1
Q
The immune system’s two intrinsic systems are:
A
- Innate (nonspecific) defense system
2. Adaptive (specific) defense system
2
Q
The immune system is a ____ system rather than ____ system.
A
functional; organ
3
Q
Innate and adaptive defenses of the immune system are ____.
A
intertwined
4
Q
Both innate and adaptive defenses release and recognise many of the same
A
defensive molecules
5
Q
How do innate defenses differ from adaptive?
A
- innate defenses have specific pathways for certain substances
- innate responses release proteins that alert cells of adaptive system to foreign molecules
6
Q
Innate defense system has two lines of defense–first and second. The first is composed of:
A
external body membranes (skin and mucosae)
7
Q
Innate defense system has two lines of defense–first and second. The second is composed of:
A
antimicrobial proteins, phagocytes, and other cells
8
Q
The second innate line of defense does what?
A
- inhibits the spread of invaders
2. has inflammation as its most important mechanism
9
Q
The adaptive defense system’s third line of defense does what?
A
It attacks particular foreign substances.
10
Q
How does the adaptive line of defense differ from the innate line of defense?
A
Takes longer to react than innate system.
11
Q
Innate defenses have ____ to ward off invading pathogens.
A
surface barriers
12
Q
The surface barriers of innate defenses are in the most general context:
A
skin, mucous membranes, and their secretions
13
Q
What are the characteristics of surface barriers of the innate defense system?
A
- they are a physical barrier to most microorganisms
- they are keratin resistant to weak acids and bases, bacterial enzymes, and toxins
- mucosae provide similar mechanical barriers
14
Q
Surface barriers of the innate defense system have protective chemicals that inhibit or destroy microorganisms. What are they?
A
- the acidity of skin and secretions–acid mantle
- enzymes
- defensins
- other chemicals
15
Q
The acidity of skin and secretions in the innate defense system does what to microorganisms?
A
inhibits growth
16
Q
What are the enzymes that inhibit microorganisms in the innate defense system?
A
- lysozome of saliva
- respiratory mucus
- lacrimal fluid
17
Q
What do the enzymes of the innate defense system do?
A
kill many microorganisms
18
Q
Defensins of the innate defense system are what? What do they do to microorganisms?
A
antimicrobial peptides; inhibit growth
19
Q
Other chemicals of the innate defense system are what? What effect do they have on microorganisms?
A
lipids in sebum, dermcidin in sweat; toxic
20
Q
Respiratory system modifications (surface barriers) of the innate defense system are:
A
- mucus-coated hairs in nose
- cilia of upper respiratory tract that sweep dust
- bacteria-laden mucus toward mouth
21
Q
Surface barriers of the innate immune system can be breached by nicks or cuts. What happens then?
A
second line of defense must protect deeper tissues
22
Q
If microorganisms invade deeper tissues, internal defenses of cells and chemicals are necessary. What are they?
A
- phagocytes
- natural killer (NK) cells
- antimicrobial proteins
- fever
- inflammatory response
23
Q
What is an example of antimicrobial proteins that protect deeper tissues upon invasion?
A
interferons and complement proteins
24
Q
What partakes in the inflammatory response to protect deeper tissues upon invasion?
A
- macrophages
- mast cells
- WBCs
- inflammatory chemicals
25
The phagocytes that participate in internal defenses are:
- neutrophils
| - macrophages
26
These are the most abundant phagocytes but die fighting.
neutrophils
27
_____ become phagocytic on exposure to infectious material.
neutrophils
28
____ develop from monocytes.
macrophages
29
The chief phagocytic cells are:
macrophages
30
____ macrophages wander through tissue spaces, e.g. alveolar macrophages.
free
31
___ macrophages are permanent residents of some organs, e.g. Kupffer cells (liver) and microglia (brain).
fixed
32
In order for phagocytosis to take place, the phagocyte must
adhere to particle
33
Some microorganisms evade phagocytic adherence with ____.
capsule
34
____ marks pathogens---coating by complement proteins or antibodies.
opsonisation
35
In phagocytosis, cytoplasmic extensions bind to and engulf the particle in a vesicle called ____.
phagosome
36
In phagocytosis, the phagosome fuses with lysosome, which creates ____.
phagolysosome
37
Pathogens are killed during phagocytosis due to acidifying and digesting with _____.
lysosomal enzymes
38
If lysosomal enzymes are unable to kill pathogens, helper T cells cause a release of enzymes of _____, which kill pathogens.
respiratory burst
39
What are the three ways that helper T cells kill pathogens that are resistant to lysosomal enzymes?
1. release cell-killing free radicals
2. produce oxidising chemicals (e.g. H2O2)
3. increase pH and osmolarity of phagolysosome
40
In phagocytosis, defensins in neutrophils pierce ____.
membrane
41
nonphagocytic large granular lymphocytes
natural killer (NK) cells
42
NK cells attack cells that lack
"self" cell-surface receptors
43
NK cells induce ___ in cancer cells and virus-infected cells.
apoptosis
44
NK cells secrete potent chemicals that enhance:
inflammatory response
45
This is triggered whenever body tissues are injured.
inflammatory response
46
This prevents the spread of damaging agents.
inflammation
47
The cardinal signs of acute inflammation are:
- redness
- swelling
- heat
- pain
- sometimes impairment of function
48
When inflammation is triggered, it disposes of what?
cell debris and pathogens
49
When inflammation is triggered, it alerts which system?
adaptive immune system
50
When inflammation is triggered, it sets the stage for what?
repair
51
The inflammatory response begins with chemicals released into _____ by injured tissues, immune cells, blood proteins.
ECF
52
Macrophages and epithelial cells of boundary tissues have ____ receptors.
Toll-like (TLR)
53
11 types of toll-like receptors (TLR) recognise specific classes of:
infecting microbes
54
Activated TLRs trigger release of _____ that promote inflammation.
cytokines
55
The three inflammatory mediators are:
- kinins
- prostaglandins
- complement
56
Inflammatory mediators dilate _____.
local arterioles
57
When inflammatory mediators dilate local arterioles, this is known as:
hyperemia
58
When inflammatory mediators dilate local arterioles, this causes:
redness and heat of inflamed region
59
Inflammatory mediators make capillaries ____.
leaky
60
Inflammatory mediators attract ____ to area.
leukocytes
61
Does edema increase capillary permeability or decrease it? What does this cause?
increase; exudate goes to tissues
62
Exudate is fluid containing ___ and ___.
clotting factors; antibodies
63
Exudate causes:
local swelling (edema)
64
When swelling occurs, it pushes on nerve endings which causes:
pain
65
Pain can also occur from:
- bacterial toxins
- prostaglandins
- kinins
66
Exudate moves foreign material into ____.
lymphatic vessels
67
Exudate delivers ____ and ____ to area of inflammation.
clotting proteins; complement
68
The clotting factors that exudate delivers to area of inflammation form _____.
fibrin mesh
69
The fibrin mesh formed by clotting factors at areas of inflammation is the scaffold for ____.
repair
70
The fibrin mesh formed by clotting factors at areas of inflammation isolates the injured area so that:
invaders can't spread
71
In phagocyte mobilisation, ___ lead, and ___ follow.
neutrophils; macrophages
72
As phagocyte attack continues, ___ arrive.
monocytes
73
12 hours after leaving bloodstream, monocytes become ____. These are called ___.
macrophages; "late-arrivers"
74
"Late-arrivers" replace ____ and remain for ____.
dying neutrophils; clean up prior to repair
75
If inflammation is due to pathogens, ____ is activated and ____ arrive.
complement; adaptive immunity elements
76
The steps for phagocyte mobilisation are:
1. leukocytosis
2. margination
3. diapedesis of neutropils
4. chemotaxis
77
the release of neutrophils from bone marrow in response to ____-inducing factors from injured cells
leukocytosis
78
neutrophils cling to walls of capillaries in inflamed area in response to CAMs
margination
79
inflammatory chemicals promote positive ___ of neutrophils
chemotaxis
80
inflammatory chemicals that promote chemotaxis are known as
chemotactic agents
81
Two different antimicrobial proteins are:
- interferons (IFNs)
| - complement proteins
82
Antimicrobial proteins attack microorganisms directly or indirectly?
directly
83
Antimicrobial proteins hinder the microorganisms' ability to ____.
reproduce
84
The family of immune-modulating proteins are known as:
interferons
85
Viral-infected cells secrete interferons to:
warn neighbouring cells
86
After viral-infected cells secrete IFNs, they enter neighbouring cells and cause the cell to do what?
produce proteins that block viral reproduction and degrade viral RNA
87
IFN alpha and beta also activate ____.
NK cells
88
IFN ____ is secreted by lymphocytes.
gamma (immune interferon)
89
IFN gamma activates ____.
macrophages
90
IFN gamma has widespread ____ effects.
immune-mobilising
91
Since IFN activates NK cells and macrophages, it indirectly fights ____.
cancer
92
Artificial IFNs are used to treat:
- hepatitis C
- genital warts
- MS
- hairy cell leukaemia
93
The complementary system is composed of ~20 blood proteins that circulate in ___ form.
inactive
94
The complement system includes which blood proteins?
- C1-C9
- factors B, D, and P
- other regulatory proteins
95
Complement is the major mechanism for destroying:
foreign substances
96
Our cells contain complement activation ____.
inhibitors
97
Complement unleashes inflammatory chemicals that:
amplify all aspects of inflammatory response
98
Complement kills bacteria and certain other cell types by ____.
cell lysis
99
Complement enhances which defense?
both innate and adaptive
100
There are three pathways to complement activation, which are:
- classical pathway
- lectin pathway
- alternative pathway
101
In the classical pathway, antibodies bind to ____ and ____. This is called _____.
invading organisms; complement components; complement fixation
102
The classical pathway is the ___ step in complement activation.
first
103
____ are produced by the innate system to recognise foreign invaders.
lectins
104
When lectins are bound to foreign invaders they can also bind and activate ____.
complement
105
Complement pathway that is triggered when activated C3, B, D, and P interact on the surface of microorganisms.
alternative pathway
106
Each complement pathway involves activation of ___ and in an orderly sequence.
proteins
107
In complement activation, each step ___ the next.
catalyses
108
Each complement pathway converges on ___, which cleaves into __ and ___.
C3; C3a; C3b
109
In complement activation, there is a common terminal pathway initiated that does three things, which are:
- enhances inflammation
- promotes phagocytosis
- causes cell lysis
110
Cell lysis begins when:
C3b binds to target cell
111
After C3b binds to target cell, what happens?
insertion of complement proteins called [membrane attack complex (MAC)] into cell's membrane
112
After MAC is inserted into cell's membrane, what happens?
MAC forms and stabilises a hole in the membrane surface
113
After MAC forms a hole in the membrane surface, what happens?
Influx of water --> lysis of cell
114
C3b also causes ____.
opsonisation
115
C3a and other cleavage products amplify ___.
inflammation
116
C3a stimulates mast cells and basophils to release ___.
histamine
117
C3a attracts ___ and ____.
neutrophils; other inflammatory cells
118
Fever is a systemic response to:
invading microorganisms
119
Leukocytes and macrophages exposed to foreign substances secrete ___.
pyrogens
120
Pyrogens act on:
body's thermostat in the hypothalamus, raising body temperature
121
The benefits of moderate fever are:
- causing the liver and spleen to sequester zinc and iron (needed by microorganisms)
- increasing metabolic rate --> faster repair
122
this system must be primed by initial exposure to a specific foreign substance
adaptive (specific defense) immune system
123
The adaptive immune system activates ___.
complement
124
The adaptive immune system amplifies ____.
inflammatory response
125
The adaptive immune system protects against ___ and ___.
infectious agents; abnormal body cells
126
part of the adaptive immune system that recognises and targets specific antigens
specific
127
part of the adaptive immune system that is not restricted to initial site
systemic
128
the adaptive immune system has ____, which leads to stronger attacks to known anitgens
memory
129
The two separate, overlapping arms of adaptive immune system are:
- humoral (antibody-mediated) immunity
| - cellular (cell-mediated) immunity
130
humoral immunity is composed of ___, produced by lymphocytes, circulating freely in body fluids
antibodies
131
in humoral immunity, antibodies bind temporarily to the target cell and do two things:
- temporarily inactivate target cell
| - mark the target cell for destruction by phagocytes or complement
132
in cellular immunity ___ act against target cell.
lymphocytes
133
lymphocytes that act against target cell act directly by
killing infected cells
134
lymphocytes that act against target cell act indirectly by
releasing chemicals that enhance inflammatory response or activating other lymphocytes or macrophages
135
substances that can mobilise adaptive defenses and provoke an immune response
antigens
136
antigens are the targets of all ___ immune responses
adaptive
137
Most antigens are large, complex molecules not normally found in
body (nonself)
138
The two important functional properties of complete antigens are:
- immunogenicity
| - reactivity
139
Examples of complete antigens are:
- foreign protein
- polysaccharides
- lipids
- nucleic acids
140
ability to stimulate proliferation of specific lymphocytes
immunogenicity
141
ability to react with activated lymphocytes and antibodies released by immunogenic reactions
reactivity
142
incomplete antigens are known as
haptens
143
incomplete antigens are not ___ by themselves
immunogenic
144
Example of haptens:
- peptides
- nucleotides
- some hormones
145
haptens may be immunogenic if attached to ____ and combination is marked foreign
body proteins
146
haptens cause the immune system to mount
harmful attack
147
Examples of mounted harmful attack as a result of haptens:
- poison ivy
- animal dander
- detergents
- cosmetics
148
antigenic determinants are also known as
epitopes
149
Only certain parts (epitopes) of entire antigen are ___
immunogenic
150
Antibodies and lymphocyte receptors bind to epitopes as enzyme binds ___.
substrate
151
Most naturally occurring antigens have numerous antigenic determinants that
- mobilise several different lymphocyte populations
| - form different kinds of antibodies against it
152
Large, chemically simple molecules (e.g. plastics) have little or no ___.
immunogenicity
153
self-antigens are also known as
MHC proteins
154
self-antigens are
protein molecules on the surface of cells that are not antigenic to self but antigenic to others in transfusions or grafts
155
Example of self-antigens:
MHC glycoproteins
156
MHC glycoproteins are coded by genes of ____ and are unique to the individual.
major histocompatibility complex
157
MHC glycoproteins have a groove holding ___ or ___.
self-antigen; foreign antigen
158
Lymphocytes only bind ___ on MHC proteins.
antigens
159
The three types of cells of the adaptive immune system are:
- B lymphocytes
- T lymphocytes
- Antigen-presenting cells (APCs)
160
B lymphocytes participate in ___ immunity.
humoral
161
T lymphocytes participate in ___ immunity.
cell-mediated
162
these do not respond to specific antigens and play essential auxiliary roles in immunity
antigen-presenting cells (APCs)
163
The five steps of lymphocyte development, maturation, and activation are:
- origin (all originate in red bone marrow)
- maturation
- seeding secondary lymphoid organs and circulation
- antigen encounter and activation
- proliferation and differentiation
164
Lymphocytes are educated as they mature, and become B cells in ___ or T cells in ___.
bone marrow; thymus
165
a lymphocyte can recognise one specific antigen by binding to it is known as
immunocompetence
166
lymphocytes unresponsive to own antigens is known as
self-tolerance
167
Thanks to immunocompetence, B or T cells display a unique receptor on their surface when they achieve maturity, so they can bind
only one antigen
168
T cells mature in the thymus under ___ and ___ pressures.
- positive selection
| - negative selection
169
selects T cells capable of regonising self-MHC proteins; failures are destroyed by apoptosis
positive selection
170
T cells capable of recognising self-MHC proteins is known as
MHC restriction
171
prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC; ensures self tolerance
negative selection
172
B cells are positively selected if they successfully make
antigen receptors
173
B cells that are self-reactive are handled by
elimination by apoptosis (clonal deletion)
174
Immunocompetent B and T cells that are not yet exposed to antigen are called
naive
175
Naive B/T cells are exported from ____ to ____.
primary lymphoid organs; "seed" secondary lymphoid organs
176
Exportation of naive B/T cells increases the chance of:
encounter with antigen
177
examples of primary lymphoid organs
- bone marrow
| - thymus
178
examples of secondary lymphoid organs
- lymph nodes
| - spleen
179
naive lymphocyte's first encounter with antigen leads to selection for further development. this is known as
clonal selection
180
If the correct signals are present in clonal selection,
lymphocyte will complete its differentiation
181
An activated lymphocyte ____.
proliferates
182
Due to lymphocyte proliferation, this leads to
exact clones
183
Most lymphocyte clones become
effector cells that fight infections
184
Few lymphocyte clones remain as
memory cells
185
Memory cells are able to respond to the same antigen
more quickly the second time
186
B and T memory cells and effector T cells circulate ___.
continuously
187
____ determine which foreign substances the immune system will recognise.
genes (not antigens)
188
Immune cell receptors are the result of
acquired knowledge of microbes (likely in environment)
189
Lymphocytes make how many different types of antigen receptors?
up to a billion
190
Lymphocytes are coded for by ~____ genes.
25,000
191
Gene segments are shuffled by ____.
somatic recombination
192
these engulf antigens
antigen-presenting cells (APCs)
193
APCs present fragments of antigens to ___ for recognition.
T cells
194
The three major types of APCs are:
- dendritic cells
- macrophages
- B cells
195
dendritic cells are located in
connective tissues and epidermis
196
macrophages are located in
connective tissues and lymphoid organs
197
dendritic cells phagocytise ___
pathogens
198
dendritic cells enter ___ to present antigens to ___ in lymph node
lymphatics; T cells
199
the most effective antigen-presenter known is
dendritic cell
200
dendritic cells are the key link between
innate and adaptive immunity
201
macrophages are widespread in ___ and ___
lymphoid organs; connective tissues
202
macrophages can activate
naive T cells
203
macrophages present antigens to T cells to
activate themselves into voracious phagocytes that secrete bactericidal chemicals
204
these do not activate naive T cells
B cells
205
B cells present antigens to ___ to assist own activation
helper T cell
206
B cells are activated when
antigens bind to its surface receptors and cross-link them
207
After antigens cross-link surface receptors, what happens?
receptor-mediated endocytosis of cross-linked antigen-receptor complexes (clonal selection)
208
After receptor-mediated endocytosis of cross-linked antigen-receptor complexes takes place, what happens?
proliferation and differentiation into effector cells
209
Most clone cells become ____ cells.
plasma
210
Plasma cells secrete ___ at a rate of ___ for how long?
specific antibodies; 2000 molecules/sec; four to five days, then die
211
Antibodies circulate in ___ or ___.
blood; lymph
212
Antibodies bind to ___ and mark for
free antigens; destruction by innate or adaptive mechanisms
213
Clone cells that do not become plasma cells become ____.
memory cells
214
Memory cells provide ____ memory and mount ___ response to future exposures of same antigen.
immunological; immediate
215
In immunological memory---primary immune response, upon first antigen exposure, what takes place?
cell proliferation and differentiation
216
The lag period for cell proliferation and differentiation in the primary immune response is:
three to six days
217
In the primary immune response, peak levels of plasma antibody are reached in ___ days.
10
218
After peak level of plasma antibodies in primary immune response of immunological memory, what happens?
antibody levels decline
219
Re-exposure to the same antigen gives ____ response. (Part of secondary immune response)
faster, more prolonged, more effective
220
(part of secondary immune response) Sensitised memory cells respond within:
hours
221
(part of secondary immune response) Antibody levels peak in ___ days at much higher levels.
two to three
222
(part of secondary immune response) Antibodies bind with ___ affinity.
greater
223
(part of secondary immune response) Antibody level can remain high for
weeks to months
224
when B cells encounter antigens and produce specific antibodies against them, this is known as
active humoral immunity
225
The two types of active humoral immunity are
- naturally acquired
| - artificially acquired
226
response to bacterial or viral infection
naturally acquired humoral immunity
227
response to vaccine of dead or attenuated pathogens
artificially acquired humoral immunity
228
most of dead or attenuated pathogens are
vaccines
229
Vaccines spare us symptoms of
primary response
230
Vaccines provide
antigenic determinants that are immunogenic and reactive
231
Vaccines can cause
- illness trying to vaccine against
| - allergic responses
232
___ and ___ help prevent illness or allergic responses induced by vaccines.
- "naked DNA"
| - oral vaccines
233
In ____ immunity, readymade antibodies are introduced into body.
passive humoral
234
In passive humoral immunity, B cells are ___ by antigens.
not challenged
235
Does immunological memory occur in passive humoral immunity?
no
236
In passive humoral immunity, protection ends when
antibodies degrade
237
Two types of passive humoral immunity
- naturally acquired
| - artificially acquired
238
antibodies are delivered to fetus via placenta or to infant through milk. this is known as
naturally acquired passive humoral immunity
239
injection of serum, such as gamma globulin, is known as
artificially acquired passive humoral immunity
240
In artifically acquired passive humoral immunity, protection is immediate but ends when
antibodies naturally degrade in body
241
the gamma globulin portion of blood is known as
immunoglobulins
242
proteins secreted by plasma cells are
antibodies
243
Antibodies are capable of binding specifically with antigen detected by ___.
B cells
244
Antibodies are grouped into one of ___ Ig classes.
five
245
four looping polypeptide chains linked by disulfide bonds
antibody monomer
246
Antibodies have T- or Y- shaped ____.
antibody monomer
247
Overall antibody shape/structure:
- two identical heavy chains with hinge region at "middles"
- two identical light chains
- variable regions at one end of each arm
- constant regions of stem
248
Variable regions at one end of each antibody arm combine to form two identical ____.
antigen-binding sites
249
Constant regions of antibody stem determine
antibody class
250
Constant regions of antibody stem serve common functions in all antibodies by dictating:
- cells and chemicals that antibody can bind
| - how antibody class functions to eliminate antigens
251
The different classes of antibodies are:
- IgM
- IgA
- IgD
- IgG
- IgE
252
Characteristics of IgM antibodies:
- pentamer (larger than others)
- first antibody released
- potent agglutinating agent
- readily fixes and activates complement
253
Characteristics of IgA antibodies:
- monomer or dimer
- in mucus and other secretions
- helps prevent entry of pathogens
254
Characteristics of IgD antibodies:
- monomer attached to surface of B cells
| - functions as B cell receptor
255
Characteristics of IgG antibodies:
- monomer; 75-85% of antibodies in plasma
- from secondary and late primary responses
- crosses placental barrier
256
Characteristics of IgE antibodies:
- monomer active in some allergies and parasitic infections
| - causes mast cells and basophils to release histamine
257
B cells can switch antibody classes but retain ____.
antigen specificity
258
B cells can switch from ___ at first; then ___.
IgM; IgG
259
Almost all secondary antibody responses are ___.
IgG
260
How do antibodies affect antigens?
inactivate and tag antigens; do not destroy them
261
When antibodies interact with antigens, they form:
antigen-antibody (immune) complexes
262
The defensive mechanisms used by antibodies are
- neutralisation and agglutination (two most important)
| - precipitation and complement fixation
263
the simplest defense mechanism is
neutralisation
264
In neutralisation, antibodies block specific sites on ___ or ___.
viruses; bacterial exotoxins
265
In neutralisation, antibodies that block sites prevent antigens from
binding to receptors on tissue cells
266
In neutralisation ____ undergo phagocytosis.
antigen-antibody complexes
267
antibodies bind same determinant on more than one cell-bound antigen
agglutination
268
In agglutination, ____ agglutinate. An example is:
cross-linked antigen-antibody complexes; clumping of mismatched blood cells
269
soluble molecules are cross-linked
precipitation
270
When soluble molecules are cross-linked, what happens?
Complexes precipitate and are subject to phagocytosis.
271
The main antibody defense against cellular antigens is:
complement fixation and activation
272
In complement fixation, several antibodies bind close together on a cellular antigen. This leads to:
complement-binding sites on stem regions aligning
273
When complement-binding sites on stem regions align, this triggers:
complement fixation into cell's surface ---> cell lysis
274
Functions of activated complement are:
- amplifies inflammatory response
- promotes phagocytosis via opsonisation
- -->positive feedback cycle that enlists more and more defensive elements
275
A commercially prepared pure antibody (also known as ____) is specific for:
monoclonal antibody; single antigenic determinant
276
Monoclonal antibodies are produced by:
hybridomas
277
cell hybrids; fusion of tumor cell and B cell
hybridomas
278
Monoclonal antibodies proliferate indefinitely and have ability to produce:
single type of antibody
279
monoclonal antibodies are used in
- research
- clinical testing
- cancer treatment
280
What do antigen-antibody complexes do to antigens?
do not destroy; prepare them for destruction by innate defenses
281
Antibodies do not invade solid tissue unless:
there is a lesion present
282
Antibodies can act intracellularly if:
attached to virus before it enters cell
| -->activate mechanisms that destroy virus
283
In the cellular immune response, T cells provide defense against ____.
intracellular antigens
284
Some T cells ___ cells; others release chemicals that:
directly kill; regulate immune response
285
In cell-mediated immune response, there are two populations of T cells based on which glycoprotein surface receptors are displayed. These are:
- CD4 cells
| - CD8 cells
286
CD4 cells usually become ____ cells.
helper T
287
Helper T (CD4) cells activate:
- B cells
- other T cells
- macrophages
- direct adaptive immune response
288
Some CD4 cells become ____.
regulatory T cells
289
Regulatory T cells moderate ____.
immune response
290
CD4 cells can also become ____.
memory T cells
291
CD8 cells become ____.
cytotoxic T cells
292
Cytotoxic T cells (CD8) destroy cells that are
harboring foreign antigens
293
CD8 cells can also become ___
memory T cells
294
Helper, cytotoxic, and regulatory T cells are ____ T cells.
activated
295
CD4 or CD8 cells are also known as
naive T cells
296
T cells only respond to processed fragments of antigens displayed on
surfaces of cells
297
Antigen presentation is vital for activation of ___ and normal functioning of ___.
naive T cells; effector T cells
298
The two types of MHC proteins important to T cell activation are:
- Class I MHC proteins
| - Class II MHC proteins
299
Both types of MHC proteins are synthesised at __ and bind to ____.
endoplasmic reticulum; peptide fragments
300
proteins that are displayed by all cells except RBCs
class I MHC proteins
301
proteins that are displayed by APCs (dendritic cells, macrophages, B cells)
class II MHC proteins
302
Class I MHC proteins bind with fragment of protein synthesised
in the cell
303
a fragment of protein synthesised in the cell is known as
endogenous antigen
304
In a normal cell, an endogenous antigen is ___. In an infected or abnormal cell it is ___.
self-antigen; nonself antigen
305
Class I MHC proteins are crucial for
CD8 cell activation
306
Class I MHC proteins inform cytotoxic T cells of
microorganisms hiding in cells (cytotoxic T cells ignore displayed self-antigens)
307
Class I MHC proteins act as
antigen holders; form "self" part that T cells recognise
308
Class II MHC proteins bind with fragments of ____ that have been engulfed and broken down in a phagolysosome.
exogenous antigens
309
Class II MHC proteins are recognised by ____.
helper T cells
310
Class II MHC proteins signal ___ cells that help is required.
CD4
311
CD4 and CD8 cells have different requirements for MHC protein that presents antigens to them. CD4 cells that become Th bind only:
class II MHC proteins typically on APC surfaces
312
CD4 and CD8 cells have different requirements for MHC protein that presents antigens to them. CD8 cells that become cytotoxic T cell bind only:
class I MHC proteins on APC surfaces
313
Once (CD8 cells that become) cytotoxic T cells are activated, they seek:
same antigen on class I MHC proteins on any cell
314
CD8 cells are activated by class __ MHC proteins.
I
315
How do APCs get endogenous antigens from another cell and display them on class I MHCs?
Dendritic cells engulf dying virus-infected or tumor cells, or import antigens via temporary gap junctions with infected cells--then display both class I and class II MHCs
316
The two-step process of T cell activation:
- Antigen binding
| - Co-stimulation
317
Both steps of T cell activation occur on surface of:
same APC
318
Both steps of T cell activation are required for ___.
clonal selection
319
T cell antigen receptors (TCRs) bind to ____ on APC surface.
antigen-MHC complex
320
TCR that recognises the nonself-self complex is linked to:
multiple intracellular signaling pathways
321
Other T cell surface proteins are involved in ____. (Ex. ___)
T cell activation; CD4 and CD8 help maintain coupling during antigen recognition
322
T cell activation--co-stimulation--requires T cell binding to:
other surface receptors on an APC (co-stimulatory signals)
323
Cytokines (interleukin 1 and 2 from APCs or T cells) trigger ___ and ___ of activated T cell.
proliferation; differentiation
324
Without co-stimulation of T cell activation, ___ occurs.
anergy
325
In anergy, T cells become:
tolerant to that antigen
326
In anergy, T cells are unable to:
divide
327
In anergy, T cells do not:
secrete cytokines
328
T cells that are activated do what?
- enlarge and proliferate in response to cytokines
| - differentiate and perform functions according to their T cell class
329
Primary T cell response peaks within:
a week
330
T cell apoptosis occurs between days:
7 and 30
331
The benefit of T cell apoptosis:
activated T cells are a hazard--produce large amount of inflammatory cytokines
-->hyperplasia, cancer
332
Effector activity wanes as amount of:
antigen declines
333
Memory T cells remain and mediate:
secondary responses
334
chemical messengers of the immune system are:
cytokines
335
Cytokines mediate:
- cell development
- differentiation
- responses in immune system
336
Cytokines include ___ and ___.
interferons; interleukins
337
____ is released by macrophages which co-stimulates bound T cells.
Interleukin 1 (IL-1)
338
Interleukin 1 co-stimulates bound T cells to:
- release interleukin 2 (IL-2)
| - synthesise more IL-2 receptors
339
IL-2 is a key growth factor, acting on cells that:
release it and other T cells
340
IL-2 encourages activated ____ to divide rapidly.
T cells
341
Other cytokines amplify and regulate:
innate and adaptive responses
342
Examples of cytokines that amplify and regulate innate and adaptive responses:
- tumor necrosis factor -- cell toxin
| - gamma interferon -- enhances killing power of macrophages
343
Helper T (Th) cells play a central role in:
adaptive immune response
344
Helper T cells activate both:
humoral and cellular arms
345
Once primed by APC presentation of antigen, helper T cells do what?
- help activate T and B cells
- induce T and B cell proliferation
- their cytokines recruit other immune cells
346
Without helper T cells, there is no:
immune response
347
Helper T cells interact directly with B cells displaying:
antigen fragments bound to MHC II receptors
348
Helper T cells stimulate B cells to ___ and ___.
divide more rapidly; being antibody formation
349
B cells may be activated by helper T cells by binding to _____. Reponse is:
T cell-independent antigens; weak and short-lived
350
Most antigens require Th co-stimulation to activate B-cells, these are called:
T cell-dependent antigens
351
CD8 cells require helper T cell activation into:
destructive cytotoxic T cells
352
Helper T cell activation of CD8 cells cause dendritic cells to express ____ required for CD8 cell activation.
co-stimulatory molecules
353
Helper T cells amplify responses of:
innate immmune system
354
Helper T cells activate ___, which leads to:
macrophages; more potent killers
355
Helper T cells mobilise _____ and ____ and attract other types of ___.
lymphocytes; macropages; WBCs
356
Helper T cells are divided into these subsets of helper T cells:
- Th1
- Th2
- Th17
357
Subset helper T cells that mediate most aspects of cellular immunity:
Th1
358
Subset helper T cells that defend against parasitic worms; mobilise eosinophils, promote allergies:
Th2
359
Subset helper T cells that link adaptive and innate immunity by releasing IL-17; may play role in autoimmune disease:
Th17
360
these cells directly attack and kill other cells
cytotoxic T cells (Tc)
361
activated cytotoxic cells circulate in blood and lymph and lymphoid organs in search of:
body cells displaying antigen they recognise
362
Cytotoxic (Tc) cell targets are:
- virus-infected cells
- cells with intracellular bacteria or parasites
- cancer cells
- foreign cells (transfusions or transplants)
363
Cytotoxic T cells bind to a ___ complex.
self-nonself
364
Cytotoxic T cells can destroy all:
infected or abnormal cells
365
Lethal hit of cytotoxic cells--two methods:
- Tc cell releases perforins and granzymes by exocytosis
| - Tc cell binds specific membrane receptor on target cell, and stimulates apoptosis
366
Perforins create pores through which:
granzymes can enter target cell
367
Granzymes stimulate ____.
apoptosis
368
Regulatory T cells dampen immune response by:
direct contact or by inhibitory cytokines such as IL-10 and TGF-beta
369
Regulatory T cells are important in preventing:
autoimmune reactions
370
By preventing autoimmune reactions, regulatory T cells do (two) things:
- suppress self-reactive lymphocytes in periphery (outside lymphoid organs)
- research into using them to induce tolerance to transplanted tissue
371
Natural killer cells recognise other (3) signs of abnormality:
- lack of class I MHC
- antibody coating target cell
- different surface markers of stressed cells
372
NK cells use same key mechanisms as ___ cells for killing their target cells.
cytotoxic T cells
373
In ___, NK and cytotoxic T cells prowl for markers they recognise.
immune surveillance
374
The four varieties of organ transplants are:
- autografts
- isografts
- allografts
- xenografts
375
graft from one body site to another in same person
autograft
376
graft between identical twins
isograft
377
graft between individuals who are not identical twins
allograft
378
graft from another animal species
xenograft
379
Sucess of graft depends on similarity of __.
tissues
380
Autografts and isografts have ideal donor tissues which are almost always successful if:
there is a good blood supply and no infection
381
There has been research into ___grafts from genetically engineered animals.
xenografts
382
The most common graft is:
allograft
383
In allograft, ___, ___, and ___ are mached as closely as possible.
ABO; other blood antigens; MHC antigens
384
In immunosuppressive therapy problems, the patient's ___ is supressed.
immune system
385
After the immune system is suppressed, it cannot:
protect from foreign agents
386
After the immune system is suppressed, bacterial and viral infections lead to:
death
387
After the immune system is suppressed, it must balance drugs for ____ but no toxicity.
graft
388
After the immune system is suppressed, it uses ___ to control infections.
antibiotics
389
After the immune system is suppressed, undr best circumstances, rejection is after ____ in __% of patients.
10 years; 50%
390
congenital or acquired condition that impairs function or production of immune cells or molecules such as complement or antibodies
immunodeficiency
391
Severe combined immunodeficiency syndrome (SCID) is a ___ defect.
genetic
392
In SCID, there is a marked deficit in ___ and ___ cells.
B; T
393
In SCID, there is a defective ___ enzyme.
adenosine deaminase (ADA)
394
SCID is fatal if untreated; it is treated with ___ transplants.
bone marrow
395
Lymphoma is an acquired ____.
immunodeficiency
396
Lymphoma is cancer of ____.
lymphocytes
397
Lymphoma leads to immunodeficiency by depressing:
lymph node cells
398
Acquired immune deficiency syndrome (AIDS) cripples the immune system by:
interfering with activity of helper T cells
399
AIDS is characterised by:
- severe weight loss
- night sweats
- swollen lymph nodes
400
With AIDS, opportunistic infections occur, such as:
- pneumocystis pneumonia
| - Kaposi's sarcoma
401
AIDS is caused by ____ transmitted by bodily fluids--blood, semen, and vaginal secretions
human immunodeficiency virus (HIV)
402
HIV enters body via:
- blood transfusions
- blood-contaminated needles
- sexual intercouse and oral sex
- vaginal secretions
403
HIV destroys ___ cells, which leads to:
helper T cells; depression of cell-mediated immunity
404
HIV multiplies in lymph nodes throughout ___ period, ~10 years if untreated
asymptomatic
405
There are symptoms of HIV when ___ collapses:
immune system
406
HIV also invades brain, which leads to:
dementia
407
HIV-coated glycoprotein complex attaches to:
CD4 receptor
408
Acquired Immune Deficiency Synrome (AIDS) arises from:
HIV reverse transcriptase
409
HIV reverse transcriptase leads to:
frequent errors; high mutation rate and resistance to drugs
410
AIDS can be treated with these antiviral drugs:
- fusion inhibitors
- integrase inhibitors
- reverse transcriptase and protease inhibitors
- antiretroviral vaginal gel
411
____ block HIV's entry into cell.
fusion inhibitors
412
____ block viral RNA integration into host's DNA.
integrase inhibitors
413
_____ inhibit viral replication enzymes.
reverse transcriptase and protease inhibitors
414
antiretroviral vaginal gel reduces AIDS risk by ___%.
50
415
immune system loses ability to distinguish self from foreign
autoimmune disease
416
in autoimmune disease, there is production of ____ and ____ that destroy body tissues.
autoantibodies; sensitised Tc cells
417
Examples of autoimmune diseases:
- MS
- myasthenia gravis
- Graves' disease
- type I diabetes mellitus
- systemic lupus erythmatosus
- glomerulonephritis
- rheumatoid arthritis
418
Autoimmune diseases are treated by suppressing the entire immune system by:
- anti-inflammatory drugs (e.g. corticosteroids)
- blocking cytokine action
- blocking co-stimulatory molecules
419
Research into autoimmune disease treatment includes:
- activating regulatory T cells
- inducing self-tolerance using vaccines
- directing antiboies against self-reactive immune cells
420
In autoimmune disease, weakly self-reactive lymphocytes may be activated by:
- foreign antigens that may resemble self-antigens
| - new self-antigens may appear
421
When foreign antigens that may resemble self-antigens appear, antibodies against foreign antigen may:
cross-react with self-antigen
422
In autoimmune disease, new self-antigens may appear, generated by:
- gene mutations
- changes in self-antigens by hapten attachment or infectious damage
- release of novel self-antigens by trauma to barrier
423
immune responses to perceived (otherwise harmless) threat cause tissue damage
hypersensitivities
424
different types of hypersensitivities are distinguished by:
1. their time course
| 2. whether antibodies or T cells are involved
425
Antibodies cause ___ and ___ hypersensitivities.
immediate; subacute
426
T cells cause ___ hypersensitivity.
delayed
427
_____ hypersensitivities begin in seconds after contact with allergen.
acute (type I) [allergies]
428
Initial contact with allergen is ____ but sensitises person.
asymptomatic
429
Allergy reaction may be ___ or ___.
local; systemic
430
Allergy reaction involves ___ secrete by ___ cells.
IL-4; Th2
431
Secreted IL-4 stimulates ____ to produce ___.
B cells; IgE
432
Produce IgE binds to ___ and ___, which leads to:
mast cells; basophils; flood of histamine release and induced inflammatory response
433
A later encounter with same allergen leads to:
allergic reaction
434
mast cells of skin and respiratory and gastrointestinal mucosa react to allergen
local reaction
435
allergic systemic response is ____.
anaphylactic shock
436
in allergic reaction, histamine release leads to
blood vessels dilated and leaky --> runny nose, hives, watery eyes
-asthma if allergen is inhaled
437
allergic reaction histamine release is controlle by
antihistamines
438
systemic response to allergen that directly enters blood and circulates rapidly
anaphylactic shock
439
in anaphylactic shock, ___ and ___ are enliste throughout the body
basophils; mast cells
440
Systemic histamine release may cause:
- constriction of bronchioles; tongue may swell
- sudden vasodilation and fluid loss from bloodstream that may cause
- >circulatory collapse (hypotensive shock) and death
441
anaphylactic shock is treate by
epinephrine
442
subacute hypersensitivities are caused by ___ and ___ transferred via blood plasma or serum
IgM and IgG
443
subacute hypersensitivities have a ___ onset and ___ duration
slow; long
444
two subacute hypersensitivities are:
- cytotoxic (type II reactions)
| - immune complex (type III) hypersensitivity
445
an example of cytotoxic (type II) reaction
mismatched blood transfusion reaction
446
an example of immune complex (type III) hypersensitivity
systemic lupus erythematosus
447
antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement-mediated lysis of cellular antigens
cytotoxic (type II) reactions
448
in immune complex (type III) hypersensitivity, ___ are widely distributed in body or blood
antigens
449
in immune complex (type III) hypersensitivity, once antigens are distributed in the body, ____ form.
insoluble antigen-antibody complexes
450
in immune complex (type III) hypersensitivity, complexes cannot be cleared from:
particular area of body
451
in immune complex (type III) hypersensitivity, complex buildup leads to:
- intense inflammation
- local cell lysis
- cell killing by neutrophils
452
delayed hypersensitivities (type IV) have a ___ onset.
slow
453
delayed hypersensitivities (type IV) mechanism depends on _____ cells.
helper T
454
in delayed hypersensitivities (type IV), ____ and ___ cause damage.
cytokine-activated macrophages; cytotoxic T cells
455
an example of delayed hypersensitivity (type IV) is
allergic contact dermatitis (e.g. poison ivy)
456
type IV hypersensitivity agents act as ____.
haptens
457
___ test depends on type IV hypersensitivity reaction.
TB skin
458
immune system stem cells develop in liver and spleen in weeks ____.
1-9
459
bone marrow becomes primary source of stem cells when?
later and through adult life
460
lymphocyte development continues in ___ and ___.
bone marrow; thymus
461
___ lymphocytes preominate in newborn; ___ system educated as person encounters antigens
Th2; Th1
462
depression, emotional stress, and grief do what do the immune response?
impair
463
vitamin ____ is required for activation of CD8 cells to produce Tc cells
D
464
vitamin D supplements reduce _____.
influenza
465
vitamin D deficiency is linked to ____.
MS
466
with age, immune system begins to ___.
wane
467
as a person ages, there is greater susceptibility to:
immunodeficiency and autoimmune diseases
468
as a person ages, there is greater incidence of:
cancer
A&P II
flashcards
Decks in class (8)
# Cards
-
Chapter 17 - Blood199
-
Chapter 16 - Endocrine System238
-
Chapter 18 - The Cardiovascular System - Heart258
-
Chapter 17 - Blood Pt. 2109
-
Chapter 19 - The Cardiovascular System - Blood Vessels219
-
Chapter 20 - The Lymphatic System and Lymphoid Organs and Tissues99
-
Chapter 21 - The Immune System - Innate and Adaptive Body Defenses468
-
Chapter 22 - The Respiratory System515
