X_Exam1 Mfm2_10

Front 1

what are the common routes of entry for pathogens:
1.
2.
3.
4.

Back 1

1. skin
2. respiratory system
3. digestive system
4. urogenital system

Front 2

once inside the body, microorganisms can reside in several key locations:

Back 2

intracellular
-vesicular
-cytoplasm

extracellular
-interstitial spaces (blood, lymph
-epithelial cell surfaces

Front 3

what are the components of the immune system:
1.
2.
3.
4.

what are the other key players:
1.
2.
3.
4.
5.

Back 3

1. lymph nodes
2. thymus
3. spleen
4. long bones

1. skin
2. mucous membranes
3. chemical factors
4. leukocytes
5. commensal bacteria

Front 4

innate immunity is our 1st line of defense, what are its general features:
1.
2.
3.
4.
5.

Back 4

1. non-specific
2. constitutively present/immediate response
3. phylogenetically ancient (found in almost every living organism)
4. limited repertoire of recognition molecules
5. no memory or lasting immunity

Front 5

innate vs. adaptive immunity, what are the key differences:
1.
2.
3.
4.
5.

Back 5

1. speed of response
2. cellular mediators differ
3. protective mechanisms vary greatly
4. adaptive response is more specific
5. adaptive response allows for immunologic memory

Front 6

place the descriptions in the correct box:

Back 6

(see figure)

Front 7

which branch of the immune system is more imperative to the survival of an organism:

Back 7

innate immunity

Front 8

what are the types of innate immune barriers:
1.
2.
3.
4.

Back 8

1. anatomical
2. chemical
3. humoral
4. celluar

Front 9

what are the anatomical barriers to infection:
1.
2.

Back 9

1. skin (epithelia)
2. mucous membranes

Front 10

fill in the sources of the chemical barriers:

Back 10

(see figure)

Front 11

fill in the chemical barriers for the sources listed:

Back 11

(see figure)

Front 12

epithelia of the skin and GI tract also has an additional layer of protection--- provided by ... bacteria

Back 12

commensal

Front 13

what are the humoral barriers to infection:
1.
2.
3.
4.
5.
6.
7.

Back 13

1. complement system
2. coagulation
3. protease inhibitors
4. lysozyme
5. interferons
6. lactoferrin and transferrin
7. cytokines

Front 14

Lectoferrin and transferrin possess antimicrobial activity by sequestering free ... that is needed for microbial function

Back 14

iron

Front 15

... and ... are protease inhibitors that work by “tricking” the bacterial protease to cleave them, forming an inactive ... bound intermediate in the process

Back 15

serpin
alpha 2-macroglobulin
covalently

Front 16

what does the following describe:

Produced by virus-infected cells
Inhibit viral replication
Signal neighboring uninfected cells to prepare for viral infection
Alerts other cells of immune system
Makes virus-infected cells more vulnerable to attack by killer lymphocytes

Back 16

type I interferons (alpha, beta, gamma)

Front 17

what are the 3 main effects of IFN secretion
1.
2.
3.

Back 17

1. alert neighboring cells
2. increases expression of antigen-presenting cell surface molecule MHC class I
3. activates nature killer (NK) cells that kill virally infected cells

Front 18

what are the 2 main types of interferons:
1.
2.

Back 18

1. alpha
2. beta

Front 19

what is the function of complement activation:

Back 19

complement or augment the immune response

Front 20

what are the 3 pathways that lead to activation of complement:
1.
2.
3.

Back 20

1. classical pathway
2. lectin pathway
3. alternative pathway

Front 21

1. what activates the classical complement pathway:

2. what activates the alternative complement pathway

Back 21

1. antibody-antigen complex
2. molecules on pathogens surface

Front 22

what are the results of complement activation:
1.
2.
3.

Back 22

1. recruitment of inflammatory cells
2. opsonization of pathogens
3. killing of pathogens by effector cells

Front 23

what is opsonization:

Back 23

when pathogens are tagged for destruction

Front 24

in the classical pathway, complement components ..., ..., and ... must be activated prior to activation of C3. In the alternative pathway, these components are replaced by ..., ..., and ... The remainder of the pathway is the same for each mechanism.

Back 24

C1
C4
C2
factor D
factor B
properdin

Front 25

what are the basic steps of complement starting with cleavage of C3:
1.
2.
3.
4.

Back 25

1. C3 is cleaved into C3a and C3b
2. C3b covalently attaches itself to bacterium
3. C3a attracts effector cells (i.e. phagocytes) to the site of infection
4. the newly arrived effector cells bind to complement "tag" on the pathogen, signaling phagocytosis and destruction

Front 26

C3 is hydrolyzed into ... and ... fragments. ... is the smaller, soluble fragment that recruits phagocytes to the site of infection while ... is the larger fragment that attaches to the surface of the pathogen, tagging it for destruction. This molecular tag is also called an ..., and ... is the process of “tagging” a pathogen.

Back 26

C3a
C3b
C3a
C3b
opsonin
opsonization

Front 27

rate of hydrolysis of C3 to C3a and C3b can be increased through formation of ...

Back 27

C3 convertase

Front 28

initial product of spontaneous hydrolysis of C3 is called ... which binds to ... in the blood or extracellular fluid, making that factor susceptible to cleavage by ... this cleavage produces a complex called ... or ... which then activates more ... molecules. The C3b fragments attach to the microbial surface and can be used either (1) ... or (2) ...

Back 28

iC3
factor B
factor D
C3 convertase
iC3Bb
C3
(1) to make more C3 convertase
(2) as an opsonin

Front 29

..., also known as ... binds to ... on the microbial surface, stabilizing and protecting it from inhibition by factor H.

Back 29

Properdin
Factor P
C3 convertase

Front 30

... activates C5 and ..., forming pores in the microbial membrane and ... This is also referred to as the ...

Back 30

C5 convertase
C6-C9
cell lysis
“membrane-attack complex” (MAC)

Front 31

The activation and cleavage of C5 also produces soluble ..., the most potent of the ..., causing significant recruitment of neutrophils and inflammation.

Back 31

C5a
anaphylatoxins

Front 32

Initiation of the alternative complement pathway on the surface of human cells is stopped at an early stage by:
1.
2.
3.

Back 32

1. decay-accelerating factor (DAF)
2. membrane co-factor protein (MCP)
3. plasma protein factor H