Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Immuno > Immunology week 3 > Flashcards

Immunology week 3 Flashcards

1
Q

Clinical Correlation- Bovine Acute Mastitis (s. Aureus)
WHAT IS IT?
WHAT 2 THINGS CAN CAUSE IT?

A

● Mastitis is inflammation of the mammary gland. It can be due to ENV
factors or passed via a contagious animal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Clinical Correlation- Bovine Acute Mastitis (s. Aureus)

can it be clinical?
subclinical?

A

Mastitis can be clinical or subclinical

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Clinical Correlation- Bovine Acute Mastitis (s. Aureus)
what 3 things can it result in?

A

can result in necrosis, fibrin clots
in milk, or an elevated somatic cell count. (acute mastitis =
contagious)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Clinical Correlation- Bovine Acute Mastitis (s. Aureus)
how can you detect SCC?

A

○ Can detect SCC via the California Mastitis Test (CMT)
■ Agglutination of DNA which forms a gel in the milk-> presence of leukocytes
○ Automated cell counting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What causes acute mastitis

A

● S.aureus is a normal commensal of our microbiota therefore there are
likely other stressors occurring causing a flare up.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What causes acute mastitis
example?
why does it happen?

A

EX: Trauma from milking
○ bacT infects & proliferates in the teat
○ bacT releases PAMPS which are noticed by macs
○ Mac release proinflammatory mediators-> changes in vasculator
○ Serum proteins (Pro-inflam proteins) and chemoattractants are released
■ What would the CS be as a result????
■ Along with CS there will be an increase in the somatic cell count

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is inflammation?

A

●** Defense rxn of living tissue against damage aimed at removing the
cause of injury & repairing the tissue**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is inflammation?
what sort of immunity is it important?

A

● It is important in innate and adaptive immunity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is inflammation?
what is Acute inflammation?
when does it occur?
what happens?
what does it show a lot of?
what does it lead to?

A

● Acute inflammation
○ Early stages of infection
○ Actively eliminates pathogens
○ There are a lot of neutrophils
○ Leads to tissue repair

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is inflammation?
What is Chronic inflammation?
what does it have a lot of?
what happens?

A

● Chronic inflammation
○ Lots of macs
○ Has not reaches healing stage the proper way

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Causes & signs of inflammation

7 signs:

A

● Exogenous
● Endogenous
● Heat
● Redness
● Swelling
● Pain
● Loss of function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes & signs of inflammation
● Exogenous
what are the 3 types?

A

○ Physical agents
○ chemical
○ Biological

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Causes & signs of inflammation
● Exogenous
○ Physical agents
what are mechanical? what are thermal?

A

● Exogenous
○ Physical agents
■ Mechanicals-foreign objects,
fractures
■ Thermal-burns and freezing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Causes & signs of inflammation
● Exogenous
○ chemical
examples?

A

■ toxic gases, acids, bases, low pH,
etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Causes & signs of inflammation
● Exogenous
○ Biological-
examples?

A

○ Biological- bacT, viruses, parasites,
fungi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Causes & signs of inflammation
● Endogenous
2 types and examples?

A

● Endogenous
○ Circulation disorders- thrombosis,
infarction, hemorrhage
○ Metabolic products- uric acid and urea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Causes & signs of inflammation
● Heat
what happens?

A

● Heat
○ vasodilation-> rise in BF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Causes & signs of inflammation
● Redness
what happens?

A

● Redness
○ Lg volume of blood

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Causes & signs of inflammation
● Swelling
what happens?

A

● Swelling
○ Vascular permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Causes & signs of inflammation
● Loss of function
when does this happen?

A

● Loss of function
○ Occurs w/ more severe/ prolonged
inflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Causes & signs of inflammation
what are PRO-INFLAMMATORY CYTOKINES:

A

PRO-INFLAMMATORY CYTOKINES:
TNF-a, IL-1, IL-6,IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Inflammatory Mediators
7-what are they?

A

● TNFa, IL1, IL6, IL8
● Complement components
● Prostaglandins
● Leukotrienes
● Vasoactive amines (histamine, serotonin)
● PAF
● Plasma Proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Inflammatory Mediators
● TNFa, IL1, IL6, IL8
what do they activate?which releases what
what do they promote? which induces what

A

● TNFa, IL1, IL6, IL8
○ Activate the coagulation cascade, release of nitric oxide, PAF,
prostaglandins, & Leukotrienes
○ IL1, IL6, IL8= promote chemotaxis, induce extravasation of
granulocytes, & degranulation of neutrophils

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Inflammatory Mediators
● TNFa, IL1, IL6, IL8
● TNF-a & IL-1 specifically do what and induce production of what?

A

● TNF-a & IL-1
○ induce fever & stress
○ Induce production of IL-6, IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Inflammatory Mediators
● TNFa, IL1, IL6, IL8
● IL-6 specifically stimulatates production of what?

A

● IL-6
○ Stimulates production of acute phase proteins (CRP)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Inflammatory Mediators
● Complement components
what are the most relevent complement components? what do they do?

A

● C3a & C5a
○ Most relevant complement component for inflammation
○ C3a & C5a increase vascular permeability which stims chemotaxis of neutrophils, eosinophils, & monocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Inflammatory Mediators
● Prostaglandins
what do they do?
PGE 2 and 2 do what?
Thromboxane?

A

Prostaglandins
○ Contribute to vasodilation, cap. Permeability, pain, & fever
○ PGE1 &2 increase the effects of histamine
○ Thromboxane-(oddball)
■ Platelet aggregation & vasoconstriction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Inflammatory mediators
● Leukotrienes
what do they induce?
what are they?

A

○ Smooth muscle contraction
○ LTB4= chemoattractant of neutrophils
○ slow reacting substances of anaphylaxis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Inflammatory mediators
● Vasoactive amines (histamine, serotonin)
where are tehy found?
result?

A

● Vasoactive amines
○ Histamine & serotonin
■ Found in mast cells
■ Result in dilation & increased
permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Inflammatory mediators
● PAF-Platelet activating factor
what do they do?
what are they?
what result?

A

○ Activates neutrophils and is a potent eosinophil chemoattractant
○ Inc. plasma proteins and results in edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Inflammatory mediators
● Plasma Proteins
what is it?
what does it do?

A

● Kinins- bradykinin (physio1 flashback)
○ Increase capillary permeability & pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Inflammatory mediators
● Clotting factors
how do they work?

A

○ Blocks the BV from losing blood and blocks
pathogens from entering

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Inflammatory mediators

PRO-INFLAMMATORY
CYTOKINES: what are they?

A

PRO-INFLAMMATORY
CYTOKINES:

TNF-a, IL-1, IL-6,IL-8

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Stages of inflammation
what are the 2 stages?

A

● Vascular stage

● Cellular stage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Stages of inflammation
● Vascular stage
what are the 3 phases?
what happens?
what clinical signs?
what result?

A

● Vascular stage
○ Phase 1- vasoconstriction
■ Short lived
■ Allows for clothing to occur
○ Phase 2- active vasodilation
■ Dilation
■ Increase in BF & cellular
metabolism
■ Causes redness and heat
○ Phase 3- passive vasodilation
■ BV stop reacting to nervous and
humoral stimuli
■ Results in swelling, pain, and
impaired function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Stages of inflammation
● Cellular stage
what happens?

A

○ Movement of leukocytes into the area of
injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Stages of inflammation
● Cellular stage
● Chemotaxis-what is it?

A

● Chemotaxis- migrate in response to a
chemical rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

**Stages of inflammation
● Cellular stage
● Rolling-what is it?

A

●** Rolling**- leukocytes slow down increase
expression of adhesion molecules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Stages of inflammation
● Cellular stage
● Migration-what happens?

A

● Migration- to the tissue spaces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Stages of inflammation
● Cellular stage
● Phagocytosis-
what happens?

A

● Phagocytosis- neutrophils and macs
engulf/ degrade the bact, etc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Leukocyte trafficking & CAMS

what are the first
cells to move out of the vasculature.

A

● Neutrophils, macs, NK are the first
cells to move out of the vasculature.

42
Q

Leukocyte trafficking & CAMS
What is the relevance of CAMS?

A

Neutrophils, macs, NK are the first
cells to move out of the vasculature.
● They do this by using CAM to migrate to
tissues where inflammation is occurring.

43
Q

Leukocyte trafficking & CAMS
who express CAM’s

A

● Both the endothelium and leukocytes
express CAM’s.

44
Q

Leukocyte trafficking & CAMS
what are the 2 ways they are expressed?

A

● CAM
○ Constitutively expressed->
■ Expressed 24/7
○ Expressed on local conditions
■ Ex. inflammation

45
Q

Leukocyte trafficking & CAMS
what are teh 4 types of CAM’s

A

● The types of CAMS
○ Selectins
○ Mucins
○ Integrins
○ Ig- superfamily CAM

46
Q

Selectins & Mucins
Selectins
what do they bind to?
what are they responsible for?
3 types of selectin, what are they?

A

● Selectins
● Bind to carbohydrate moieties
●** Responsible for leukocyte interaction
with the endothelium during the
initial vascular phase of
inflammation**
● Selectin L (CD62L)
● **Selectin E (CD62E)
● **Selectin P (CD62P)

47
Q

Selectins & Mucins
● Selectins
● Selectin L (CD62L)
how is it expressed?

A

● Selectin L (CD62L)
○ Expressed on leukocytes

48
Q

Selectins & Mucins
● Selectins
● **Selectin E (CD62E)
when is it synthesized?

A

● **Selectin E (CD62E)
○ Synthesized following stimulation

49
Q

Selectins & Mucins
● Selectins
selectin P (CD62P)
where is it contained?
what happens?

A

● **Selectin P (CD62P)
○ Contained in granules in endo. Cells
○ Released granules fuse w/ the cell
membrane

50
Q

Selectins & Mucins
● Mucins
name 2

A

CD34 aka GlyCAM-1
PSGL-1

51
Q

Selectins & Mucins
● Mucins
● CD34 aka GlyCAM-1
what does it bind to?

A

● CD34 aka GlyCAM-1 binds to CD62L

52
Q

Selectins & Mucins
● Mucins
● PSGL-1
where is it?
what does it bind to?
where does it bind?

A

● PSGL-1 on neutrophils binds to
selectins E and P on endothelial cells

53
Q

integrins & Ig Superfamily
● Integrins
what are they?

A

● Heterodimeric proteins that contain an
A & B chains which forms a binding site
that the ig- superfamily can bind to

54
Q

integrins & Ig Superfamily
● Integrins
divide into subgroups based on what?

A

● Divided into subgroups based on beta
chain (B1-B7)

55
Q

integrins & Ig Superfamily
● Integrins
B2 is expressed by what?
what does a deficiency in B2–>

A

B2=expressed by leukocytes
○ Deficiency in B2-> LAD

○ Leukocyte adhesion deficiency-

56
Q

integrins & Ig Superfamily
● Integrins
what is: Leukocyte adhesion deficiency

A

**Leukocyte adhesion deficiency-
autosomal recessive disease

(recurrening bacT infections)b/c
neutrophils cannot extravasate.**

57
Q

integrins & Ig Superfamily
● IG superfamily
what is it?
what does it bind to?
how is it expressed?
4 kinds?

A

IG superfamily
○ Immunoglobulin like domains
○ Binds to integrins
○ Expressed on endothelial cells
○ ICAM-1 (CD154)
○ ICAM-2 (CD102)
○ ICAM-3 (CD50)
○ VCAM (CD106)

58
Q

integrins & Ig Superfamily
● IG superfamily
○ MadCAM-1contains what? what does it bind to?

A

○ MadCAM-1 contain IG-like domains
and mucin domains
■ Able to bind to both selectins
and integrins

59
Q

Leukocyte extravasation
4 steps, what are they?

A
  1. Rolling
  2. Activation
    ● Adhesion
    ● Diapedesis (migration)
60
Q

Leukocyte extravasation
1. Rolling
what happens?
what binds to what, where?
what result?

A

Rolling
○ Leukocytes mucin CAMS bind to selectin
E & P on endothelial cells.
■ They slow down and they roll on
the endothelium

61
Q

Leukocyte extravasation
Activation
what happens?
an increase in what by whatand and increase of what leads to what?

what happens at this stage?

A

Activation
○ Increase in chemokine secretion by
endothelial cells and increased
chemokine receptor expression on
leukocytes results in the activation of
leukocytes
○ Integrins on leukocytes change to
high- affinity state

62
Q

Leukocyte extravasation
Adhesion
what binds to what?
what happens here?

A

Adhesion
○ Integrins bind firmly to the endothelium
○ Immobilization (handcuffed) -> this is
where migration will occur!

63
Q

Leukocyte extravasation
Diapedesis (migration)
who does what here and goes where?
who binds, how?

see slide 14 for diagram

A

Diapedesis (migration)
○ Leukocytes squeeze between endo. Cells
and go to the site of inflammation
○ Leukocytes bind to endo via PECAM-1
(CD131)!

64
Q

Neutrophil and monocyte extravasation
● Neutrophil extravasation

when do they arrive?
when do they bind?
what are they activated by?
does Selectin L bind?
PSGL-1 causes what to bind?
An increase of what, where allowas for what to happen?

A

● Neutrophil extravasation
○ First cell to arrive!!!
○ Only bind to endo if there is
inflammation
○ IL-8 & MIP-B activate neutrophils
○ Selectin L (binds to glycam)
○ PSGL-1 (binds selectins P & E)
○ Increase ICAM on endo and CD11a/
CD18 & CD11b/ CD18 (LFA-1 & MAC-1)
on neutrophil allows for adhesion and
migration

65
Q

Neutrophil and monocyte extravasation
● Monocyte extravasation
when does it arrive?
what is expressed when?

A

● Monocyte extravasation
○ Late to the party!
○ VCAM and ICAM-1 is only expressed
after activation

66
Q

Neutrophil and monocyte extravasation
Monocyte extravasation
what is Homeostatic migration
what is it regulated by
what leads to rolling?
what leads to activation
what leads to migration?

A

Homeostatic migration
○ Small amount of monocytes can
extravasate under normal conditions to
replenish macs!
○ Regulated by CXCL14
○ CD62L (selectin L)-> rolling
○ MCP-1 -> activation
○ PECAM-1-> migration

67
Q

Neutrophil and monocyte extravasation
Monocyte extravasation
what do complement receptors do?

A

Complement receptors such as CR3 &
CR4 bacT peptides participate in
extravasation of monocytes into
inflamed tissue

68
Q

Neutrophil and monocyte extravasation
PRO-INFLAMMATORY CYTOKINES:

A

PRO-INFLAMMATORY CYTOKINES:
TNF-a, IL-1, IL-6,IL-8

69
Q

Lymphocytes
Lymphocyte extravasation
what can they do, resulting in what?
what can they pass through?
what are involved?

A

● Lymphocyte extravasation
○ Can recirculate and they live longer!
○ They pass through capillary venules
called endothelial venules (HEV)
○ Selectins E and P, mucins, GlyCAM-1,
ICAM-1, 2, 3, VCAM-1 and MadCAM-1=
are involved

70
Q

Systemic manifestations of inflammation
Typically we want the inflammatory
response to stay where?

A

Typically we want the inflammatory
response to stay in a localized area but
this may not always happen.

71
Q

Systemic manifestations of inflammation
name 4

A

Manifestations of systemic inflammation
■ Acute phase response
■ Alterations in WBC count
■ Pyrexia
■ Sepsis and septic shock

72
Q

Systemic manifestations of inflammation
Systemic effects of inflammation
name 5

A

Systemic effects of inflammation
○ Loss of appetite
○ Altered sleep patterns
○ Lethargy
○ Muscular wasting
○ Metabolic acidosis

73
Q

Inflamation
Manifestations of inflamation
Name 9

A

Inflamation
Manifestations of inflamation
-acute phase proteins
leukocytosis and leutopenia
high fever
sepsis, septic shock
anorexia
altered sleep patterns
lethargy
muscular wasting
metabolic acidosis

74
Q

inflammation
what happens to acute phase proteins?
what are they?

A

Acute phase proteins ○ Serum proteins that either increase or
decrease in number during infection ■ Complement ■ C-reactive proteins ■ Haptoglobin ■ Serum amyloid
○ IL6 is the main proinflam cytokine that
signals for APP

75
Q

Inflammation
what constitutes a minor, moderate, major positive APP- Increase?

A

Positive APP- increase ○ Major- increase over 100-1000 fold &

peaks at 24-48 hrs
○ Moderate increases 5-10 fold peaks at
48-72 hrs
○ Minor gradually increases 50-100%

76
Q

Inflammation
what is a negative APP?

A

● Negative APP- decrease

77
Q

Resolution of inflammation
if not terminated what happens?

A

If not terminated chronic inflammation and cellular destruction will occur

78
Q

Resolution of inflammation
what is released?

A

TGF Beta from macs are released

79
Q

Resolution of inflammation
what is down regulated?

A

IL-4 and IL-10 downregulate proinflammatory cytokines
● Downregulation of leukotrienes

80
Q

Resolution of inflammation
what is upregulated?

A

Upregulation of anti-inflammatory molecules like Interleukin 1 receptor
antagonist or the double tumor necrosis factor receptor

81
Q

Resolution of inflammation
Apoptosis of what?

A

Apoptosis of proinflammatory cells

82
Q

Resolution of inflammation
pro-inflammatory cytokines have what sort of life?

A

Also the pro-inflammatory cytokines have a short half life

83
Q

Resolution of inflammation
Neutrophils undergo what?

A

Neutrophils undergo apoptosis

84
Q

Resolution of inflammation
Resolvins and protectins from where cause what to what?

A

Resolvins and protectins (from omega 3 polyunsaturated fatty acids) cause
apoptosis of neutrophils*

85
Q

Resolution of inflammation
what happens to macs?

A

It ends with macs leaving through the lymphatics
○ Why does it make sense that macs would be the last to leave? (Think about M2)

86
Q

outcomes

what happens in short lived inflammation?

A

Resolution- complete restoration of the
inflamed tissue
○ Occurs in short lived inflammation

87
Q

outcomes
what can happen with fibrosis and functional impairment?

A

Fibrosis- forms a scar & functional
impairment can occur

88
Q

outcomes
what might form?

A

Abscess formation

89
Q

outcomes
chronic inflamatio causes what?

A

Chronic inflammation- prolonged
inflammation
○ Tissue destruction

90
Q

You are trying to explain the clinical signs of
inflammation to your coconut retriever. Which of the
following is not a sign of inflammation?
A. Heat
B. Redness
C. Increase production of IL4
D. Increase production IL1
E. Loss of function

A

C

91
Q

You are taking a study break and watching the lion king.
While you were watching it, you started thinking about
immunology because you are a bomb a$$ immunology
student. Which outcome of inflammation is paired
correctly?

a. Fibrous- scar
b. Resolution- abscess
c. Chronic- complete recovery
d. None of the above are correct

A

A

92
Q

You are laying on the beach and all of the sudden your
immunology TA comes up to you and asks “Why are
monocytes/ macrophages late to the party?” What do
you tell her?
A. They need sleep
B. Don’t trick us they’re first!
C. VCAM is only expressed after activation
D. Selectin E has to be induced
E. GO AWAY

A

C

93
Q

DYour Immunology TA wont take a hint and keeps asking you
about immunology. What do you say to her when she asks what
must undergo a high affinity conformational change to allow for
adhesion?
A. Chemokines
B. Leukocytes
C. Chemotaxis
D. Integrins
E. Selectins
F. TLR

A

D

94
Q

You are explaining to your techs why the serum protein
levels from malibu (your patient) look off. What is true
about major acute phase proteins?
A. You’re making things up
B. They decrease over 100- 1000 fold at 24-48 hrs
C. They increase 5-10 fold peaks @ 48-72 hrs
D. They increase over 100-1000 fold
E. They gradually increase to 1000x over an extended period of time

A

D

95
Q

You’re laying in bed at aprox. 1:59 am thinking about immunology.
Which mediators aid in the resolution of inflammation?
A. TNF B
B. IL1
C. IL2
D. IL6
E. IL8
F. IL7
G. TNF y
H. TNF a
I. IL4
J. IL10

A

A I J

96
Q

You are still in bed but now it is 3 am. You’ve tried counting sheep
but nothing is working so you are still thinking about immuno. Which
of the following are proinflammatory cytokines
A. TNF b
B. IL1
C. IL2
D. IL6
E. IL8
F. IL7
G. TNF y
H. TNF a

A

BDEH

97
Q

What are manifestations of inflammation?

A

What are manifestations of inflammation?
● Manifestations of inflammation
○ Acute phase proteins
○ Leukocytosis and leukopenia
○ High fever
○ Sepsis, septic shock
○ Anorexia
○ Altered sleep patterns
○ Lethargy
○ Muscular wasting
○ Metabolic acidosis

98
Q

You are currently living your best life being a DOGtor and you are
explaining to Fluffys owners why he has inflammation but you went on a
rant and brain dumped all of your second semester knowledge from
immunology on them. Which of the following is something you may have
told fluffy’s humans?
A. Selectins bind to Ig superfamily
B. Integrins bind to mucins
C. MadCAM-1 contains IG- like domains and mucin domains so it is able to
bind to mucin and selectins
D. Selectin E and P are expressed only after being stimulated

A

D

99
Q

You have a patient, fireball, who has been suffering from
recurrent severe BacT infections.which of the following
could be an explanation on why they are constantly
having BAcT infections????

A. We haven’t had BacT yet
B. Genetics
C. Evolution
D. There is a B2 deficiency which results in LAD and as a result neutrophils
cannot extravasate.

A

D

100
Q

Your Grandma calls you because she thinks you are just living on
an island hanging out and you have all of the time in the world to
chat. As a result, you decided to start explaining to her how
monocytes extravasate. What would part of your explanation
say???
A. Monocytes can undergo homeostatic migration to replenish macrophages
to tissues.
B. Selectin L is important for rolling
C. MCP-1 is important for activation
D. PECAM-1 is important for migration
E. All of the above
F. Monocytes don’t extravasate, macrophages do.

A

E

Immuno (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions