Immunology Test 2

Front 1

List 4 types of epithelial barriers.

Back 1

mechanical
antimicrobial substances
phagocytes
normal microbial flora

Front 2

"Cleansing" mechanisms of the skin and GIT

Back 2

skin = desquamation
GIT = mucus and peristalsis

Front 3

"Cleansing" mechanisms of eyes and respiratory tract

Back 3

eyes = tears and lashes
respiratory = mucus and cilia

Front 4

Lysozyme

Back 4

antimicrobial substance that breaks down cell wall

Front 5

2 iron-binding proteins

Back 5

transferrin and lactoferrin

Front 6

2 ways that normal microbial flora inhibit establishment of new organisms

Back 6

competing for nutrients and space.
releasing antimicrobial substances.

Front 7

ileus (and its results)

Back 7

lost of peristalsis.

results in overgrowth of flora and crossing of GI bacteria into bloodstream

Front 8

2 professional phagocytes
(1 cell capable, but not professional)

Back 8

neutrophils and macrophages
(eosinophil)

Front 9

Where is neutrophil normally found?

When is it recruited during infection?

Is it long or short lived?

Back 9

found in blood

recruited early in infection

short lived

Front 10

3 phases of phagocytosis

Back 10

recognition and attachment
internalization
killing/destruction

Front 11

2 types of recognition/attachment in phagocytosis

Back 11

direct (PRR); recognize cell membrane)
indirect (recognize opsonins attached to cell membrane)

Front 12

2 significant opsonins in indirect recognition in phagocytosis

Back 12

C3b
IgG

Front 13

3 types of killing/destruction in phagocytosis

Back 13

O2 dependent (antimicrobial lysosymes)
O2 independent (respiratory burst)
NO dependent

Front 14

2 molecules that generate nitric oxide (NO) radicals

Back 14

macrophages
INF- gamma

Front 15

Where are complement proteins found?

Back 15

plasma
interstitial fluid
secretions

Front 16

3 complement pathways

Back 16

classical (activated by IgM or IgG)
alternative (actvated by microbial cell walls)
lectin (activated by collectins)

Front 17

How is the classical complement pathway activated?

Back 17

IgG or IgM

Front 18

How is the alternative complement pathway activated?

Back 18

bacterial cell walls and basement membrane

Front 19

How is the lectin complement pathway activated?

Back 19

collectins

(a type of PRR- pattern recognition receptor)

Front 20

4 functions of complement

Back 20

mast cell activation
chemotaxis (neutrophil recruitment)
opsonization
pore formation (microbe killing)

Front 21

What complement mediators activate mast cells?

Back 21

C3a
C5a

Front 22

What complement mediator activates the recruitment of neutrophils (via chemotaxis)?

Back 22

C5a

Front 23

What complement mediator activates phagocytosis?

Back 23

C3b

Front 24

What complement mediator activates pore formation?

Back 24

C5b678(9)n

Front 25

4 types of cell signaling

Back 25

juxtacrine
autocrine
paracrine
endocrine

Front 26

What is chemokine's effect on WBC movement?

Back 26

WBCs move from low to high concentration (travel to inflammation site)

Front 27

2 types of chemokines (proteins that attract WBCs)

Back 27

interleukins (IL)
colony-stimulating factors (CSF)

Front 28

4 cytokine families (based on function)

Back 28

hemotopoietic
inflammatory
antiviral
immunologic

Front 29

Action of G-CSF (cytokine)

Back 29

promote neutrophil production

Front 30

3 pro-inflammatory cytokines

Back 30

IL-1
IL-6
TNF-alpha

Front 31

Which cytokine activates eosinophils?

Back 31

IL-5

Front 32

3 anti-viral cytokines

Back 32

INF-alpha
INF-beta
INF-omega
(all are Type 1 interferons)

Front 33

What 2 things is inflammation intending to eliminate?

Back 33

eliminate cause of cell injury
eliminate dead cells and tissue

Front 34

2 functions of ACUTE inflammation

Back 34

dilute/remove injuring agent
prepare tissue for healing

Front 35

3 microvascular processes in acute inflammation

Back 35

vasodilation
increased vascular permeability
leukocyte emigration

Front 36

What is the role of increased vascular permeability in acute inflammation?

Back 36

allows plasma proteins (complement, Abs) to "leak" to infection site

Front 37

2 features of infection that the sentinel cells recogize

Back 37

PAMPs
DAMPs

Front 38

4 types of sentinel cells

Back 38

epithelial cells
macrophages
dendritic cells
mast cells

Front 39

What 3 inflammation mediators activate vasodilation?

Back 39

histamine
seratonin
prostaglandin E2

Front 40

Role of C5a, chemokines, and bacterial peptides in acute inflammation

Back 40

chemotaxis

Front 41

Role of interferons?

Back 41

inhibit VIRAL replication

Front 42

What cells secrete Type 1 interferons?

Back 42

any cell infected by viruses

Front 43

What cells secrete Type 2 interferons (responsible for immume and inflammatory responses)?

Back 43

Th1 lymphocytes and NK cells

Front 44

What type of interferon is INF-gamma?

Back 44

Type 2

Front 45

What class of lymphocyte is part of innate immunity?

Back 45

NK cells

Front 46

How do NK cells activate macrophages?

Back 46

Secrete INF-gamma

Front 47

Function of MHC

Back 47

transport intracelllar antigens to the cells surface where TCR (T-cell receptor) can see it

Front 48

Which MHC class presents antigens to CD8 T-cells?

Back 48

MHC class 1

Front 49

Which MHC class presents antigens to CD4 T-cells?

Back 49

MHC class 2

Front 50

Which MHC class and T-cell type are responsible for intracellular antigens?

Back 50

MHC class 1
CD8

Front 51

Which MHC class and T-cell type are responsible for extracellular antigens?

Back 51

MHC 2
CD4

Front 52

4 key features of lymphocytes

Back 52

re-circulation (blood->lymph tissue->blood)

1 lymphocyte for 1 antigen

clonal proliferation

confer memory to adaptive immunity

Front 53

Which lymphocyte secretes antibodies?

Back 53

B cells

Front 54

Where are B-cells located in lymphoid tissue?

Back 54

follicles/nodules

Front 55

Where are T-cells located in lyphoid tissue?

Back 55

diffuse tissue

Front 56

Identifying surface molecule of B-cells

Back 56

CD79

Front 57

Identifying surface molecule of Tcells

Back 57

CD3

Front 58

Identifying surface molecule of helper T-cells (Th1, Th2, T17, Tfh)

Back 58

CD4

Front 59

Identifying surface molecules of cytotoxic T-cells (Tc)

Back 59

CD8

Front 60

What type of lymphiod tissue are bone marrow, thymus,a nd cloacal bursa?

Back 60

primary

Front 61

Where do B and T-cells mature?

Back 61

primary lymphoid tissue

Front 62

What type of lymphoid tissue are spleen, lymph nodes, and MALT?

Back 62

secondary

Front 63

Where do lymphocytes respond to antigens?

Back 63

secondary lymphoid tissue

Front 64

Describe the circulation pattern of "naive" lymphocytes?

Back 64

circulate between blood and secondary lymphoid tissues

Front 65

Describe the circulation pattern of memory lymphocytes

Back 65

return to the type of lymphoid tissue in which they were 1st activated

Front 66

Pro/Con of intranasal vaccine for mucosal infection.

Back 66

pro = provide better local immunity

con = duration of immunity is not as long as if vaccine was administered systemically

Front 67

What central tolerance selection process occurs in primary lymphoid tissue?

Back 67

Negative selection
Immature lymphocytes that have affinity to ANY antigen are destroyed (since they are likely self antigens)

Front 68

Describe positive selection process in the cortex of thymus

Back 68

Immature lymphocytes that do NOT recognize MHC are destroyed

Front 69

If an immature lymphocyte recognizes MHC class 1, it will become _______.

Back 69

a mature CD8 T-cell

Front 70

If an immature lymphocyte recognizes MHC class 2, it will become _________.

Back 70

a mature CD4 T-cell

Front 71

Describe the negative selection process in the medulla of the thymus

Back 71

Immature lymphocytes that have HIGH affinity for MHC molecules are destroyed

Front 72

4 phases of antibody responses

Back 72

lag
log
plateau
decline

Front 73

4 features/steps of lymphocyte activation (cell-mediated immunity)

Back 73

recognition
activation
proliferation
differentiation

Front 74

2 types of cells produced in differentiation during CMI

Back 74

effector and memory cells

Front 75

Compare primary and secondary immune responses in terms of kinetics, magnitude, Ab class, affinity for Ag, and TCR affinity for Ag

Back 75

kinetics = 2nd is faster
magnitude = 2nd is greater
Ab class= 1st(IgM) 2nd(IgA, IgG, IgE)
Ab affinity = 2nd Ab's have greater affinity
TCR affinity = no change

Front 76

3 ways immune responses are terminated

Back 76

antigen is eliminated (no longer a stimulus)

IgG antibodies inhibit B-cell activation (feedback inhibition)

Treg cells secrete suppressive cytokines that inhibit T and B-cell activation

Front 77

Where is IgG made? Where are they found?

Back 77

made in systemic immune system.

found in plasma and tissue fluids

Front 78

Where is IgM made? Where is it found?

Back 78

made is systemic immunse system and MALT.

found in plasma

Front 79

Which antibody is secreted in pentomeric form?

Back 79

IgM

Front 80

Where is IgA made? Where is it found?

Back 80

made in MALT.

found in secretions and plasma (low)

Front 81

Where is IgE made? Where is it found?

Back 81

made in MALT.

found in mast cells

Front 82

Which antibody is secreted as a dimer?

Back 82

IgA

Front 83

5 functions of antibodies

Back 83

neutralization
complement activation
opsonization
antibody dependent cellular cytotoxicity (ADCC)
mast cell activation

Front 84

Inhibition by binding and preventing attachment to cellular receptors is called _____.

Back 84

neutralization

Front 85

__________ is the process by which a cell internalizes fluids and soluble molecules.

Back 85

pinocytosis (cell drinking)

Front 86

________ is the reaction of an antibody or antigen receptor with more than one antigen receptor

Back 86

cross reaction

Front 87

What is an epitope?

Back 87

the site on an antigen that is recognized by an antigen receptor

Front 88

The most important cell that presents Ags to naive CD4 cells are ________.

Back 88

myeloid dendritic cells

Front 89

5 types of effector CD4 cells

Back 89

Th1
Th2
Th17
Tfh
Treg

Front 90

Where is IgA made? Where is it found?

Back 90

made in MALT.

found in secretions and plasma (low)

Front 91

Where is IgE made? Where is it found?

Back 91

made in MALT.

found in mast cells

Front 92

Which antibody is secreted as a dimer?

Back 92

IgA

Front 93

5 functions of antibodies

Back 93

neutralization
complement activation
opsonization
antibody dependent cellular cytotoxicity (ADCC)
mast cell activation

Front 94

Inhibition by binding and preventing attachment to cellular receptors is called _____.

Back 94

neutralization

Front 95

List 3 mediators that induce acute-phase response

Back 95

IL-1
IL-6
TNF-alpha

Front 96

List the disease progression from SIRS (systemic inflammatory response syndrome) to death.

Back 96

SIRS-->sepsis-->severe sepsis-->septic shock-->MODS (multi-organ dysfunction)-->death

Front 97

_____ is a uncontrollable inflammatory response to an infection.

Back 97

sepsis

Front 98

List at least 3 clinical signs for SIRS

Back 98

hyperthermia/hypothermia
tachycardia
leukopenia (low WBC count)
leukocytosis (high WBC count)
tachypnea

Front 99

Disregulation of coagulation is a clinical sign of _________.

Back 99

sepsis

Front 100

During sepsis, is the immune response too weak or too strong?

Back 100

Either. Too weak to fight infection or so strong it damages organs.

Front 101

Describe the PIRO staging system for sepsis.

Back 101

P = predisposition (genetic, environmental)
I = infection (source, severity)
R = response (proof, via labwork, clinical signs)
O = organ dysfunction (# and magnitude)

Front 102

List atleast 2 conventional treatments for sepsis

Back 102

plasma (increase Abs)
fluid therapy
broad spectrum Abs
flush inflammed areas

Front 103

List at least 2 non-traditional treatments for sepsis.

Back 103

insulin therapy
glucocorticoids (immune suppresant)
activated protein C

Front 104

3 characteristics of a "good" antigen

Back 104

large size
complexity
foreigness