immune system test Flashcards

1
Q

2 parts of immune response

A

innate and adaptive

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2
Q

the innate immune system is

A

nonspecific, 2 parts

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3
Q

part 1 of innate immune system

A

physical/chemical barriers to keep contaminants out

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4
Q

part 2 of innate immune system

A

responses like macrophages, inflammation, and fever to keep microbes at bay

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5
Q

adaptive immune response

A

how the body learns to specifically target and eliminate contaminants

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6
Q

skin

A

(normally) solid barrier that stops bacteria from getting inside inside the body

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7
Q

the outer layer of the skin is coated in

A

protein keratin

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8
Q

function of keratin in the skin

A

works with other lipids and proteins to form a tight seal separating inside from out

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9
Q

The outer cells of the skin

A

is continuously shedding , this is called desquamstion

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10
Q

desquamation takes

A

attached microbes with them

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11
Q

the skin secretes waxy, oily

A

sebum

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12
Q

sebum gives the skin a pH of about what

A

5.5

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13
Q

pH of sebum is

A

acidic compared to body’s 7.4

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14
Q

change in pH due to sebum can cause

A

denature enzymes in bacteria, slows their function

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15
Q

95% of infections from

A

begin in the mucous membranes

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16
Q

5% of infections result from

A

vector bites

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17
Q

Other pH barriers to microbes

A

saliva
stomach
vagina

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18
Q

saliva pH

A

roughly neutral (7)

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19
Q

pH of stomach after a meal

A

2

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20
Q

pH of stomach at rest

A

3.5

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21
Q

inside of vagina pH

A

4

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22
Q

what are the OTHER physical barriers to microbes

A
mucus, 
urinations,
defectation, 
vomitting, 
tears, hairs 
and cilia
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23
Q

where is MUCUS found

A

airway, esophagus, stomach, intestines, cervix (females)

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24
Q

how does mucus affect microbes

A

microbes stick to it and are broken down by protein and/or expelled from the body

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25
what washes microbes out of the body
urination, defcetation, vomiting and tears
26
hairs in the nose and cilia in the windpipe can....
stop microbes from entering the lungs
27
because of cilia.... bacteria are pushed
up and away from the lungs through the mucociliary elevator
28
if a particle is detected in the airway
extremely sensitive nerves in the airway will force a cough reflex
29
lysozyme (a chemical barrier)
lysozyme is an enzyme in tears, mucus, breast milk, saliva
30
lysozyme function
breaks apart peptidoglycan, kills bacteria
31
what is peptidoglycan
main component of bacterial cell walls,
32
normal flora
bacteria living on it in a mutualistic relationship
33
instead of harming the body.........
many benefits
34
benefits of normal flora
- nutrients that the body can't normally provide (B12) - competition for space and nutrients, - create compounds that kill other bacteria - modify the pH of an area to make it inhospitable to other bacteria
35
competition for space and nutrients causes
makes it hard for bad bacteria to survive
36
how much human cells in the body
10^13
37
how much symbiotic bacteria in the human body
10^14
38
first step of phagocytosis
- chemotaxis and adherence of microbes to phagocyte
39
second step of phagocytosis
- ingestion of microbe by phagocytosis
40
step 3 phagocytosis
formation of a phagosome
41
step 4 phagocytosis
fusion of the phagosome with a lysosome to form a phagolysosome
42
step 5 phagocytosis
digestion of ingested microbe by enzymes
43
step 6 phagocytosis
formation of residual body containing indigestible material
44
step 7 phagocytosis
discharge of waste materials
45
phagocytes
white blood cells that eat and destroy foreign contaminants through phagocytosis
46
types of phagocytes
neutrophils macrophages dendritic cells
47
neutrophils function
eat bacteria
48
macrophages function *
eat everything that dosen't have a proper ID
49
dendritic cells function*
eat surroundings that show PAMPS
50
macrophages and dendritic cells
present digested guts to surrounding cells, especially T cells
51
what is PAMPs
micro-associated patterns
52
PAMPs
pathogen-associated molecular patterns
53
peptidoglycan (PAMPs)
main bacterial cell wall component, gram positive
54
peptidoglycan chemical surrounds
membranes of many bacteria
55
if a bacterial membrane contains a thick layer of peptidoglycan
gram positive
56
why is something gram positive
turns purple when dyed w/ Gram method
57
if it does NOT turn purple hen dyed with the gram method
gram negative... turns pink instead
58
LPS (PAMPs)
main bacterial membrane component, gram negative
59
LPS
lipopolysaccharides
60
what are LPS
long chains of sugars that attach to membranes of gram-negative bacteria with thin peptidoglycan layer
61
Flagellin (PAMPs)
a protein found in bacterial flagella
62
many bacteria have a flagellum
to help them move through the body
63
many flagellum
flagella
64
main protein in flagella
flagellin, is a PAMP
65
Double stranded RNA (PAMPs)
found in viruses
66
glucans (PAMPs)
major component of fungal cell walls
67
PRRs
Pattern Protein Receptors
68
where are PRRs found
they are proteins found on the plasma membrane of macrophages
69
job of PRRs
recognize PAMPs
70
2 main types of PRRs;
Phagocytosis receptors | TLRS
71
Phagocytosis receptors
binding to a PAMP causes the onset of phagocytosis..
72
phagocytosis receptors are only found in
phagocytes
73
TLRs
toll-like receptors
74
TLRs function
bidning to PAMP causes the activation of genes coding for cytokines
75
what are cytokines
signalling proteins
76
where are TLRs found
phagocytes, epithelial cells and MORE
77
there are many kinds of TLRs that each
recognize specific microbial compoents
78
each TLRs trigger the
release of some cytokines
79
cytokines are....
small proteins produced by various white blood cells
80
cytokines are produced in response to
PAMP binding to a TLR
81
cytokines can be
autocrine paracrine endocrine
82
autocrine (cytokine)
meaning they act on the red blood cell that secrets them
83
paracrine (cytokine)
they act on nearby cells
84
endocrine (cytokine)
travel longs distances in the body
85
3 things tat cytokines cause to happen
- vasodilation of blood vessels - upregulation or downregulation of genes - white blood cell hematopoiesis
86
3 OTHER THINGS that cytokines can cause
- production of antobodies - apoptosis - inhibition of viral replication
87
chemokines
are a type of cytokine, attract molecules through chemical signals
88
two categories of chemokines
homeostatic | inflammatory
89
homeostatic chemokines
attract various types of white blood cells to the area and invoke diapedesis
90
what is diapedesis
jumping through the walls of a vessel into infected tissue
91
what is chemically attracted to chemokines
white blood cells
92
inflammatory chemokines
initiate the inflammatory response by causing vasodilation
93
vasodilation caused by inflammatory chemokines....
leads to more blood, and in turn more white blood cells in the area
94
inflammation can be
acute or chronic
95
acute
quick onset
96
chronic
long term
97
signs of inflammation
redness, heat, swelling, pain
98
positive feedback loop of cytokines
cytokines made to recruit WBS, which release cytokines to recruit even more WBCs
99
the positive feedback loop of cytokines is supposed to be
localized and shut off at a certain point
100
if an infection gets too big
the body does not to shut down the cytokines >>> CYTOKINE SToRM
101
result of a cytokine storm
widespread inflammation
102
widespread inflammation from a cytokine storm can cause
ARDS>>> DEATH??!??!?
103
ARDS
acute respiratory distress syndrome
104
cytokine storm can also cause
severe damage to blood vessels when they dilate too much
105
damage to blood vessel can lead to
blood spilling the extracellular space
106
blood spilling the extracellular space causes
reddish splotches on the skin (petichaie LOOK It up), shock
107
fever invoked
by pyrogen
108
pyrogens can be classified as
endogenous or exogenous
109
exogenous pyrogens
come from outside and bind to PRRs to trigger the release of endogenous pyrogens
110
example fo exogenous pyrogen
LPS . (lipopolysaccharide)
111
endogenous pyrogens
are cytokines made by macrophages in RESPONSE to exogenous pyrogens
112
examples of endogenous pyrogens
interleukin-1 (IL-1) and interleukin-6 (IL-6)
113
endogenous pyrogens travel
to the hypothalamus in the brain..... send hormonal signals across the body to increase temperature
114
fevers help stop
bacterial growth (deature?!)
115
fevers increase
ability of certain macrophages to do their jobs by altering their membrane fluidity.
116
how does inflammation cause its symptoms
- capillary widening - increased capillary permeability - attraction of white blood cells - systemic response
117
capillary widening can cause
increased blood flow
118
increased capillary permeability can cause
release of fluid
119
attraction of white blood cells can cause
migration of WBCS to injury
120
systemic responses can cause
fever and proliferation of white blood blood cells
121
antibodies
small y shaped proteins
122
antibodies structure
the same except the two tips of the Y
123
two tips of the Y structure
heavily variable , infinite shapes, almsot every molecule
124
stem of the Y of antibodies
Fc region
125
branches of the Y
FA=ab regions
126
antigens
the shreds resulting from pathogens being broken down by phagocytes
127
how are antigens sensed
by antigen binding sites on antibodies
128
another name for antibodies
immunoglobulins
129
Ig
immunoglobulins
130
5 types of immunoglobulins
IgG*, IgM, IgD, IgA, and IgE.
131
most common Ig
IgG
132
B cells
white blood cells who create antibodies
133
Each B cell..
creates just one specific antibody
134
how do B cells create antibodies
through V(D)J recombination
135
After a B cell's antibody recognized a pathogen and has treated the body
B cell becomes a memory B cell
136
what do memory B cells do after becoming one?
travel to lymph node and lies dormant
137
memory B cells lie dormant in lymph nodes until
the same antigen is spotted
138
what happens when the same antigen (already been treated by a memory B cell) is seen again
dormant B cells rapidly creates antibodies (MUCH FASTER) >>>>>>>>
139
When dormant B cells rapidly create antibodies... the body
bodies is quickly cured .. often before sickness is felt
140
B cell phenomenon is basis for
vaccination
141
T cells
type of white blood cell produced in the thymus
142
thymus location
JUST SUPERIOR TO THE HEART
143
Like B cells, T cells are also
antigen-specific
144
TCRs
T cell receptors
145
t cell receptors
special receptors on the membranes of T cells
146
what do TCRs do
look for digested pieces of stuff that macrophages and dendritic cells have broken apart during phagocytosis
147
if TCRs see "bad stuff" >>> 3 reactions for what 3 cell types
cytotoxic T cells, helper T cells regulatory T cells
148
cytotoxic T cells
hunt down and kill cells that contain a certain anitgen
149
helper T cells
begin producing cytokines
150
cytokines released by helper T cells....
will attract B cells, cytotoxic T cells and macrophages, and will cause white blood cell hematopoiesis
151
regulatory T cells
shut down other T cells at the end of an immune response
152
smaller sub-region of an antigen
epitopes
153
what are epitopes recognized by
paratopes on antigens
154
most pathogens
have many epitopes, can be recognized by many antibodies
155
4 MAIN METHODS FOR ANTIBODIES FIGHTING PATHOGENS
Neutralization Agglutination Precipitation Complement Activation
156
when the Fab region(s) of an antibody bind to the antigen...
Fc ragion dangles off
157
many phagocytes have special....
special receptors called opsonin receptors...
158
opsonin receptors
increase the chemical attraction between themselves and dangling Fc regions
159
main idea of opsonin receptors
makes marked antigens look more delicious to phagocytes
160
neutralization
antibody physically blocks the antigen from having its effect
161
example of antibody neutralization
Corynebacterium diphtheriae
162
Corynebacterium diphtheriae
bacteria that secretes small protein diphtheria toxin
163
diphtheria can...
ENTER CELLS AND BREAK THE eEF-2 protein
164
eEF-2 protein
vital part of protein synthesis in human cells
165
antibody for diptheria
blocks diphtheria from binding to receptors and entering the cell
166
so if dipheria toxin is neutralized by the antibody
eEF-2 is never turned off
167
agglutination
the clumping together of molecules
168
in agglutination some antibodies will cause
bacteria or mother molecules to stick together in large groups
169
when agglutination happens it makes it
easier for phagocytes to engulf them after opsonization
170
agglutination also plays a major role in
blood types
171
blood types
A, B, AB, or O
172
Type A blood
have A antigen on RBCs (and B antibody in blood
173
Type B blood
have B antigen on RBCs (and A antibody in blood)
174
Type AB blood
have A and B antigen on RBCs (no antibodies in blood)
175
Type O blood
have neither A or B antigen on RBCs (both antibodies in blood)
176
when would a blood transfusion go bad
a person gains a transfusion of blood with an antigen they have antibodies fo
177
if a person gains a transfusion of blood with an antigen they have antibodies for
the antibodies will cause RBCs to agglutinate and then lyse.
178
if red blood cells agglutinate then lyse
free hemoglobin clogs the kidneys >> shut down
179
some antigens, but usually...........
usually harmful pieces of a virus, are solube
180
soluble antigens
hide in the body by dissolving in serum
181
what can antibodies to to fight the antigens that dissolve to hide
bind to them and force them out of solution to form a solid precipitate
182
when antibodies bind to antigens to form a solid precipitate
makes them easier targets for phagocytosis
183
in order for precipitaion to work
Roughly equal part of antigen and antibody
184
precipitation is often coupled with
agglutination
185
complement pathway is cool because...
shared component of adaptive and innate immune systems
186
complement pathway is turned on by
presence of PAMPS or signal from antigen-antibody complexes
187
_______ released because of PAMPS or antigen-antibody complexes
cytokines, lead to a cascade that makes many different proteins together
188
cytokines and cascade that makes many different proteins together
form a giant pore in a pathogen membrane>> KILLS it
189
autimmune disease
are a broad class of diseases where the body “attacks itself
190
what happens in an autoimmune disease
antibodies in the body mistake “self” cells for “nonself” cells and begin attacking them.
191
what things to autoimmune diseases cause
tissue damage increased tissue growth altered tissue function
192
primary immune response
first time the body sees an infection.... takes while to gather the troops
193
secondary immune response
each subsequent time the body sees an infection... faster and stronger reaction
194
vaccinations
expose the body to a pathogen without getting youu sick
195
what are the three ways a bacterium or virus is prepared for a vaccine
attenuated killed/inactivated subunit
196
attenuated vaccine
bacterium/virus is alive.... genetically modified so that bad genes are removed
197
killed/inactivated vaccine
bacterium/virus is grown in lab then killed by heat or formaldehyde.... dead specimen injected
198
subunit vaccine
bacterium/virus grown in lab... ... ...only one part (a single epitope) is placed into vaccine and injected
199
what parts are usually injected in a subunit vaccine
capsid in viruses, membrane or wall component in bacteria
200
examples of attenuated vaccination
MMR, Measles, Mumps, Rubella
201
examples of killed/inactivated vaccination
Polio
202
example of subunit
hep. B
203
pros of attenuated vaccination
- small dose - usually no booster - giver STRONGEST IMMUNITY
204
cons attenuated vaccination
- must be refrigerated - small risk of mutation to regain pathogenicity - may cause adverse reaction
205
pros of killed/inactivated vaccination
- no risk of mutation to regain pathogenicity | - does not need to be refrigerated
206
cons of killed/inactivated vaccination
- much larger doses required -often needs booster shots | - may cause adveerse reaction
207
which is more likely to cause adverse reaction: killed or attentuated
attenuated
208
pros of subunit vaccination
- no risk of mutation to regain pathogenicity - does not need to be refrigerated - not likely to overwhelm immune system and cause adverse reaction
209
cons of subunit vaccination
- gives "weakest" immunity b - much larger doses required - often requires boosters
210
why does subunit vaccination give the weakest immunity
only one or a few epitopes recognized
211
what disease did we eradicate
small pox
212
what type of immunity do vaccines provide
active (artificial)
213
what is the basis of active immunity
causes your body to make memory B cells that recognie | antigens and spring into action the next time encountered
214
active immunity generally lasts....
for life
215
when is passive immunity usually used
time-sensitive cases
216
examples of uses for passive immunity
snakebites... tetanus infection for unimmunized ...... patient w a weakened immune system
217
what is the basis for passive immunity
injecting neutralizing antibodies harvested froma different host into the patient
218
passive immunity generally lasts...
days to months (TEMPORARY)
219
active natural immunity
patient catches disease, develops own antibodies and build up memory B cells that will fight it the next tuime
220
active artificial immunity
patient receives (attenuated, dead, subunit) vaccine, gains memory B cells without actually fighting it
221
passive natural immunity
infant patient drinks breastmilk, receives mother's antibodies, temporary protection form many disease
222
passive artificial immunity
patient receives injection of antibodies from donor organisms that neutralize antigens and give temporary immunity.
223
what are often donors for passive artificial immunity
horses, pigs etc