X_Exam1 Mfm2_13

Front 1

white blood cells are also know as ...

Back 1

leukocytes

Front 2

what are the 3 most abundant leukocytes (in order of abundance):
1.
2.
3.

Back 2

1. neutorphil
2. lymphocyte
3. monocyte

Front 3

what type of leukocytes are derived from a common myeloid precursor in the bone marrow:
1.
2.
3.
4.
5.
6.

Back 3

1. neutorphils
2. eosinophils
3. basophils
4. monocytes
5. dendritic cells
6. mast cells

Front 4

what type of leukocytes are derived from a lymphoid precursor:
1.
2.

Back 4

1. B and T cells
2. natural killer cells

Front 5

what type of blood cells are derived from an erythoid precrusor:
1.
2.

Back 5

1. platelets
2. erythrocytes

Front 6

what are macrophages:

Back 6

monocytes that have moved out of the bloodstream into tissue

Front 7

... are usually the first effector cells/phagocytes that a pathogen encounters when it invades the body

Back 7

Macrophages

Front 8

Macrophages are (long/short) -lived and participate in (innate/adaptive/both) immunity

Back 8

long
both

Front 9

Macrophages are activated upon binding of specific ... to several types of cell-surface receptors. Activation leads to enhanced ... and release of ...

Back 9

ligands
phagocytosis
inflammatory cytokines

Front 10

macrophages and other phagocytes utilize ... that recognize conserved molecular moieties called ... that are frequently found on bacteria, viruses, and fungi

Back 10

pattern recognition receptors (PRR)
pathogen-associated molecular patterns (PAMPs)

Front 11

binding of ... ligands to ... by ... induce intracellular signaling in the phagocyte, leading to enhanced phagocytosis and cytokine secretion

Back 11

PAMP
PRRs
macrophages and other phagocytes

Front 12

fill in the table:

Back 12

(see figure)

Front 13

what are the macrophage receptors discussed in class:
1.
2.
3.
4.
5.
6.

Back 13

1. LPS receptor (CD14)
2. CR3, CR4
3. Mannose receptor
4. Scavenger receptor
5. Glucan receptor
6. Toll-Like Receptors (TLRs)

Front 14

toll-like receptors are 10 receptors with specificities for ... and the activation of TLRs results in increased production and secretion of ... by ...

Back 14

different microbial products
cytokines
macrophages

Front 15

identify the important cytokines

Back 15

(see figure)

Front 16

..., ..., and ... are referred to as endogenous pyrogens because they result in heat production in the body and act on temperature-control sites in the ..., and on ... and ..., altering energy mobilization to generate heat.

Back 16

IL-1
IL-6
TNF-alpha
hypothalamus
muscle
fat cells

Front 17

what causes fever:
1.
2.

Back 17

1. hypothalamic response to cytokines
2. muscle and adipose cells alter energy mobilization to generate heat

Front 18

what are the effects of fever:
1.
2.
3.
4.

Back 18

1. bacterial and viral replication decreased
2. antigen processing is enhanced
3. adaptive immunity more potent
4. human cells become more resistant to negative effects of TNF-alpha

Front 19

In addition to causing fever, IL-1, IL-6, and TNF-alpha act on ...(cell type) in the ... to induce synthesis of acute-phase proteins. These acute-phase proteins include ... and ... both of which act as opsonins and complement activator, and ... a protein involved in blood clotting.

Back 19

hepatocytes
liver
C-reactive protein
mannose-binding lectin
fibrinogen

Front 20

why is mannose-binding lectin highly specific for only bacterial cells:

Back 20

due to the proper spacing of mannose and fucose residues on the bacterial cell surface

Front 21

C-reactive protein and mannose-binding lectin both act as ... and ...

Back 21

opsonins
complement activators

Front 22

what are the 5 main facts about neutrophils discussed in class:
1.
2.
3.
4.
5.

Back 22

1. recruited to sites of infection by macrophage inflammatory mediators (esp. CXCL8)
2. NOT found in normal healthy tissue
3. most abundant circulating WBC
4. short-lived (less than 2 days)
5. about 60% of hematopoietic activity in bone marrow devoted to neutrophil production

Front 23

the primary function of neutrophils is ... and they form ... upon death

Back 23

powerful phagocyte
pus

Front 24

During phagocytosis, there is an increase in ... and ... consumption which is referred to as the ... which allows for ... killing of bacteria through the generation of reactive oxygen species. In addition, bacteria can be killed by pre-formed substances released from ... or ... when they fuse with the phagosome. This is referred to as ... killing.

Back 24

glucose
oxygen
respiratory burst
oxygen-dependent
granules
lysosomes
oxygen-independent

Front 25

Chronic Granulomatous Disease:
1. caused by:
2. what gets impaired:
3. what is the result:
4. and what is also the result:

Back 25

1. inherited deficiency in NADPH oxidase
2. phagocytic oxygen-dependent killing
3. chronic, recurrent infections with catalase-positive microorganisms (Staphylococcus, Klebsiella, Serratia, Aspergillus)
4. chronic inflammatory symptoms like gingivitis, enlarged lymph glands, tumor-like granuloma masses

Front 26

Neutrophils are usually the (first/second) effector cell encountered by a pathogen. because they must migrate from out of the ... into the ... in response to ... cytokine and chemokine release.

Back 26

second
bloodstream
infected tissue
macrophage

Front 27

how do neutrophils migrate from blood into infected tissue:

Back 27

they roll along vascular endothelial surface becuase selectin-mediated adhesion to s-Lex is weak

Front 28

what are the 4 steps in neutrophil extravasation:
1.
2.
3.
4.

Back 28

1. Weak rolling adhesion of the neutrophil along the endothelial wall mediated by E-selectin
2. Tight binding between the neutrophil and endothelial cell that traps neutrophil - mediated by ICAM-1
3. Diapedesis involves the ameoboid-like movement of the neutrophil in between two adjacent endothelial cells
4. Migration of the neutrophil through the interstitial fluid to the site of infection - mediated by CXCL8

Front 29

important things to remember about the adhesion molecules selectins do:
1.
2.
3.
4.

Back 29

1. stored in Weibel-Palade bodies inside vascular endothelial cells
2. expressed at cell surface in response to inflammatory mediators
3. weakly bind to sialyl-Lewisx carbohydrates of cell-surface glycoproteins on leukocytes
4. allow for neutrophil “rolling”

Front 30

adhesion molecules to remember (and why): integrins:
1.
2.
3.
4.

Back 30

1. LFA-1 and CR3 on neutorphil cell surface
2. ICAM-1 on endothelial cells
3. CXCL8 stops neutorphil rolling
4. LFA-1 and CR3 in diapedesis

Front 31

1. what casues Leukocyte Adhesion Deficiency:

2. what effect does it have on leukocytes:

3. what does not get formed:

4. what are the symptoms:

Back 31

1. absence of CD18 – the common β2 chain of many integrin molecules
2. unable to undergo adhesion-dependent migration
3. abscess or pus
4. recurrent, chronic bacterial infections (omphalitis common in infants)

Front 32

NK cells are the effector cells that kill .... and ... NKs are very important in combating ... infections (along with interferons).

Killing is accomplished through the release of ... and ... that form pores in the target cell membrane, leading to the induction of apoptosis.

Back 32

infected cells in the body
pre-cancerous and cancer cells
viral
granular perforins
granzymes

Front 33

cytotoxicity of NKs is increased dramatically by ..., ..., and ...

Back 33

IFNs
IL-12
TNF-alpha

Front 34

..., ..., and ... increase the proliferation and activation of NK cells to quickly eliminate viral infections

Back 34

IFNs
IL-12
TNF-alpha

Front 35

NK cells express a variety of receptors that help them recognize ... present on the surface of infected cells. NK receptors can either be ...-like or ...-like in structure. In addition, NK receptors are either ... or ... in function.

Back 35

ligands
immunoglobulin
lectin
activating
inhibitory

Front 36

NK cells have ... and ... receptors that interact with ligands, Upon interaction with a ... of a healthy cell, the inhibitory signal always dominates, preventing activation of the NK cell

Back 36

activating
inhibitory
MHC class I molecules

Front 37

what happens to MHC class I molecules of infected cells:

Back 37

its conformation may change or its expression may be lost

Front 38

alloreactions are mediated by ...

Back 38

NKs

Front 39

what are the important facts about eosinophils:
1.
2.
3.
4.

Back 39

1. second most abundant granulocyte
2. defend against helminth worms and other intestinal parasites
3. involved in allergies and asthma
4. release cytokines, lipid mediators, and reactive oxygen species through degranulation

Front 40

what are the important facts about basophils:
1.
2.
3.

Back 40

1. least abundant granulocyte
2. degranulate releasing histamine and other powerful cytokines, as well as proteolytic enzymes and other inflammatory mediators
3. allergic responses

Front 41

what are the minority subpopulations of B and T cells that contribute to innate immunity:
1.
2.
they are considered to be a component of the innate immune response due to their ...

Back 41

1. B-1 lineage of B cells
2. γ:δ T cells
presence at birth

Front 42

what are the Major sequence of events in the innate immune response:
1.
2.
3.

Back 42

1. Complement activation
2. Macrophage activation
3. Neutrophil extravasation and activation

Front 43

Recruitment of neutrophils into tissue, peaks within ...hours
Neutrophil-derived chemoattractants recruit more monocytes, macrophages, and eosinophils within ... hours

Back 43

6
5 to 6

Front 44

what are the major players of the innate immune response:
1.
2.
3.
4.
5.

Back 44

1. Complement
2. Macrophages
3. Neutrophils
4. Chemokines and cytokines
5. NK cells

Front 45

what are the hallmarks of inflammation:
1.
2.
3.
4.

Back 45

1. calor (heat)
2. dolar (pain)
3. rubor (redness)
4. tumor (swelling)

Front 46

Phagocytes like ... and ... become “antigen-presenting cells” that activate .... Cytokines released during the innate immune response “prime” the adaptive immune response.

Back 46

macrophages
dendritic cells
T cells

Front 47

Inflammation results from vascular changes that occur in local blood vessels in response to cytokines: (1) ... and (2) ...

Back 47

1. Blood flow increases to the site of infection (to get more effector cells there more quickly)
2. vascular permeability increases (spaces between adjacent endothelial cells widen to allow for easy extravasation of phagocytes out into infected tissue)