Exam 2 Flashcards
1
Q
what does the first line of defense in innate immunity consist of
A
nonspecific external barriers
- skin and mucous membranes
2
Q
what does the second line of defense in innate immunity consist of
A
innate immune response
- phagocytic and NK cells, inflammation, and fever
3
Q
what does the third line of defense in innate immunity consist of
A
adaptive immune response
- cell-mediated immunity and humoral immunity
4
Q
characteristics of innate immunity
- specificity, are we born with it, does it function immediately, does it have memory, what does it recognize
A
- nonspecific
- we are born with it
- functions immediately
- no memory
- recognizes PAMPs
5
Q
characteristics of adaptive immunity
- specificity, what does it recognize, is it immediate, are we born with it, does it have memory
A
- highly specific
- recognizes antigens
- takes time to develop
- develops throughout light (not born with it)
- generates memory
6
Q
what happens when our bodies encounter a bacterium but we don’t get sick
A
first line of defense
- physical, chemical, and cellular barriers
7
Q
how does the skin help with being in the first line of defense
A
- the skin has tightly packed cells that don’t let microbes penetrate it
- it is slightly acidic
- the outermost layer sheds off
8
Q
mucous membrane is involved in the first line of defense, what characteristics about it make it helpful
A
- it lines the digestive, respiratory, and genitourinary tracts
- mucus traps microbes, contains chemicals
9
Q
what are some mechanically moving microbes
A
- mucociliary escalator
- peristalsis
- lacrimal apparatus (tears)
- saliva
- urine and vaginal secretion
10
Q
what does the mucociliary escalator do
A
move microbes out of respiratory tract
11
Q
what and where is peristalsis
A
it moves the food down and along in the gut
12
Q
what does lacrimal apparatus (tears) wash out
A
the eyes
13
Q
what does saliva flushes out
A
the mouth
14
Q
urine and vaginal secretions flush out the
A
genitourinary tract
15
Q
what does normal microbiota do as a first line of defense physical barrier
A
- compete with pathogens for cellular binding sites and available proteins
16
Q
what does normal microbiota secrete
A
antimicrobial products and waste products that are toxic to pathogens
17
Q
what is involved in the chemical barriers of the first line of defense in innate immunity
A
- lysozyme
- peroxidase
- lactoferrin
- salt
- sebum
- low pH in stomach and vagina
18
Q
what is the function of lysozyme
A
cleaves bond between NAG and NAM in peptidoglycan
19
Q
what does peroxidase generate
A
ROS
20
Q
what is the function of lactoferrin
A
sequester iron that microbes need for growth
21
Q
what does sebum seal off
A
the pore of the hair follicle
22
Q
what does salt accumulate from
A
perspiration
23
Q
where is there a low pH and normal microbiota
A
in the vagina
24
Q
what are the components of the innate immune response
A
- recognition of PAMPs
- inflammation and phagocytosis
- complement proteins
- type 1 IFNs
- NK cells
- fever
25
what are leukocytes
white blood cells (WBC's)
26
what is a lymphocyte
a specific type of WBC
27
what do lymphocytes recognize
antigens
28
what immune response do lymphocytes participate in
adaptive
29
what is the goal of acute inflammatory response
to contain, destroy, and remove pathogens and initiate the process of healing
30
how does acute inflammation work
moves immune cells and inflammatory proteins from the blood to the site of infection where they destroy pathogens
31
what is the goal of chronic inflammation response
to contain, destroy, and remove persistant pathogens
32
what happens if chronic inflammatory response fails
it contains the infection until the adaptive immune response fully develops which will clear the infection
33
are PAMPs shared by humans
no
34
how do innate immune cell recognize pathogens
non-specific recognition
35
true or false - pattern recognition receptor (PRR) is an example of a toll-like receptor
true
36
what are three toll-like receptors (TLRs)
- lipopeptide
- flagellin
- peptidoglycan
37
mannose binding protein is another type of what
PRR
38
what is an opsonin
it is a soluble host protein
- coats the outer surface of a pathogen allowing phagocytes to bind and engulf more efficiently
39
what are the two major opsonins
- C3b -> recognize PAMPs
- IgG Ab -> recognize antigens
40
what are the eight steps to acute inflammatory response
1. macrophage releases vasoactive substances and cytokines
2. mast cell degranulates
3. histamine releases (vasoactive)
4. vasodilation
5. increased permeability and edema
6. diapedesis - PMNs traveling to site of infection
7. chemotaxis - movement towards or away gradient - towards site of infection
8. phagocytosis
41
true or false - C5a is also chemotactic
true
42
what process are TNF-alphas apart of
phagocyte migration
43
what are the six steps in phagocyte migration
1. circulating blood
2. endothelial cells receive signals from tissue to upregulate adhesion proteins
3. roll along inside vessel (selections)
4. stable adhesion (ICAM1)
5. diapedesis (WBC squeezes out between endothelial cells of the blood vessel to go to tissue)
6. chemotaxis
44
at the start of inflammation what is the most abundant
neutrophils
45
at the end of inflammation what is the most abundant
monocytes
- turn into macrophages when leave the blood vessel
46
when pathogen destruction is occurring by phagocytes what does the pH go down to
4-5
47
what happens in nonoxidative killing
once the phagosome fuses with the lysosome, the engulfed bacteria are degraded by lysosomal enzymes (lysozyme, phospholipase, and proteases)
48
why is it important that the fusion of phagosome and lysosome enhance acidification
for activation of pH-dependent lysosomal enzymes
49
what happens in oxidative killing
activated phagocytes undergo a respiratory burst
- increase their uptake and consumption of oxygen
50
the increased oxygen in oxidative killing is metabolized into
ROS
- reactive oxygen species
51
what does ROS degrade
bacteria
52
which cells do phagocytosis
- neutrophils
- macrophages
- dendritic cells
- all of the above
all of the above
53
what are cytokines
they are proteins secreted by WBCs that act on other cells to regulate their activity
54
true or false - cytokines can only act locally
false
- act locally or systemically
55
what do cytokines include
- chemokines
- IFN's
- TNF-alpha
- interleukins
56
what are three pro-inflammatory cytokines
- interleukins = subfamily of cytokines that are in both adaptive and innate immune responses
- chemokines = direct migration of WBCs to a site of infection (chemotaxis)
- TNF-alpha = stimulates production of adhesion proteins (selections) on endothelial cells
57
what are other inflammatory mediators
- histamine = vasodilation and increased vascular permeability
- prostaglandins and leukotrienes = vasodilation, pain, fever, and vascular permeability
- C3a and C5a = chemotaxis and mast cell degranulation (anaphylatoxin)
58
what can macrophages do in chronic inflammation
they become activated by cytokines (which are released by Th2 cells from adaptive)
- stimulate ROS production = increased phagocytic power
- secrete large quantities of cytokines that maintain the inflammatory response
59
what do lymphocytes (T and B cells) do in chronic inflammation
- major players in adaptive immune response
- direct the attack against persistent pathogens
60
does a granuloma form everytime with chronic inflammation
no
- only sometimes
61
what happens if activated macrophages fail to destroy microbes
the macrophages will fuse together to form giant multinucleated cells
62
what three things form granulomas
- giant multinucleated cells
- macrophages
- T cells
63
true or false - granulomas in infectious diseases may interfere with normal tissue function
true
64
what are granulomas called when they form in the lungs of TB patients
tubercles
65
what are granulomas called in syphilis
gummas
66
the proteins in the complement system are made where, circulate where, and enter where
- made in the liver
- circulate in the blood
- enter the tissue
67
true or false - the serum proteins are normally inactive in the complement system
true
68
how are the proteins in the complement system activated
- alternative pathway = C3b binding to microbial invaders
- lectin pathway = mannose-binding lectin binding to microbial invaders
- classical pathway (only if re-exposure) = antibodies binding to microbial invaders
69
what does C3b cause
opsonization
70
what does C3a + C5a cause
inflammation
71
what does C5b + C6-C9 cause
membrane attack complex (MAC) -> lysis
- create pores in membrane disrupting integrity of cell
72
how can something produced during the adaptive response activate the innate response
from the first exposure the body produced antibodies.
- memory of pathogen develops and antibodies are ready at re-exposure
- antibodies can easily activate classical pathway at re-exposure
73
what are the three effects of complement activation (pathways)
- inflammation
- opsonization -> enhanced phagocytosis
- membrane attack complex -> lysis
74
what kind of toxins are C3a and C5a
anaphylatoxins
- bind mast cells and basophils and degranulate to release histamine (vasodilation)
75
what do C5a attract
phagocytes (chemotactic)
76
a patient with a genetic disorder resulting in defective complement would be most affected by a mutation in which of these?
- C1
- C3
- C5
- C9
C3
77
how is a fever induced
by pyrogens
78
what are pyrogens
endogenous or exogenous
79
what is the function of prostaglandins in a fever
they reset hypothalamic thermostate
80
do you vasoconstrict or vasodilate in fever
vasoconstrict because sweating and shivering
81
what are the three benefits of a fever
- inhibits growth of temperature-sensitive microbes
- speeds up phagocytosis and the repair of tissue
- increased leukocyte motility
82
would complement proteins and phagocytosis be effective in fighting off pathogens that replicate inside cells such as viruses?
no
83
IFN-alpha and beta are apart of which immune response
innate
84
IFN-gamma is apart of which immune repsonse
adaptive
85
how are IFN-alpha and beta produced
by virally-infected cells
86
what do IFN-alpha and beta cause
neighbor cells to produce antiviral proteins - inhibit viral replication
87
how are IFN-gamma produced
by lymphocytes
88
what does IFN-gamma induce
neutrophils and macrophages to phagocytize bacteria
89
are NK cells innate or adaptive
innate
90
true or false - NK cells are a type of lymphocyte
true
91
true or false - NK cells kill virally
true
92
how do NK cells differ from T-cells
in the way they recognize their target
93
what are the two major immune responses
innate and adaptive
94
what are the two branches of the adaptive immune response
- cell-mediated immunity
- humoral immunity
95
what are the subcategories of cell-mediated immunity
- cytotoxic T-lymphocytes
- activated macrophages
96
what are the subcategories of humoral immunity
- B lymphocytes
- antibody proteins
97
is cell-mediated immunity intracellular or extracellular
intracellular
98
is humoral immunity intracellular or extracellular
extracellular
99
in cell-mediated immunity what do lymphocytes act against
target cell
100
describe how lymphocytes in cell-mediated immunity directly act against target cells
by killing infected cells
101
how to lymphocytes in cell-mediated immunity act indirectly against target cells
by releasing chemicals that enhance inflammatory response
- or by activating other lymphocytes or macrophages
102
in humoral immunity where are the antibodies circulating
freely in body fluids
103
what do B cells activate
antibodies
104
in humoral immunity do the antibodies bind permanently or temporarily to the target cell
temporarily
105
what happens in humoral immunity when the antibody temporarily binds to the target cell
- temporarily inactivate
- mark for destruction by phagocytes or complement
106
what are the two types of response in adaptive immunological memory
- primary response = occurs after initial contact with Ag
- secondary response = occurs after subsequent exposures
107
B cells differentiate into
plasma cells and memory cells
108
T cells differentiate into
helper T cells, cytotoxic T cells, and memory cells
109
does BCR recognize whole antigen or parts of antigen
whole antigen
110
does TCR recognize whole antigen or parts of antigen
parts of antigen
111
where do B cells and T cells develop
bone marrow
112
where do B cells mature
bone marrow
113
where do T cells mature
thymus
114
what are the primary lymphoid organs
thymus and bone marrow
115
what are the secondary lymphoid organs/tissues
- lymph nodes
- spleen
- clusters of lymphoid tissue in gut (GALT) and tonsils and breast (MALT)
116
____ but still ___ lymphocytes leave the thymus and bone marrow
immunocompetent and naive
117
___ cells and effector ___ cells circulate continuously in the blood and lymph and throughout the secondary lymphoid organs
memory and T
118
what are naïve lymphocytes
they are lymphocytes that have antigen receptors, but have not yet encountered their specific antigen
119
what are activated lymphocytes
they are lymphocytes that have bound antigen to their antigen receptor and have received a co-stimulatory signal
- they are able to expand and differentiate into effector and memory cells
120
what are effector lymphocytes
they are short-lived descendants of activated lymphocytes
- can carry out specific immune functions
121
what are memory lymphocytes
long-lived descendants of activated lymphocytes
- can quickly become active effector lymphocytes on second exposure to antigen
122
what is an antigen
a foreign substance recognized by a BCR, TCR, or antibody (Ab)
123
true or false - each microbe or noninfectious foreign substance has the same antigen
false
- antigens are unique to each one (like a name tag)
124
how did antigen get its name
antibody generator
125
what can be antigens
- proteins
- polysaccharides
- conjugates of lipids with proteins and polysaccharides
126
what is immunogenicity
has the ability to induce humoral and/or cell-mediated immune response
127
what is an immunogen
a substance that induces response
128
what is antigenicity
has the ability to combine specifically with Abs or TCR/MHC or BCR but may or may not induce an immune response
129
true or false - not all antigens are immunogenic
true
130
what are haptens
they are too small to induce a response
- lack immunogenicity
131
if hapten is coupled to a carrier protein is it able to induce an immune reponse
yes
132
what are epitopes apart of
antigens
133
what can recognize an epitope
- BCR
- TCR
- antibody (Ab)
134
true or false - a typical protein only has one unique epitope
false
- a typical protein has multiple epitopes
135
predict which of the following is the most immunogenic (ie which elicits the strongest immune response)
- ss DNA
- self (host) protein
- piece of plastic
- bacterial cell
- bacterial pilus protein
bacterial cell
136
what makes a good antigen
- large size (more epitopes)
- complexity/heterogeneity
- proteins generally elicit strong response
137
what are the two that elicit weak responses
- polymers
- lipids are haptens
138
how many antigen-binding sites do the BCR's recognize
two
139
how many antigen-binding sites do TCR's recognize
one
140
what kind of antigens do BCR bind to
free soluble antigens
141
what kind of antigens do TCR bind to
binds processed antigens that are presented to them by MHC receptor
- don't bind soluble antigen
142
true or false - each B and each T cell express a unique BCR or TCR that recognizes one single epitope
true
143
can B or T cells bind to identical antigens
yes
144
do BCRs and TCRs vary from cell to cell
yes
145
genetic rearrangement in T cell: what makes up the alpha chain
one V-alpha segment and one J-alpha segment
146
genetic rearrangement in T cell: what makes up the beta chain
one V-beta segment, one D-beta segment, and one J-beta segment
147
all of the genetic rearranging in the T cell provide
genetic diversity
148
for negative selection of autoimmune clones, lymphocytes that react with self antigens (autoimmune) undergo apoptosis (negative selection) in
bone marrow (B cells) or in thymus (T cells)
149
what is the purpose of lymphocytes in negative selection to undergo apoptosis
prevents self-reacting T and B cells from reaching the bloodstream and potentially causing autoimmune disease
150
what do activated CD4+ T cells differentiate into
helper T cells and memory cells
151
what are the two types of helper T cells
Th1 and Th2
152
why do helper T cells secrete cytokines
to activate other cells of the immune response
153
what does IL-2 activate
CD8+ T cells
154
what does IFN-gamma activate
macrophages
155
what does IL-4,5 activate
B cells
156
what does CTL mean
cytotoxic T cell
157
what do activated CD8+ T cells differentiate to
cytotoxic T cells and memory cells
158
CTL bind ___, make ___, and kill
bind cells, make holes (perforin) and kill (granzymes)
159
what are CTL effective against
intracellular pathogens particularly viruses
160
true or false - T cells only recognize short fragments of antigens (peptides of about 8-25 aa's)
true
161
what are APCs
professional antigen presenting cells
162
what are APCs
they are specialized cells that internalize antigen by phagocytosis or endocytosis and then express parts of the antigen on their cell surface via MHC receptors
163
APCs are distinguished by what two properties:
1. express MHC 2 receptors
2. provide co-stimulatory signals necessary for activation of T cells
164
what are the three kinds of APCs
- macrophages
- dendritic cells
- B cells
165
what do dendritic cells do
phagocytize pathogens
- most effective antigen presenter known
- strongest initiator of T cell activation
- key link between innate and adaptive immunity
166
where are macrophages located
they are widespread in lymphoid organs and connective tissues
167
what do macrophages in APCs present
they present antigens to T cells to activate themselves into mean phagocytes that secrete bactericidal chemicals
168
what is the function of B cells in APCs
- do not activate naive T cells
- present antigens to helper T cell to assist own activation
169
what are the two types of MHC receptors
- MHC 1 present to CD8+ T cells -> cytotoxic T cells
- MHC 2 present to CD4+ T cells -> helper T cell
170
where are MHC 1 receptor found
on all nucleated cells (not RBC)
171
with MHC 1 receptor how is the degradation of cytosolic proteins done
by proteasome
172
do MHC 1 receptors present endogenous or exogenous antigens
endogenous
173
what cells to the MHC 1 receptor present the processed antigen to
CD8+ T cells
174
MHC 2 receptors are found on
professional antigen presenting cells
- APCs also express MHC 1 receptors
175
how are the peptides generated in MHC 2
by lysosomal enzymes
176
true or false - antigens presented on MHC 2 receptors are exogenous (most bacteria, toxins, and fungi)
true
177
what cells do MHC 2 receptors present the peptides to
CD4+ T cells
178
which type of molecule is responsible for presenting an exogenous antigen on the surface of the appropriate cell?
- TCR
- MHC 1
- MHC 2
- CD4
- CD8
CD4
179
where in the body do APCs go to present endogenous antigens to CD8+ T cells?
- lymph nodes
- thymus
- liver
- bone marrow
lymph nodes
180
samantha johnson has bare lymphocyte syndrome due to a lack of MHC 1 expression. this disease would be expected to result in an inability of APCs to....
- present endogenous antigen to T cells
- bind to any T cells in the lymph node
- activate any CD4 T cells
- A and C are correct
- A and B are correct
present endogenous antigen to T cells
181
what are the two major phases of primary T and B cell response
1. selection and activation of naïve lymphocytes
2. execution of the effector function
182
what happens in clonal selection
upon entry into immune system, each antigen is recognized by a genetically distinct lymphocyte with the "right" receptor
183
what happens in clonal activation
signals from another cell are usually needed
184
what happens in clonal expansion
upon activation, the lymphocyte proliferates and differentiate into a larger population of identical cells (ie clones) that can react to that antigen
185
what are the three steps in activating CD4+ T cells
1. requires interaction between TCR and the peptide presented on MHC 2 on the APC
2. requires a co-stimulatory signal (B7-CD28)
3. CD4+ T cells up-regulates IL2R and produces IL-2 to expand and differentiate into effector and memory T cells
186
what do Th1 cells differentiate into
- IFN-gamma -> macrophages
- Il-2 -> CD8+ T cells
187
what do Th2 cells differentiate into
IL-4,5 -> B cells
188
with activated macrophages phagosome will be more ____ fused to the lysosomes
efficiently
189
in activated macrophages, what are the three highly reactive and microbicidal molecules
- oxygen radicals
- nitric oxide
- proteases
190
activated macrophages are a good defense against what
intracellular bacteria
- eg: mycobacterium tuberculosis
191
which type of lymphocytes is responsible for virus-infected host cells?
- B lymphocyte
- helper T cell
- cytotoxic T cell
- plasma cell
cytotoxic T cell
192
what are the four steps in the activation of CD8+ T cells
1. requires the interaction between TCR and peptide presented on MHC 1 on the APC
2. requires a co-stimulatory signal from B7-CD28
3. requires IL-2 from Th1 cell
4. CD8+ T cell up-regulates IL2R and produces IL2 to expand and differentiate into effector and memory T cells
193
can B cells recognize antigen directly
yes
194
when B cells are activated what do they differentiate into
plasma cells
195
what do plasma cells make and secrete
antibodies (Ig)
196
when antigens activate B cells, they clone, and give rise to __ cells and __ cells
plasma and memory
197
what are the two mechanisms of B cell activation
1. B cell receptor bind to antigen
- endocytose (engulf) the antigen, process it, and present on MHC 2 to Th2 cells
- Th2 cells release IL-4,5 -> strong activation = T dependent
2. co-stimulatory signal
- some antigens crosslink BCR -> weak activation = T-independent
198
true or false - T independent antigens are rare and highly repetitive molecules
true
199
do T-independent B cells produce memory cells or class switch
no
200
in T-independent B cell activation - B cells are weakly stimulated to make what class of antibodies
IgM
201
children don't activate ___ cells independently of ___ cells
B and T
202
T-dependent B cells present their antigen on their MHC ___ to __ cell
2 and Th2
203
in T-dependent B cell activation - Th2 cell produces cytokines that strongly activate the __ cell
B
204
in T-dependent B cell activation - can B cells undergo class switching to make antibodies other than IgM
yes
205
what are most antigens, T-dependent or T-independent
T-dependent
206
a patient infected with HIV becomes severely immunocompromised. This is because HIV infects and destroys CD4+ T cells. Low CD4+ T cell count would result in an inability to fight off infections by which of the following?
- RNA viruses
- extracellular bacteria
- intracellular bacteria
- fungi
- all of the above
all of the above
207
can an organism be wholly intracellular at all times
no
208
transmission must occur between what kind of cells
the host's cells
209
what does the extracellular phase in the development of the pathogen provide
an opportunity to control infection through defense mechanisms
- phagocytosis, presentation on MHC 2, Ab, and complement
210
can an APC engulf "dead" parts of viruses
yes
211
antibodies are especially effective against ___ pathogens
extracellular
- eg bacteria
212
what is the structure of an immunoglobulin
- Ab's are heterodimers
- 2 identical light chains and heavy chains
- disulfide bonds join heavy, light chains, and Fc segment
213
on the immunoglobulin structure how many Fab's and Fc's are there
two Fab's and one Fc
214
the Fc on the immunoglobin structure binds to what kind of cell
host cell
215
true or false - each antibody recognizes any general antigen
false
- each antibody recognizes a specific antigen
216
the BCR heavy chain is made up of what segments
V, D, and J
217
the BCR light chain is made up of what segments
V and J
218
what do antibodies do
they circulate through the blood and lymph
- only interacts with specific target antigen
219
what happens when Ab find its antigenic match
it binds to the antigen and initiates several events that destroy the targets
220
what are four antibody functions
1. agglutination = crosslink antigen to reduce number of infectious units to be dealt with (each side of Y attaches to a bacteria)
2. fixes and activates complement = the stick of the Y (Ab) attaches to complement and then causes inflammation and cell lysis
3. opsonization = enhances phagocytosis
4. neutralization = blocks adhesion of bacteria and viruses to mucosa (also blocks attachment of toxin) - the Abs will bind to every binding spot on the bacteria, virus, and toxin so that they have no where to bind onto our mucosa
221
what are the five different heavy chain constant regions
IgM,IgG, IgA, IgD, and IgE
222
amino acid sequence in the constant region of the ___ chain determines Ig class
heavy chain
223
IgM serves as an ___ receptor on B cells
antigen
224
what Ab class is first produced in primary response
IgM
225
what does IgM activate
complement
226
why is IgM good at agglutination
because it has 10 antigen binding sites
- 5 antibodies
227
what does the M stand for in IgM
multi/mega
228
what does the G stand for in IgG
generic/general
229
what Ab is the most abundant in serum
IgG
230
which Ab is the only one that can cross the placenta
IgG
231
what can IgG do
- opsonization
- activate complement
- neutralize toxins and viruses
232
what does IgA protect, what does it exist as, and what secretions is it in
- protects mucosal surfaces
- exists as a dimer
- is in breastmilk, mucus, tears, and saliva
233
what does IgD function as
a BCR
234
what can IgE do
lysis of parasitic worms and allergic reactions
235
upon first exposure which Ab is first made
IgM
236
what does IgM change into by default
IgG
237
in other situations, what can IgM class switch to
IgE or IgA
238
what does class switching not alter
the antigen specificity
239
are NK cells innate or adaptive, what kind of cells do they kill, their mechanism of killing is similar to what other cell
- innate cells
- kill infected host cells (intracellular)
- similar mechanism of killing as CTL (make pores, induce apoptosis -> perforin, granzyme)
240
immunological memory has two different responses, what are they
primary and secondary
241
what happens in the primary immune reponse
- cell proliferation and differentiation upon first antigen exposure
- lag period: 4-7 days or longer
- peak levels of plasma Ab are reached in 10 days
- Ab levels then decline
242
what happens in secondary immune response
- re-exposure to same antigen gives faster, more prolonged, more effective response
- sensitized memory cells respond within hours
- Ab levels peak in 3-5 days at much higher levels
- Ab's bind with greater affinity
- Ab level can remain high for weeks to months
- pathogens usually eliminated before causing harm
243
what Ab is the Ab of memory
IgG
244
when there is a second exposure, does IgM need to be made first and then change to IgG
no
- can produce IgG Ab without having to first make IgM and then class switch
245
what does immunization mean
exposure to antigen
246
what does immunodiagnosis use
antibody-antigen interactions to identify pathogens and diagnose infection
247
what is a serological test
in vitro diagnostic test of serum
248
what is serum
plasma with all clotting factors removed
- the blood fraction that contains antibodies
249
what is the percent of plasma, WBCS and platelets, and RBCs in immunodiagnosis
- 55% plasma
- 1% WBCs and platelets
- 44% RBCs
250
what do serological tests identify
antibodies
251
what do immunological tests identify
antigen
252
a positive Ab-Agn interaction is usually evident as some visible sign such as ___ ___ or ___
color change; clumping
253
what occurs with latex agglutination test to detect Ab
- latex beads coated with an antigen
- agglutinate when mixed with patient serum if they have IgM Abs against the antigen
- agglutinated complexes settle out and form visible clumps
254
in the latex agglutination test, the agglutinated particles will be spread throughout the test tube or mostly concentrated at the bottom with the most positive reaction
at the bottom
255
what happens with latex agglutination test to detect antigen
- latex beads coated with Abs
- agglutinate when mixed with patient serum if serum contains antigens specific to the antibodies
256
why are labeled Ab tests used
to detect either antigens or Abs
257
what are two examples of labeled Ab tests
1. fluorescent Ab tests (immunofluorescence)
2. ELISA
258
what is the indicator for ELISA
the enzyme linked to Ab
- product has color
259
how does ELISA detect Abs
- a patient's serum is added to wells in 96-well plate that has a known antigen
- patient's Abs bind to antigen
- patient's Abs are detected by a secondary Ab that is labeled with an enzyme
- when substrate is added, the enzyme-antibody complex hydrolyzes the substrate, which releases a dye
- wells that develop color are positive for the Ab
- colorless wells are negative
260
what does indirect ELISA detect
antibodies
261
what does direct ELISA detect
antigens
262
true or false - classifying adaptive immunity has active and passive immunity
true
263
how is active immunity acquired
through direct stimulation of the immune system by an antigen
- produces Abs
- takes time to develop
- develops memory, lasting
264
how is passive immunity acquired
indirectly by the donation of performed Abs produced by another human or animal
- protection without prior experience
- acts immediately
- does NOT create memory, short term
265
what is an example of natural acquired and artificial acquired passive immunity
- natural = breastmilk
- artificial = blood donation
266
what is an example of natural acquired and artificial acquired active immunity
- natural = getting the illness itself
- artificial = through vaccine
267
what are specific types of immunotherapy
- convalescent serum = serum from donor(s) who has a known exposure to a specific pathogen
- synthetic monoclonal Abs = Abs produced in the lab-specific to an antigen on a pathogen
- antitoxin = an Ab that recognizes and binds to a bacterial exotoxin or toxin in snake venom
268
what is immunotherapy used for
- patients at risk for rapidly fatal diseases
- patients at risk for bacterial diseases involving exotoxin (ie botulism and tetanus)
- patients who are immunodeficient (ie HIV patients and chemo patients)
269
true or false - immunotherapy is part of artificially acquired passive immunity
true
270
what does a vaccination do
- deliberately expose a person to material that is antigenic but not pathogenic
- stimulate a primary adaptive response to prepare the immune system for future exposure to a virulent pathogen (ie generate memory cells)
- response to exposure to the virulent pathogen will be immediate and powerful due to the secondary response
271
what does a vaccine contain
dead or weakened or subunits (parts) of pathogens that stimulates your immune system to produce Abs or CTL's, exactly like it would if you were exposed to the disease
272
true or false - vaccines = pathogen imposters
true
273
how is herd immunity achieved
when critical portion of population is immune to disease
274
herd immunity - the higher the immunization rate in a population, the less likely an ___ agent can spread due to insufficient susceptible hosts
infectious
275
what does herd immunity confer
indirect protection for those who can't become immune
276
what is herd immunity responsible for
dramatic declines in childhood diseases and for prevention of epidemics
277
who is unable to be immunized
- immunocompromised (AIDS patients, patients taking immunosuppressive drugs)
- pregnant women (risk to fetus)
- elderly or babies
278
one measure of contagiousness is ___
R0
279
what does R0 represent
the number of people on average that an infected individual spreads an infection to
280
what is the herd immunity threshold equation
(R0 - 1) / (R0)
281
why do we still vaccinate against uncommon disease
to maintain herd immunity
