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bio265 > unit 5 study guide > Flashcards

unit 5 study guide Flashcards

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1
Q

body’s defense against any kind of pathogen

A

innate immunity

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2
Q

first and second lines of defense are

A

innate immunity

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3
Q

why are most infections subclinical?

A

there are no signs/symptoms due to innate immune response repelling infection

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4
Q

properties of skin that make it a good barrier to infection

A

dry, constantly shedding, hypertonic

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5
Q

mucous membranes most common as a portal of entry

A

in upper respiratory tract

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6
Q

leukocytes capable of phagocytosis

A

neutrophil, macrophage, dendritic cell, B cell

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7
Q

IgM

A

10 binding sites
1st antibody produced upon exposure
classical pathway activated by IgM

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8
Q

IgE

A

basophil receptor
2 binding sites
allergic response
releases histamine once attached to basophil

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9
Q

IgG

A

most common and lasts longest
2 binding sites
can cross into placenta and small tissue

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10
Q

IgA

A

secretory Ig
4 binding sites (identical)
found in breast milk

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11
Q

IgD

A

B cell receptor
2 binding sites
purpose unknown

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12
Q

Ig found in breast milk

A

IgA

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13
Q

most common Ig and can cross into placenta

A

IgG

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14
Q

Ig that is a B cell receptor

A

IgD

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15
Q

1st to show in presence of exposure

A

IgM

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16
Q

basophil receptor Ig

A

IgE

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17
Q

6 steps of phagocytosis

A
  1. chemotaxis - phagocyte moves toward chemokine source
  2. adhesion - phagocyte bingds to target
  3. ingestion - phagocyte eats target
  4. digestion - digesting begins due to enzymes
  5. residual body - former phagolysosome
  6. elimination - residual body shits out contents; exocytosis
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18
Q

leukocyte involved in body’s resistance to a tape worm

A

eosinophil

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19
Q

chemotaxis

A

1st step of phagocytosis
helps bring phagocytes to infection site

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20
Q

digestion of ingested microbe begins with

A

formation of phagolysosome

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21
Q

cytokine that virally infected cells produce to slow spread of virus across tissue

A

interferons

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22
Q

complement proteins involved in classical pathway

A

c1, c2, c3, c4, c5

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23
Q

c1 function in classical pathway

A

binds to antibodies bound to their target antigen
cleaves c2 and c4 into c2a/c2b and c4a/c4b

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24
Q

c2 function in classical pathway

A

cleaved by c1 into c2a/c2b
c2a binds to c4b and becomes c2ac4b

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25
c3 function in classical pathway
cleaved by c2ac4b c3a is chemokine; activates inflammation c3b is opsonin
26
c2ac4b function in classical pathway
cleaves c3
27
c3a function in classical pathway
chemokine that activates inflammation
28
c3b function in classical pathway
opsonin that enhances phagocytosis cleaves c5 into c5a/c5b
29
c5 function in classical pathway
cleaved by c3b c5a activates inflammation; chemokine c5b joins c6, c7, c8, c9+ to form MAC direct cell killer
30
MAC
membrane attack complex; pokes holes in invader membrane and kills it
31
how does classical pathway activate
once antibodies bind to their antigen, then c1 binds
32
complement proteins that cause chemotaxis and inflammation
c3a and c5a
33
opsonin comp protein
c3b
34
does complement interfere w viral replication?
yes - activates inflammatory response
35
comp proteins involved in MAC
c5b, c6, c7, c8, c9
36
is classical pathway adaptive or immune
adaptive
37
complement cascades
series of antimicrobial proteins circulating in blood plasma
38
protein kinase r
enzyme in interferon that prevents ribosome formation
39
ribonuclease L
enzyme in interferon that chops up mRNA
40
first step in inflammation pathway
release of histamine by mast cells following tissue damage
41
adherence of phagocytes to the lining of blood vessels is called
margination
42
what happens first, diapedesis or margination?
margination
43
at what point in the cascades do both alternative and classical pathways of complement activation become the same?
once c3 is cleaved into c3a/c3b
44
5 hallmarks of inflammation
rubor, calor, tumor, dolor, functio laesa
45
rubor
redness
46
calor
heat
47
tumor
swelling
48
dolor
pain
49
functio laesa
loss of function
50
what effect does fever have on phagocytes?
fever increases phagocyte response to pathogens and infected cells
51
ways a fever slows infection spread
slows bacterial pathogen growth increases complement function liver removes transferrin from blood to starve pathogen interferon production increases
52
what activates adaptive immune cells?
antigen activates B and T cells
53
leukocytes involved in adaptive immune response
t lymphocytes, NK cells, b lymphocytes, dendritic cells, macrophage
54
cells of immune system involved in humoral immunity
b cells
55
branch of adaptive immunity that produces antibodies
humoral
56
branch of adaptive immunity that directly kills infected cels
cellular
57
do lymphatic vessels have valves to control fluid flow?
yes; like veins
58
what direction does fluid in lymphatic system flow?
from body tissue back into cardiovascular system
59
b cells mature in
bone marrow
60
t cells mature in
thymus
61
where do b and t cells activate?
in lymph nodes
62
relationship between antigen and epitope
epitope - region of antigen recognized by BCR or TCR one antigen can have many epitopes
63
biomolecule that stimulates strongest immune response in humans
proteins
64
exogenous antigen
originate outside of cells most bacterial pathogens have exogenous antigens
65
endogenous
originate inside of cells, but not self viral pathogens
66
autoantigens
originate inside of your cells; your own antigens immune system should ignore these
67
class of MHC that presents endogenous antigens
MHC class I
68
MHC class I
found on all body cells containing nucleus
69
presents antigen to Tc cells
MHC class I
70
MHC class II
found on antigen-presenting cells only
71
antigen presenting cells
macrophages, b cells, dendritic cells
72
presents exogenous antigens to Th cells
MHC class II
73
result of negative selection in the thymus during t cell maturation
negatively selected t cells are killed via apoptosis
74
role of TCR during clonal selection
TCR interacts w antigen presented in MHC class I (Tc) or HMC class II (Th) t cells lack TCR = negatively selected TCR binds to autoantigen = negatively selected TCR binds to MHC = positive selection
75
all t cells must have a
t cell receptor (TCR)
76
fate of autoreactive b cell
selected for apoptosis
77
why is apoptosis considered “clean” cell death?
cells do not lyse, instead they bleb
78
two cell surface proteins found on all Tc cells
TCR and CD8
79
which class of MHC presents antigen to activate Th?
MHC class II
80
characteristics of b cells (4)
each b cell has a BCR they recognize antigens with their BCR they can produce antibodies they mediate the immune memory response
81
do b cells interact with MHC class I or II to recognize antigens?
no; they PRESENT antigen to T cells using classes
82
areas of Ig molecule that are variable and bind to antigen
Fab (antigen binding region)
83
areas similar for all antibodies
Fc (constant)
84
antibody found in mucus saliva and tears
IgA
85
highest affinity antibody
IgG
86
IgD is a BCR, so
humoral immune response is limited without IgD
87
how does antibody-dependent cell cytotoxicity work?
antibodies bind to antigens on the cell membrane of an infected cell and NK cells then destroy the cell via apoptosis
88
function of MHC II on APC
presents antigen to Th cells
89
cytokine that acts as communication between leukocytes
interleukin (IL)
90
IL thats stimulatesTh proliferation
IL-2
91
methods Tc cells use to kill microbe infected cells
cytotoxic granule release; initiates apoptosis in infected cell
92
cytotoxic granule that initiates apoptosis
granzyme
93
cytotoxic granule that pokes holes in cell membrane
perforin
94
when an NK cell encounters a cell with no MHC class I, it
releases cytotoxic granules to kill the cell
95
how will NK respond to virally infected cells bound by antibodies
releases cytotoxic granules to kill the cell
96
releases cytotoxic granules to kill the cell

bio265 (9 decks)

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