Immune System Flashcards
1
Q
antigen
A
anything in out body that generates an immune response
2
Q
pathogens
A
antigens that cause problems for our body
3
Q
3 levels of immunity (informally)
A
- keep things out
- isolate thing to specific spot
- specifically kill those things
4
Q
nonspecific immune system
A
- our immune system going after ANYTHING that is a foreign substance
- anything that prevents entry of foreign things into the body
5
Q
innate immunity is another term for…
A
nonspecific immunity
6
Q
t/f the immune system is an organ system
A
false!
it is a “functional system”
7
Q
specific immune system
A
- process of B and T lymphocytes going after only the specific pathogens that they are immunocompetent for
- slower process
8
Q
external body membranes are an examples of specific or nonspecific immunity?
A
nonspecific
9
Q
which immune system is faster? specific or nonspecific
A
nonspecific
10
Q
adaptive immunity is another term for…
A
specific immune system
11
Q
superficial nonspecific defenses
A
nonspecific immunity mechanisms that occur outside of body
- skin
- mucous membranes
12
Q
how does skin work in immunity?
A
prevents entry of foreign substances into body
there are layers of dead skin cells on outside of epidermis to help too
13
Q
why does it matter for immunity that the epithelium (skin) is avascular?
A
that means the foreign substance has to get very deep into the body from skin to get into circulation
14
Q
when does skin provide an entry path for antigens to get in??
A
when it is broken
15
Q
what parts of body do mucous membranes cover that are considered “outside” of body?
A
GI tract
reproductive tract in females
16
Q
how do mucous membranes work in immunity?
A
- produces mucus
- is barrier of epithelial tissue
- may produce lysozyme and enzymes
17
Q
how does mucus in mucous membranes help in immune response?
A
it can act as a trap
it may have an acidic pH which kills foreign things
18
Q
skin-acid mantle
A
thin layer on skin that’s acidic, helps kill pathogens
19
Q
how do digestive enzymes work in immunity?
A
enzymes denature the proteins of a foreign thing to shut it off
20
Q
almost all internal nonspecific defenses will promote________
A
inflammatory response
21
Q
internal nonspecific defenses
A
- phagocytes (macrophages, neutrophils, eosinophils)
- mast cells
- natural killer cells
- inflammation
- antimicrobial proteins (interferon, complement system)
- fever
22
Q
major phagocytes in body
A
macrophages
23
Q
2 types of macrophages? What does this mean?
A
- fixed or free
- some in interstitial space, some in lymph, some in reticular bundles
24
Q
how do neutrophils work as an internal nonspecific defense?
A
these cell don’t become phagocytic until they encounter something foreign
25
how do eosinophils work as an internal nonspecific defense?
they are phagocytic against parasitic worms
26
mast cells
type of internal nonspecific defense
| binds, ingests, and destroys bacteria
27
NK cells are a type of _____
T cell
28
are NK cells specific or nonspecific?
nonspecific!
29
natural killer cells are able to kill _____; they tend to go after _____
anything
| abnormal body cells
30
how do NK cells kill cells?
lysis
| they have lytic chemicals to break cells down
31
how do lytic chemicals from NK cells break down cells?
the chemicals go through cell membranes and break down cell into pieces from the inside
32
t/f: NK cells do not need to be activated by foreign things to start working
true
33
cardinal signs of inflammation
redness
heat
swelling
pain
34
what causes inflammation?
skin's barrier is broken
| body tries to isolate anything that may have gotten into that spot
35
inflammation attracts _____ cells, which do what?
phagocytic cells; dispose of cellular debris and set the stage for repair
36
antimicrobial proteins
interferon
| complement system
37
interferons
- chemical secreted by infected cell that is a signal to start WBC production
- protects neighboring cells from getting infected by same virus
38
complement system
group of over 20 different proteins floating (inactive) in bloodstream
activated when antigen is present --> causing inflammation and other cells to kill foreign things
39
what happens when complement system protein is activated
inflammation
| other cells kill foreign thing
40
which internal nonspecific defenses are localized?
```
phagocytes
mast cells
NK cells
inflammation
antimicrobial proteins
```
41
which internal nonspecific defenses are systemic?
fever
42
fever
elevated body temp
| systemic response to infection (retards spread)
43
general (informal) process of phagocytes
- antigen is surrounded by phagocytic cell
- phagocyte engulfs antigen and puts it into a little vesicle
- vesicle binds with another vesicle that contains enzymes
- enzymes break down antigen
- cell eliminates waste products
44
phagocytic mechanism (process)
1. phagocyte recognizes pathogen's carbohydrate surface marker
this is enhanced via opsonization
2. cytoplasmic extensions adhere to pathogen
3. pathogen pulled inside cell (called phagosome) in vacuole
4. lysosome binds with phagosome --> forming phagolysosome
5. lysosomal enzymes digest pathogen
6. residual body formed and then expelled
45
opsonization
antibodies bind to foreign markers on antigen --> mark it as foreign so macrophages know what to go after
46
what do macrophages create to adhere to pathogen?
cytoplasmic extensions
47
adhesion/adherence
when cytoplasmic extensions created by macrophage adhere to pathogen
48
name of vacuole that pulls pathogens into macrophage
phagosome
49
what is the waste called which is formed/expelled in phagocytic mechanism
residual body
50
t/f NK mechanism has a relatively long lag time
false!
| it has no lag time
51
NK mechanism
1. NK cells detect infected/cancerous cells based on lack of "self" markers or presence of certain sugars
2. NK cells release perforins
3. channels appear in target cells and nucleus disintegrates (lysis)
52
perforins
```
class of cytolytic chemicals
break cell into pieces
released by NK cells
```
53
inflammatory mechanism
1. toll-like receptors (TLRs) on surface of macrophages recognize pathogens
2. TLRs release cytokines
3. other cells release other inflammatory mediator chemicals
4. vessels in injured area dilate and increase permeability
5. hyperemia occurs
6. exudate accumulates, causing edema
54
cytokines
"cell chemicals" (inflammatory chemicals)
released by TLRs in inflammatory response
promote inflammation and attract WBCs when they encounter antigen
55
inflammatory mediator chemicals
chemicals released by other cells (not TLRs) which aid in inflammation
ex incl histamines and prostaglandins (signaling molecules)
56
what stimulates other cells to release inflammatory mediator chemicals in the inflammation response?
TLRs
57
why might vessels leak plasma during the inflammation response?
because vessels in injured area increase permeability (and dilate)
58
hyperemia
accumulation of blood
| leads to redness and heat
59
redness and heat are 2 characteristics of inflammation that are caused by what?
hyperemia
60
exudate
stuff exiting blood vessel in inflammation bc it is dilated
61
edema
swelling
62
why does edema cause pain?
edema signals nociceptors, which causes pain
63
swelling and pain are two characteristics of inflammation that are caused by what?
edema
64
advantages of exudate accumulation at site of infection
- brings oxygen and nutrients to help tissue repair (to close breach)
- brings clotting proteins and antibodies
- dilutes harmful substances
65
how do exudates dilute harmful substances?
if you have a bunch of antigens clumped together, antigens in the middle are protected and survive (like body guards around celeb)
exudates dilute and separate the substances so they are easier to attack
66
results of inflammation (9)
- injured cells release leukocytosis-inducing factors
- causes neutrophil release by red bone marrow
- loss of fluids slows blood flow locally
- production of selections on endothelial cells
- margination occurs
- neutrophils escape capillaries
- inflammatory chemicals act as chemotaxic agents
- monocytes follow neutrophils
- monocytes become macrophages after leaving capillaries
67
function of leukocytosis-inducing factors
stimulate production of WBCs (especially neutrophils)
| promote leukocytosis
68
leukocytosis
abnormally high number of WBCs
69
how does loss of fluids slow blood flow locally?
- diluted blood vessel allows more blood to accumulate
| - as we pull fluid out of that blood, we have more formed elements accumulating, which slow blood flow
70
selectins
- adhesion molecule specifically for neutrophils
- product of inflammation
- found on endothelial cells
71
margination
adherence of neutrophils along wall of blood vessel
72
how are neutrophils in the exudate?
because they escape capillaries
73
t/f inflammation promotes diapedesis
true!
| neutrophils escape capillaries
74
monocytes follow _____
neutrophils
75
t/f more monocytes move to affected area in inflammation because we produce more
false!
| monocytes are chemotaxically attracted to the area
76
monocytes become _____ after leaving capillaries
macrophages
77
monocytes produce ______ when they leave the capillaries and become macrophages
lytic chemicals (lysozymes)
78
interferon mechanism
1. cells infected by virus release interferons
2. IFNs diffuse to nearby cells
3. PKR protein synthesis is stimulated
4. PKR interferes with viral replication
5. IFNs also activate macrophages and NK cells
79
while a virus-infected cell is dying, it secretes ______ to warn/protect nearby cells
interferon
80
protein that interferes with viral replication, so virus can no longer replicate
PKR
81
why do interferons activate macrophages and NK cells?
to kill the virus before it tries to replicate
82
role of PKR
interfere with viral replication
83
Complement System Mechanism I (Classical)
1. antibodies bind to pathogens (which have been opsonified)
2. complement proteins bind to antibody-pathogen complexes
3. lysis, phagocytosis, and inflammation result (to destroy foreign thing)
84
what do complement proteins bind to in the antibody-pathogen complexes? antibodies or pathogens?
antibody
85
what destroys the antigen in complement system mech I?
complement proteins
86
complement system mechanism II (Alternate)
1. complement proteins bind to polysaccharide molecules on pathogens
2. lysis, phagocytosis, and inflammation result
87
which complement system uses antibodies?
mechanism I (classical)
88
in complement system mechanism 2, when do complement proteins activate?
when they bind to polysaccharide molecules on pathogens
89
fever mechanism
1. leukocytes and macrophages exposed to pathogens secrete pyrogens
2. pyrogens cause hypothalamus to raise body temp
90
what part of body determines body temp?
hypothalamus
91
pyrogens
chemical secreted by leukocytes and macrophages during fever that causes hypothalamus to raise body temp
92
when is it good to take zinc?
if you have a viral infection
93
when body temperature increases, that decreases the amount of stores of which minerals?
iron and zinc
94
bacteria feed on which minerals to replicate?
iron and zinc
95
does fever increase or decrease metabolic activity?
increases
96
how do fevers work as immune response?
- increase metabolic activity
| - denature enzymes in antigen
97
antigenic properties
antigenic determinants
immunogenicity
reactivity
98
antigenic determinants promotes ___________ which promotes __________
immunogenicity; reactivity
99
antigenic determinants
things on surface of antigen act activate immune system
| stimulates specific immune response
100
major histocompatibility complex
self markers
101
self antigens
marker we produce that tells immune system we belong
| not immunogenic to us, so does not activate immune system
102
t/f our own self antigens do not activate our immune system
true
103
characteristics of specific immunity
- pathogen specific
- not immediately active (lag time)
- systemic
- provides "memory"
104
what does it mean that specific immunity provides memory?
when specific immune cells have been activated, they produce copies of themselves to activate quicker and better if exposed to same thing in the future
105
specific immunity pathways
humoral
| cell-mediated
106
antibody-mediated response is another term for
humoral pathway
107
humoral pathway
- b lymphocytes in body become activated then produce antibodies, which float around in the body via the circulatory system
- these antibodies are specific to certain antigenic properties
- antibodies mark antigen for destruction
108
antibodies work for _____ antigenic properties; antigens have ___ antigenic properties on it
only one; more than one
109
cell mediated pathway
- when our own body cells are infected/weird --> not saying 'self'
- t lymphocytes attack those directly and kill them by lysis
110
all lymphocytes are produced by _______ in ___________
stem cells; red bone marrow
111
t/f all lymphocytes are virtually identical when first formed, then differentiate
true
112
t cells become immunocompetent where?
thymus
113
b cells become immunocompetent where?
bone marrow
114
where do immunocompetent cells mature?
in secondary lymph organs
115
t/f lymphocytes are fully functional even before they are bound with an antigen
false
| not fully mature yet
116
why is there a time lag for specific immunity?
because the lymphocytes are not fully functional until they are bound to antigen
117
antigen presenting cells (APC)
cells that engulf pathogen and present its fragments as antigens
still activate specific immune system even if their markers started out as "self" but got messed up
118
antigen challenge
first encounter between a naive immunocompetent lymphocyte and antigen
119
where does antigen challenge usually occur?
in secondary lymph tissue or organ
120
naive immunocompetent lymphocyte
hasn't ever encountered anything foreign yet
121
when does primary humoral response happen?
the first time we encounter a foreign thing
122
primary humoral response
1. antigens bind with surface receptors on naive immunocompetent B lymphocyte
2. clonal selection occurs
3. most clones become plasma cells with produce antibodies
4. some clone cells become memory cells
123
which lasts longer: antibodies or memory cells?
memory cells
124
clonal selection
b lymphocyte producing copies of itself by dividing
| bc if there is one antigen floating around, there are probably more, so we need more receptors
125
how long do plasma cells last?
4-5 days; then they die
126
when does the secondary humoral response occur?
when we are exposed to the same antigen for a second time
127
t/f secondary humoral response is the same mechanism as primary?
true
128
how is the secondary humoral response different from the primary?
secondary response.....
- is faster
- lasts longer
- is more effective
129
why is the secondary humoral response more effective than the first?
because it is effectively producing lots of copies
130
sources of humoral immunity
active
passive
natural
artificial
131
active immunity
(becoming infected)
we produce our own antibodies
foreign substance got inside and we are acting on it
132
passive immunity
getting antibodies are did not produce; comes from external source
133
natural active immunity
we have been infected and produce antibodies
134
natural passive immunity
how mom delivers antibodies to baby through breast milk or placenta
135
artificial active immunity
vaccination
| given a vaccine to activate production of antibodies by b lymphocytes
136
artificial passive immunity
being given a shot of antibodies, injected into our bodies
137
components of antibody structure
- 2 identical heavy chains
- 2 identical light chains
- variable region
- constant region
- antigen binding site
138
variable region of antibody
where light chains and heavy chains overlap
| determines what it can bind to (varies)
139
second humoral response is ______ to _______ x higher than primary
1000 to 10,000
140
constant region of antibody
only heavy chains
always the same
determines how antigen gets destroyed
141
antigen-binding site is determined by _______
variable region
142
t/f type of antibody cannot change over course of infection
false! it can!
143
monomers IgD, IgG, and IgE each have ___ binding sites
2
144
classes of antibodies
```
IgD
IgG
IgE
IgA
IgM
```
145
IgD
receptors on surface of B lymphocytes
146
IgG
most abundant antibody in blood
constant region binds with complement proteins, which destroy antigen
use complement system "classical pathway"
can cross placenta
produced late in primary or early in secondary response
147
IgE
```
bind to mast cells and basophils
not many in blood (only traces in plasma)
cause release of histamine
evoke inflammation
activate immune system
activated during allergic reaction
located in mucosae
```
148
IgA
dimer (2 monomers)
4 binding sites
in mucus
binds with antigen, prevents antigen from binding with other body cells
149
IgM
```
pentamer
10 binding sites
produced during primary response (first)
increased # IGM means recently infected
fix/activate complement protein
agglutination
```
150
antibody functions
- formation of antigen-antibody complex
- provide site for binding of complement proteins
- block sites on pathogens
- cause clumping of antigen-containing cells
- cause clumping of soluble antigen molecules
151
neutralization
antibody function of blocking sites on pathogen so pathogen cannot bind
152
monoclonal antibodies
commercially produced
| used to be used in lab, then to treat cancer, now to treat covid patients
153
cell mediated immune response
1. t cell binds with antigen infected body cell
2. co-stimulatory signals are present
3. t cell is activated
4. clones are produced
5. some clones become memory cells
154
when are co-stimulatory signals released?
due to binding of secondary sites
155
t/f both helper t cells and cytotoxic t cells are active as part of specific immunity
true!
156
t cell activators
- class I MHC protein-linked antigens
| - class II MHC protein-linked antigens
157
endogenous
produced by the body/cell itself
158
exogenous
produced by something other than own cell
159
are class I MHC protein-linked antigens endogenous or exogenous?
endogenous
160
are class II MHC protein-linked antigens endogenous or exogenous?
exogenous
161
CD4 cells
helper t cells
162
cancerous cells are examples of Class __ MHC protein-linked antigens
1
163
bacterial infected macrophages are examples of class __ MHC protein-linked antigens
2
164
____ are activated by class II MHC protein-linked antigens
CD4 (helper t cells)
165
___ are activated by class I MHC protein-linked antigens
CD8 cells (cytotoxic t cells)
166
what do CD8 cells do when activated by class I MHC protein-linked antigens
produce copies/memory cells and produce cytolytic chemicals
167
antigen binding
t cell antigen receptors bind to antigen-MHC complex
168
secondary binding produces ________
co-stimulators
169
co-stimulators
t cell binding to other receptors on APC, cytokines, interleukins
170
t/f each co-stimulator produces the same response
false! they all promote different response
171
response of co stimulators
either facilitates or disables activation
| slows down immune system or produces clones
172
cytotoxic t cell functions
directly attack/kill our body's infected cells
| secrete lytic chemicals/perforins that cause cell lysis
173
helper t cells
regulatory cells
class II
activate cytotoxic t cells to kill infected cells
174
suppressor t cells
stops cloning
regulatory
releases chemicals that slow B and T cells from cloning
175
CD8 cells
cytotoxic t cells
176
types of immune disorders
immunodeficiencies
autoimmune diseases
hypersensitivities
177
immunodeficiencies
any condition that causes immune cells to behave abnormally or don't have enough
178
autoimmune diseases
immune system attacks our own body cells
| cannot accurately distinguish "self" cells
179
hypersensitivities
responses to allergens
| harmless to most, but activates immune system for some
180
t/f you can be born with an immunodeficiency or acquire it
true
181
severe combined immunodeficiency syndrome (SKIDS)
mutation in DNA that attacks lymphocytes, lacking specific immunity
congenital (genetic)
182
AIDS
acquire something that kills T lymphocytes
| die of another complication bc lacking lymphocytes
183
signs of AIDS
lymph node swelling
184
MS is what kind of immune disorder
autoimmune disease
185
multiple sclerosis
immune cells attack white fiber in brain
| lose neural connectivity
186
myasthenia gravis is what kind of immune disorder?
autoimmune disease
187
myasthenia gravis
immune system attacks neuromuscular junction
| inhibits nervous muscle control
188
graves' disease is what kind of immune disorder?
autoimmune disease
189
graves' disease
immune system attacks thyroid gland
| produce extra thyroid hormone
190
signs of graves' disease
bulging eyeball
191
juvenile diabetes is what kind of immune disorder?
autoimmune disease
192
juvenile diabetes
attacks pancreas
| don't produce sufficient insulin
193
lupus is what kind of immune disorder?
autoimmune disease
194
lupus
attacks tissue in kidneys, heart, lungs, skin
| butterfly red marks/wolf bite
195
rheumatoid arthritis is what kind of immune disorder?
autoimmune disease
196
rheumatoid arthritis
attacks synovial joints
| joint deformity, stiffness, pain
197
cause of autoimmune diseases
unknown
| maybe bacterial infection
198
types of hypersensitivities
immediate, subacute, or delayed
199
example of immediate/acute hypersensitivity
anaphylaxis
200
immediate/acute hypersensitivity
happens within seconds of contact with allergen
first encounter (warning) causes sensitivity, not full blown allergic reaction
second encounter worse
this encounter could die
201
anaphylaxis
body floods with histamine --> causes systemic vasodilation
usually get a warning
bp drops then death
202
subacute hypersensitivity
a couple hours between exposure and response
203
transfusion reaction is an example of which type of sensitivity?
subacute
204
transfusion reaction
injected with wrong blood type
| eventually... shiver; blue;die
205
what happens when you are given the wrong blood type
after a few hours you get the shivers
hours later you turn blue
hours later you die
206
delayed hypersensitivity
can take days from exposure to response
207
poison ivy reaction is an example of which type of hypersensitivity
delayed
208
t/f transplants have high likelihood of success
false
| High probability of rejection of transplant because self is different than our self
209
autograft
tissue from ourself
| rejection risk is low
210
isograft
tissue from identical twin, same MHC
| rejection risk is low
211
allograft
tissue from someone else
| lower risk of rejection if you are more closely related to them
212
xenograft
tissue from different species
generally rejected
use medication to shut off immune system for the transplant to establish
