Chap 16 Flashcards
(337 cards)
1
Q
Nonspecific defenses of the host
A
Innate immunity
2
Q
Mature cell that releases antibodies
A
Plasma cell
3
Q
Cells that make up innate immunity
A
-Basophil
-Eosinophil
-Mast cell
4
Q
Granulocytes
A
-Basophil
-Eosinophil
-Mast cell
-Neutrophil
5
Q
Both innate and adaptive cells
A
-Neutrophil
-Monocyte
-Dendritic cell
- Natural Killer cell
6
Q
Adaptive immunity cells
A
Plasma cell
B cell
T cells
7
Q
Types of T cells
A
-T helper
-Cytotoxic T cells (lymphocytes)
-T regulatory cell
8
Q
Agranulocyte with many surface projections
A
Dendritic cells
9
Q
Releases histamines that cause inflammation
A
Basophil
10
Q
Kills parasites with oxidative burst
A
Eosinophil
11
Q
Antigen-presenting cells; produce antibacterial peptides
A
Mast cell
12
Q
Phagocytizes bacteria and fungi
A
Neutrophil
13
Q
Precursor to macrophages. Some macrophages can be fixed in certain organs while others wander tissues, causing inflammation. All perform phagocytosis.
A
Monocyte
14
Q
In skin and respiratory and intestinal mucosa, phagocytizes bacteria and presents antigens to T cells
A
Dendritic cell
15
Q
Kills cancer cells and virus-infected cells
A
NK cell
16
Q
Recognizes antigens and produces antibodies
A
Plasma cell, B cell
17
Q
TH (T helper cell)
A
secrete cytokines
18
Q
They are CD4+ cells that bind MHC class II molecules on APCs.
A
Helper T cells
19
Q
recognize and kill specific “non-self” cells. They are CD8+ cells that bind to MHC class I molecules. T
A
Cytotoxic T lymphocyte CTL
20
Q
Cells are CD4+ cells that destroy cells that do not correctly recognize “self” cells.
A
T regulatory cells
21
Q
measure leukocytes in the blood
A
White blood cell (WBC) counts
22
Q
High WBC counts may indicate
A
bacterial infections, autoimmune diseases, or side effects of medications
23
Q
Low WBC counts may indicate
A
viral infections, pneumonia, autoimmune diseases, or cancers
24
Q
Normal WBC range
A
5,000-10,000 WBCs per cubic milimeter or 5.0-10.0 x 10^9 WBCs per liter
25
Normal neutrophils percentage
60-70%
26
Normal lymphocytes percentage
20% to 25%
27
Normal monocytes percentage
3% to 8%
28
Normal Eosinophils percentage
2% to 4%
29
Normal basophils percentage
0.5% to 1%
30
Immunity
ability to ward off disease
31
Susceptibility
lack of resistance to a disease
32
Innate immunity
defenses against any pathogen; rapid, present at birth
33
Adaptive immunity:
immunity or resistance to a specific pathogen; slower to respond, has memory component
34
Toll-like receptors (TLRs)
on host cells attach to pathogen-associated molecular patterns (PAMPs)
35
TLRs bound to PAMPs induce
the release of cytokines from the host cell that regulate the intensity and duration of immune responses
36
First line defenses
Skin
Mucous membranes
37
Innate (Non-specific) Defenses
1. First-line defenses
2. Phagocytosis
3. inflammation
4. Complement system
38
Two main divisions of adaptive defense
1. humoral immunity
2. Cell-mediated immunity
39
Antigen presenting/processing cells aid in
activation of adaptive defenses
40
humoral immune response
consists of the activity of B cells and the antibodies they produce
41
Cell-mediated immunity
host defense used to fight intracellular pathogens and abnormal body cells such as cancer cells.
42
Protagonists of cell-mediated immunity are
T lymphocytes
43
Helper T cells
secrete cytokines to activate other cells of the immune system
44
Cytotoxic T cells
attack infected cells directly
45
Dermis
inner portion made of connective tissue
46
Epidermis
outer portion made of tightly packed epithelial cells containing keratin, a protective protein
47
Shedding and dryness of skin inhibits
microbial growth
48
Mucous membranes
Epithelial layer that lines the gastrointestinal, respiratory, and genitourinary tracts
49
Mucus
viscous glycoproteins that trap microbes and prevent tracts from drying out
50
Lacrimal apparatus
drains tears; washes eye
51
Ciliary escalator
transports microbes trapped in mucus away from the lungs
52
Earwax
prevents microbes from entering the ear
53
Urine
cleans the urethra via flow
54
Vaginal secretions
move microorganisms out of the vaginal tract
55
Other physical factors
Peristalsis, defecation, vomiting, diarrhea
56
Sebum
forms a protective film and lowers the pH (3–5) of skin
57
To what level does sebum lower pH?
3-5
58
Lysozyme
in perspiration, tears, saliva, and urine destroys bacterial cell walls
59
60
gastric juice
destroys most bacteria and toxins
61
pH of gastric juice
1.2-3.0
62
Low pH (3–5) of vaginal secretions inhibits
microbes
63
pH of Vaginal secretions
3-5
64
Normal microbiota
compete with pathogens via microbial antagonism (competitive exclusion)
65
microbial antagonism
(competitive exclusion)
66
Competitive advantage for space and nutrients
normal microbiota
67
Produce substances harmful to pathogens
normal microbiota
68
Alter conditions that affect pathogen survival
normal microbiota
69
Commensalism:
one organism benefits while the other (host) is unharmed
70
Probiotics
live microbial cultures administered to exert a beneficial effect
71
Formed Elements in Blood
Cells and cell fragments suspended in plasma
72
Types of formed elements in blood
Erythrocytes (red blood cells)
Leukocytes (white blood cells)
Platelets
73
How are formed elements created?
Created in red bone marrow stem cells via hematopoiesis
74
Granulocytes
leukocytes with granules in their cytoplasm that are visible with a light microscope
75
Neutrophils
phagocytic; work in early stages of infection
76
Basophils
release histamine; work in allergic responses
77
Eosinophils:
phagocytic; toxic against parasites and helminths
78
60-70% of leukocytes
function: Phagocytosis
Neutrophils
79
80
Basophils percentage
(0.5-1%)
81
Basophils function
Production of histamine
82
Eosinophils percentage
2-4%
83
Eosinophils function:
Production of toxic proteins against certain parasites; some phagocytosis
84
Agranulocytes
leukocytes with granules in their cytoplasm that are not visible with a light microscope
85
Monocytes
mature into macrophages in tissues where they are phagocytic
86
Dendritic cells found in
found in the skin, mucous membranes, and thymus; phagocytic
87
Lymphocytes
T cells, B cells, and NK cells; play a role in adaptive immunity
88
Monocytes percentage
3-8%
89
Function of monocytes
Phagocytosis (when they mature into macrophages)
90
Dendritic cells function
phagocytosis and initiation of adaptive immune responses
91
92
Lymphocytes percentage
20-25%
93
NK cells function
Destroy target cells by cytolysis and apoptosis
94
T cells function
Cell-mediated immunity
95
B cells function
Produce antibodies
96
Lymphatic system components
Lymph, lymphatic vessels, lymphoid tissue, and red bone marrow
97
Lymphatic system contains which cells?
lymphocytes and phagocytic cells
98
Lymph carries microbes to
lymph nodes
99
What happens at lymph nodes
lymphocytes and macrophages destroy the pathogen
100
Act against all pathogens; not specific to a given pathogen
Innate defenses
101
recognize a specific pathogen
Adaptive defenses
102
must be activated by APCs before they can work
adaptive, specific defenses
103
Examples of adaptive defenses
antibodies, cytotoxic cells
104
Innate and adaptive defenses make it very difficult for pathogens to
penetrate, colonize and cause disease
105
Phago:
from the Greek, meaning eat
106
Cyte
from the Greek, meaning cell
107
Fixed macrophages
are residents in tissues and organs
108
Free (wandering) macrophages
roam tissues and gather at sites of infection
109
Chemotaxis
Chemical signals attract phagocytes to microorganisms
110
Adherence
Attachment of a phagocyte to the surface of the microorganism
111
Ingestion
Opsonization: microorganism is coated with serum proteins, making ingestion easier
112
Digestion
Microorganism is digested inside a phagolysosome
113
The Mechanism of Phagocytosis steps
1. Chemotaxis
2. Adherence
3. Ingestion
4. Digestion
114
Ingestion of a solid - such as a microorganism or cellular debris by a eukaryotic cell
Phagocytosis
115
Used by some protozoans for obtaining nutrients
Phagocytosis
116
Used by certain cells of the immune system to fight infection
Phagocytosis
117
Examples of phagocytes
Macrophages, neutrophils
118
Movement of a cell towards or away from a chemical stimulus
Chemotaxis
119
Phagocytes use pseudopods to
move towards microorganisms or damaged cells at the site of infection. Arrive only minutes after infection
120
Chemotactic chemicals that attract phagocytes include:
1. microbial products
2. Components of damaged cells
3. Chemicals released by other white blood cells
4. Peptides derived from the complement system
121
The plasma membrane of phagocytes usually attaches to glycoproteins on the microorganism's surface. This process is called ____________.
adherence
122
Adherence is made easier through
opsonization
123
opsonization
antibodies or complement proteins from the host coat the microbe's surface, serve as handles so phagocyte can more easily attach to the microorganism.
124
Opsonins
proteins that coat the microbe are called
125
pseudopods fuse, forming a sac called a
phagosome
126
The phagosome enters the cytoplasm where it fuses with
lysosomes
127
Digestion of most bacteria within lysosome is complete within
10-30 mins
128
elimination (exocytosis)
after phagocytosis,
Phagolysosome fuses with the plasma membrane and expels the contents
129
Some of the contents of the phagolysosome may also be presented on the cell membrane through a process called
antigen processing and presentation
130
Phagocytes are able to detect foreign cells by looking for molecules on
the surface of those invaders that are not found on the human body
131
look for a specific antigen on the surface of invaders
adaptive defenses
132
When immune surveillance cells such as macrophages are looking for invaders, they search for surface molecules that are not found on host surfaces, such as
peptidoglycan
133
capsules protect microbes because
they're made of polysaccharides similar to molecules found on host cells.
134
When a macrophage encounters an encapsulated bacterium
It doesnt recognize it as foreign and ignores it
135
Examples of encapsulated bacterium
Streptococcus pneumoniae, common cause of bacterial pneumonia
136
are all bacteria killed after being swallowed by a phagocyte
no
137
how does the tuberculosis bacterium survive phagocytosis?
by preventing the fusion of lysosome and phagosome. This keeps digestive enzymes away from the bacterium
138
These two bacteria can actually escape the phagosome and live within the cytoplasm of the phagocyte
shigella and listeria
139
Some microbes are not affected by lysosomal activity
Leishmania, a protozoan, can resist lysosomal enzymes
140
inhibit the pathway that leads to oxidative killing within a phagocyte
legionella and some staphylococci
141
Some bacteria actually reproduce within the
phagocyte
142
Capable of hiding from host defenses by changing surface antigens ___________.
frequently
143
Changing surface antigens can result from
mutations, genetic recombinations
144
Viruses that frequently exhibit genetic recombination
RNA viruses such as:
influenzavirus, HIV
145
Trypanosoma causes
sleeping sickness
146
has a surface glycoprotein that undergoes frequent changes
Trypanosoma
147
Complement
group of proteins that when activated, undergoes a series of reactions leading to inflammation, opsonization and cell lysis.
148
Some bacteria simply invade complement by
covering the binding sites with a capsule
149
Other bacteria have peptidases that
destroy key complement proteins and block the cascade
150
mimic a control molecule that the human body uses to keep complement inactive when it is not needed.
Neisseria and some viruses
151
Produce molecules called leukocidins
1.Pseudomonas,
2.group A streptococci
3.bacterial pathogens.
152
Leukocidins cause
destruction of phagocytes, such as neutrophils and macrophages.
153
Species of Neisseria that cause meningitis and gonorrhea secrete an enzyme called
IgA protease
154
IgA protease destroys
a class of antibodies called IgA that are located in mucous membranes
155
meningitis and gonorrhea are less likely to be detected in which regions
mucous membranes
156
Examples of pathogens that can cause generalized suppressions of the immune system
HIV, measles and several viruses
157
How do viruses cause generalized suppression
suppress activity of cytokines, or reproduce within macrophages and T cells.
158
Superantigens role in invasion
toxins that distract adaptive defenses, causing them to produce a non-specific exaggerated response, and fail to respond to the actual invader
159
Signs and symptoms of inflammation:
pain, redness, immobility, swelling (edema), heat
160
Function of inflammation
Destroys injurious agent or limits its effects on the body
161
inflammation repairs
and replaces tissue damaged by the injurious agent
162
Inflammation activates
acute-phase proteins by the liver
163
Acute phase proteins by the liver cause
vasodilation and increased permeability of blood vessels
164
acute-phase proteins
Serum proteins whose concentration changes by at least 25% during inflammation.
165
Histamine
1. Vasodilation
2. Permeability
3. Smooth muscle contraction
166
Kinin
A substance released from tissue cells that causes vasodilation.
167
Prostaglandin
A hormonelike substance that is released by damaged cells, intensifies inflammation.
168
Leukotrienes made by
1. produced by mast cells and basophils
169
Leukotrienes produced by
mast cells and basophils
170
Leukotrienes cause
increased permeability of blood vessels
171
Leukotrienes help
phagocytes attach to pathogens.
172
cytokine
A small protein released from human cells that regulates the immune response; directly or indirectly may induce fever, pain, or T cell proliferation.
173
Histamine comes from
Mast cells, basophils, platelets
174
kinins come from
Blood plasma
175
Prostaglandins come from
damaged cells
176
Leukotrienes come from
Mast cells and basophils
177
complement comes from
blood plasma
178
cytokines come from
fixed macrophages
179
Effects of histamine
Vasodilation & increased permeability of blood vessels
180
effects of kinins
chemotaxis by attracting neutrophils
181
effects of prostaglandins
intensify the effects of histamine and kinins, and help phagocytes move through capillary walls.
182
Effects of leukotrienes
increase permeability of blood vessels and help attach phagocytes to pathogens
183
effect of complement
stimulates release of histamine, attracts phagocytes and promotes phagocytosis
184
effect of cytokines
vasodilation and increased permeability of blood vessels
185
First step of inflammation
histamines, kinins, prostaglandins, leukotrienes and cytokines are released by damaged cells
186
step 2 of inflammation
blood clot forms
187
step 3 of inflammation
Abscess starts to form
188
Step 4 of inflammation
margination- phagocytes stick to the endothelium
189
step 5 of inflammation
phagocytosis of invading bacteria occurs
190
Things that can trigger inflammation
sunburn, chemical burns, cuts, microbial infections
191
Inflammation is a type of
general, nonspecific, defensive response
192
Three main functions of inflammation
1. Destroy agent causing injury
2. Limit the effects of the agent on the rest of the body
3. Repair or replace damaged tissue
193
certain components of the complement system can also stimulate the release of ______
histamines
194
histamines can result in
vasodilation
195
Vasodilation results in
more blood (more phagocytes), more oxygen, and more nutrients being delivered to the site of injury.
196
increased blood flow also results in
redness, heat and some of the pain associated with inflammation.
197
What has a direct effect on the capillaries in the area of the injury?
histamines, prostaglandins and leukotrienes
198
Cause the walls of the capillaries to become leakier
histamines, prostaglandins and leukotrienes
199
Leaky capillaries cause
more fluid to leave the capillary and enter tissue spaces, causing swelling or edema
200
Increased blood flow delivers
phagocytes such as monocytes and neutrophils to the scene.
201
phagocytes stick to the walls of the blood vessels in a process called
margination
202
After margination, the cells squeeze through the gaps in a process called
Diapedesis or emigration
203
within about an hour of tissue damage, the phagocytes begin to
destroy the invading microorganisms by phagocytosis.
204
After engulfing large numbers of microorganisms and damaged tissues,
the phagocytes die, forming pus
205
other components of the blood lead to the formation of ______ _________ which seal off the site of injury
blood clots
206
final stage of inflammation is
tissue repair
207
The increased delivery of nutrients and oxygen aids in
tissue repair
208
sticking of phagocytes to blood vessels in response to cytokines at the site of inflammation
margination
209
Phagocytes squeeze between endothelial cells of blood vessels via
diapedesis
210
tissue repair cannot be completed until
all harmful substances are removed or neutralized
211
Stroma
is the supporting connective tissue that is repaired
212
Parenchyma
is the functioning part of the tissue that is repaired
213
regenerated epidermis
parenchyma
214
Regenerated dermis is
Stroma
215
Fever
Abnormally high body temperature
216
Hypothalamus is normally set at
37 C
217
cause the hypothalamus to release prostaglandins that reset the hypothalamus to a higher temperature
cytokines
218
The body maintains the higher temperature until
the cytokines are eliminated
219
crisis
The phase of a fever characterized by vasodilation and sweating.
220
As body temperature falls (crisis),
vasodilation and sweating occurs
221
How is fever beneficial?
Damaging pathogens
Fevers increase the temperature of infected tissues to a level that damages pathogens.
Impairing pathogen replication
The systemic temperature increase caused by a fever can make it harder for pathogens to replicate if they have spread.
222
Complement system is made of
Serum proteins produced by the liver that enhances the immune system in destroying microbes
223
The complement system acts in
a cascade in a process called complement activation
224
Proteins are designated with
uppercase C and numbered in order of discovery
225
226
Activated fragments are indicated with
lowercase a and b
227
set of proteins that circulate in the blood serum
complement system
228
When the complement system is activated these proteins destroy foreign cells by
cytolysis
229
the complement system also activates
the inflammatory response, and assists in phagocytosis
230
The main components of the complement system are called
C1 through C9
231
Complement can be activated through 3 different pathways
1. Classical pathway
2. Alternative pathway
3. Lectin patway
232
first activation pathway of complement system to be discovered
Classical pathway
233
The classical pathway begins when
a pair of antibodies attaches to antigens on the surface of a bacterium
234
Antigens can be
proteins or large polysaccharides on the surface of a bacterium
235
The antibodies bind and activate
C1
236
C1 then cleaves
several copies of C2 and C4
237
Together, the C2a and C4b fragments form
an enzyme that cleaves C3, activating the complement system
238
was named so because it was discovered after the classical pathway
Alternative pathway
239
Classical pathway requires antibodies specific to the
invading microorganism
240
The alternative pathway requires
three complement proteins called factor B, factor D and factor P
241
Factor P stands for
properdin
242
243
243
244
Factors B, P, & D are attracted to
microbial cell-surface material such as the lipid-carbohydrate complexes of certain bacteria and fungi
245
Together with C3, these proteins (B,P,D) result in the cleavage and activation of
C3 proteins
246
C3 proteins in turn activate the
rest of the complement system
247
Most recently discovered pathway of complement activatio is the
lectin pathway
248
What stimulates the production of lectins?
Macrophages ingest materials through phagocytosis, they release chemicals that stimulate the production of lectins
249
carbohydrate binding proteins
lectins
250
The lectins bind to
distinctive patterns of carbohydrates on the surface of certain bacteria and viruses.
251
the lectins themselves can act as
opsonins for phagocytosis, but also activate C2 and C4
252
the activation of C2 and C4 leads to the activation of C3 which
leads to the activation of the rest of the complement pathway
253
Step 1 classical pathway
Antibodies bind to antigens, activating C1
254
Step 2 classical pathway
C1 splits and activates C2 and C4
255
256
Step 3 classical pathway
C2a and C4b combine and activate C3
257
C3a functions in
inflammation
258
C3b functions in
cytolysis and opsonization
259
Step 1 alternative pathway
C3 present in the blood combines with factors B, D, and P on microbe surface
260
step 2 alternative pathway
C3 splits into C3a and C3b, functioning the same as in the classical pathway
261
What happens in the lectin pathway ?
Macrophages ingest pathogens, releasing cytokines that stimulate lectin production in the liver
262
Mannose-binding lectin (MBL) binds to
mannose, activating C2 and C4
263
C2a and C4b activate
C3, which functions the same as in the classical and alternative pathways
264
cytolysis
The destruction of cells, resulting from damage to their cell membrane, that causes cellular contents to leak out.
265
Activated complement proteins create a membrane attack complex (MAC) leads to
cytolysis
266
Promotes attachment of a phagocyte to a microbe
Opsonization
267
Activated complement proteins bind to mast cells, releasing histamine
inflammation
268
Outcomes of complement activation
1. Cytolysis
2. Opsonization
3. Inflammation
269
The complement system is another way the body
fights infection and destroys pathogens
270
This component of innate immunity
“complements” other _______ _________.
immune reactions.
271
The cascade can be activated by
a pathogen directly or by an antibody–antigen reaction
272
Together these proteins destroy microbes by
cytolysis, (2) enhanced phagocytosis, and (3) inflammation
273
C3a and C5a act as
chemotactic factors, attract phagocytes to the site of infection.
274
C3a and c5a also bind to
mast cells , release histamine and cause inflammation. also relase other chemicals
275
C3b acts as an
opsonin, coating the invading cell
276
This coat makes it easier for the phagocyte to
adhere to the invading cell during phagocytosis
277
C5b binds to C6 and C7 which attach to the
plasma membrane of the invading cell
278
C8 and several C9 molecules bind to the C5b, C6, C7 complex and
forming a cylinder shaped membrane attack complex
279
MACs make holes in membrane causing
water and ions to leave, cytolysis, killing the cell
280
regulation of complement
Regulatory proteins readily break down complement proteins, minimizing host cell destruction
281
282
Complement and disease
Lack of complement proteins causes susceptibility to infections
283
Evading the complement system
Capsules prevent complement activation
284
Interferons
Cytokines produced by cells; have antiviral activity
285
IFN-α and IFN-β
produced by cells in response to viral infections; cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication
286
IFN-γ
causes neutrophils and macrophages to kill bacteria
287
Antiviral Action of Alpha and Beta Interferons (IFNs) step 1
Viral RNA from
an infecting virus
enters the cell.
288
Antiviral Action of Alpha and Beta Interferons (IFNs) step 2
The virus induces the host cell to
produce interferon mRNA
(IFN-mRNA), which is translated
into alpha and beta interferons.
289
Antiviral Action of Alpha and Beta Interferons (IFNs) step 3
Interferons make contact with uninfected
neighboring host cells, where they bind either
to the plasma membrane or to nuclear
receptors. Interferons induce the cells to
synthesize antiviral proteins (AVPs).
290
Antiviral Action of Alpha and Beta Interferons (IFNs) step 4
AVPs degrade viral mRNA and
inhibit protein synthesis—and
thus interfere with viral replication.
291
Iron-Binding Proteins
1. Transferrin
2. Lactoferrin
3. Ferritin
4. Hemoglobin
292
Transferrin found in
blood and tissue fluids
293
Lactoferrin found in
milk, saliva, and mucus
294
Ferritin found in
Liver, spleen, and red bone marrow
295
Hemoglobin found in
located in red blood cells
296
Bacteria produce
siderophores
297
siderophores compete with
iron-binding proteins
298
Antimicrobial Peptides
Short peptides produced in response to protein and sugar molecules on microbes
299
What do antimicrobial peptides do?
Inhibit cell wall synthesis
Form pores in the plasma membrane
300
have a Broad spectrum of activity
antimicrobial peptides
301
Genetic resistance
Confers a selective survival advantage
E.g., sickle cell trait and Plasmodium falciparum
302
Age
Confers a selective survival advantage
E.g., sickle cell trait and Plasmodium falciparum
303
Observing healthy protocols
another factor that helps prevent infection
304
20-25%
Lymphocytes
305
3-8%
Monocytes
306
2-4%
Eosinophils
307
0.5-1%
Basophils
308
60-70%
Neutrophils
309
viral infections, pneumonia, autoimmune diseases, or cancers
Low WBC
310
bacterial infections, autoimmune diseases, or side effects of medications
High WBC
311
PAMPs stand for
pathogen-associated molecular patterns (PAMPs)
312
Innate or adaptive: 1. First-line defenses
Innate
313
Innate or adaptive: 2. Phagocytosis
Innate
314
Innate or adaptive:
3. inflammation
Innate
315
Innate or adaptive:
4. Complement system
Innate
316
Innate or adaptive:
4. Complement system
Innate
317
found in the skin, mucous membranes, and thymus; phagocytic
Dendritic cells
318
T cells, B cells, and NK cells; play a role in adaptive immunity
Lymphocytes
319
Destroy target cells by cytolysis and apoptosis
NK cells
320
Opsonization:
microorganism is coated with serum proteins, making ingestion easier
321
(IFN-mRNA), which is translated
into
alpha and beta interferons.
322
(IFN-mRNA), which is translated
into
alpha and beta interferons.
323
Arrive only minutes after infection
Phagocytes
324
Complement activation leads to
inflammation, opsonization and cell lysis.
325
A substance released by tissue cells that causes vasodilation, capillary permeability, and smooth muscle contraction.
Histamine
326
Activates acute-phase proteins by the liver
Inflammation
327
Serum proteins whose concentration changes by at least 25% during inflammation.
Acute phase proteins
328
A substance released from tissue cells that causes vasodilation.
Kinin
329
Leukotrienes cause
increased permeability of blood vessels
330
Leukotrienes help
help phagocytes attach to pathogens.
331
A small protein released from human cells that regulates the immune response;
Cytokine
332
directly or indirectly may induce fever, pain, or T cell proliferation.
Cytokine
333
Help phagocytes attach to pathogens
Leukotrienes
334
increase permeability of blood vessels and help attach phagocytes to pathogens
Leukotrienes
335
stimulates release of histamine, attracts phagocytes and promotes phagocytosis
Complement
336
cause neighboring cells to produce antiviral proteins (AVPs) that inhibit viral replication
IFN a and IFN b
