaves 1 Fab and 1 Fc

Fab can still bind 2 ags
Fc dissociates

Fab now called F(ab’)2

164
Q

what ags antibodies recognize

A

proteins
nucleic acids
polysaccharides

165
Q

proteins that abs recognize as ags

A

in conformational form
linear form
or cut form

166
Q

T cells can only recognize ____ ags

A

protein ags

167
Q

affinity

A

how tight an ag binds to an ab

increases w/ second exposure

168
Q

avidity

A

strength of an ag-ab complex

depends on affinity and valence

increases as valence increases

169
Q

valence

A

the number of ags that can bind to an ab

typically minimum is 2

170
Q

ag binding site for b cell receptor and TCR

A

binds to variable heavy and light chains

binds to variable alpha and beta

171
Q

type of ag that binds to b cell receptor and TCR

A

proteins, polysaccharides, lipids

proteins only – in linear form

172
Q

binding affinity: b cell receptors and TCR

A

higher

less than B cell binding

173
Q

B cell receptors

A

IgM and IgD

174
Q

immature B cells always produce _____ first

A

IgM

175
Q

mature B cells produce membrane ____ and _____ which are ?

A

IgM and IgD

mature B cell receptors

176
Q

mature B cells produce membrane ____ and _____ which are ?

A

IgM and IgD

mature B cell receptors

177
Q

activated B cells can maintain what ? and form ?

A

maintain memb IgM, IgD

form secretory abs (A,G,E)

178
Q

activated B cells can form secretory abs but is dependent upon ?

A

on T cells and cytokines they produce

179
Q

plasma cells have constant secretion of ?

A

abs

secretory abs only

180
Q

isotype switching requires ________.

to switch causes changes in ?

A

cytokines

change of heavy chain Fc portion
Fab stays the same

181
Q

compare structure of abs

A

G, E, D = normal monomers

M = pentamer w/ J chain

A = dimer w/ J chain + secretory section

182
Q

location of IgG

A

serum

highest level in serum (not body)

can invade tissues

183
Q

location of IgM

A

serum

naïve b cells

184
Q

location of IgE

A

mast cells

185
Q

location of IgA

A

mucosal areas

highest in these areas of the body

186
Q

location of IgD

A

naïve b cells only

187
Q

function of IgG

A

phagocytosis
can pass from mom to fetus
can be secreted
highest during 2ndary response

**highest in serum

188
Q

function of IgM

A 
complement activation
memb bound
**always present first
highest during primary response
high avidity
low affinity
189
Q

function of IgE

A

allergic response
can be secreted
acute inflammation
infections by worms

190
Q

function of IgA

A

mucosal defense
can be secreted
can cross endo memb

transferred in breast milk

191
Q

function of IgD

A

only found on b cells

192
Q

IgE is present during _____ responses via ______ cell activation.

A

allergic

mast cell activation

193
Q

cytokines that stimulate each ab

A 
G = IFN-y
M = IL-2,4,5
E = IL-4
A = TGF-B
194
Q

types of T cells

A

Th0
CD4
CD8

195
Q

Th0 = ?

A

naïve t cell

196
Q

CD4 T cells

A

T helper cells

recognize ags on MHC II on APCs

197
Q

types of t helper cells

A

Th1 = intracell pathogens
produce IFN-y

Th2 = extracell pathogens
help develop B cell to memory cells

198
Q

Cd8 t cells

A

cytotoxic T cells

associated w/ MHC class I

fights intracell pathogens

199
Q

describe T cell receptors (TCR)

A

only on t cell memb’s

most are made of alpha n beta chains

can only bind processed protein ag

200
Q

regions of TCRs

A

TM region w/ alpha/beta chains

constant regions
variable regions — have ag binding site

201
Q

ysigma T cells

A

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
Q

components of TCR complex

A

TCR - a n b chains
CD3
zeta chain
CD4 or CD8 (which bind to MHCs)

203
Q

CD3

A

–found on ALL t cells
–used as diagnostic tool to find t cells
–sends signals into t cell
= production/release of cytokines

204
Q

zeta chain

A

apart of TCR complex

–signaling part of complex

205
Q

MHC class I – loci genes

A

HLA-A
HLA-B
HLA-C

206
Q

MHC class II – loci genes

A

HLA - DQ
HLA - DR
HLA - DP

207
Q

MHC loci genes

A

each person gets 6 HLA genes

3 from mom/3 from dad
–allowing for variations

208
Q

MHC - class I properties

A
  1. on all nucleated cells (so not RBCs)
  2. contains 1 a chain
  3. **B-macroglobulin
  4. intracell pathogens
209
Q

MHC class I molecules bind to ?

A

short linear peptides

to CD8 t cells – binds to a chain

210
Q

there is enhanced expression of MHC - I with ?

A

IFNy

IFN-a/B

211
Q

MHC class II properties

A
  1. expressed on prof APCs
  2. two chains - a n B
  3. typically extracell peptides
212
Q

MHC class II molecules bind to ?

A

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
Q

enhanced expression of MHC-II under ?

A

IFN-y

214
Q

co-stimulation

A

CD40 – macrophages/DCs/B cells

CD40L – t cells

important for co-stimulation of t cell and activation of APC

215
Q

MHC-I processing pathway

A
  1. virus peptides tagged/destroyed
  2. TAP
  3. MHC-I created
  4. MHC-I:Ag complex sent to golgi
216
Q

virus peptides

A

tagged by ubiquinase

sent to proteasome for degradation

217
Q

TAP

A

this takes peptide fragments to ER

218
Q

creation of MHC-I

A

in ER

meets up and binds w/ virus peptides

219
Q

MHC-I:Ag complex is sent to ?

A

to golgi
to exocytotic vesicle
to memb

220
Q

MHC-II processing pathway

A
  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
Q

MHC-II processing — extracellular proteins are taken in via _______ and fuse ?

A

endocytosis

fuse w/ lysosome = phagolysosome

222
Q

creation of MHC-II

A

made in ER
processed by golgi
sent via exocytotic vesicle
fuses w/ phagolysosome

223
Q

CLIP

A

in the vesicle this binds MHC-II so that nothing else will bind it

224
Q

HLA-DM

A

removes clip

stabilizes binding of peptide to MHC-II

225
Q

define cross presentation

A

sometimes extracell pathogens are brought in via endocytosis
and leak into cytoplasm

226
Q

steps in cross presentation

A

extracell pathogens leak into cytoplasm

get tagged - Ub
–once tagged go thru MHC-I pathway

227
Q

results of cross presentation

A

results in extracell pathogens presented on MHC-I to be bound by CD8+ T cells

228
Q

peptide binding/recognition

A

LY

low yield

Immunology Exam 1 (8 decks)

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