Lesson 12 Flashcards
1
Q
pathogens
A
agents capable of producing disease
2
Q
pathogens include
A
- viruses
- bacteria
- fungi
3
Q
first line of defense against pathogens
A
skin and mucous membranes which serve as barriers
4
Q
second line of defense
A
protections against pathogens that break the skin, mucous membrane barriers
5
Q
what is included in the second line of defense?
A
- leukocytes
- macrophages
- antimicrobial proteins
- natural killer cells
- fever
- inflammation
6
Q
third line of defense
A
adaptive immunity, mechanisms that defeat a specific pathogen and leave the body with a memory of it
7
Q
immune system
A
widely distributed population of cells diverse chemical, physical barriers, and physiological responses
8
Q
what are the two types of immune defenses?
A
- innate
- adaptive
9
Q
innate immunity
A
- defenses we are born with
- protect us from broad spectrum of disease agents
10
Q
innate immunity has a ___ effect
A
local
11
Q
local effect of innate immunity
A
defends at point of invasion but there are exceptions
12
Q
what in an exception to the local effect of innate immunity?
A
fever
13
Q
innate immunity is _____
A
nonspecific
14
Q
non-specificity of innate immunity
A
defenses are against a broad spectrum of disease agents rather than one particular pathogen
15
Q
innate immunity lacks ____
A
memory
16
Q
memory lacking in innate immunity
A
does not remember exposure to a specific pathogen
17
Q
adaptive immunity
A
defenses against specific pathogens developed only upon exposure and maintain immune memory
18
Q
protective features of the skin
A
- toughness of keratin, difficult to penetrate
- too dry and nutrient-poor to support much microbial growth
- acid mantle
- peptides that kill microbes present
19
Q
what happens to microbes that are adhered to the skin
A
skin is continually shed with dead keratinocytes of the stratum corneum of the epithelium
20
Q
acid mantle
A
thin filament of lactic and fatty acids from sweat and sebum that inhibits bacterial growth
21
Q
what peptides are present in the skin that kill microbes
A
- dermcidin
- defensins
- cathelicidins
22
Q
what protects all tracts open to the exterior
A
mucous membranes
23
Q
protective features of mucous membranes
A
- sticky mucus physically traps microbes
- presence of lysozyme
24
Q
lysozyme
A
enzyme that destroys bacterial cell walls
25
____ is in skin and mucous membranes
subepithelial areolar tissue
26
subepithelial areolar tissue of skin and mucous membranes contain
viscous barrier of hyaluronic acid in ground substance
27
hyaluronic acid
large glycosaminoglycan
28
pathogens can release
hyaluronidase
29
hyaluronidase
enzyme to make hyaluronic acid less viscous
30
what is waiting when skin and mucous membranes are penetrated?
- phagocytes
- leukocytes
31
what are the five types of leukocytes?
- neutrophils
- eosinophils
- basophile
- monocytes
- lymphocytes
32
neutrophils
- wander in connective tissue
- function to kill bacteria
33
neutrophils can ensnare bacteria by releasing
neutrophil extracellular trap
34
neutrophil extracellular trap (NET)
web of nuclear chromatin and proteins
35
how can neutrophils kill
phagocytizing and digesting microbe or by releasing bactericidal chemicals to create killing zone around neutrophil
36
eosinophils found especially in
mucous membrane
37
eosinophils guard against
large parasites like tapeworms and roundworms
38
eosinophil participate in
inflammation and allergic reactions
39
basophils secrete chemicals that do what?
aid mobility and action of other leukocytes
40
leukotrienes
- vasodilator
- increases blood flow and speeds delivery of leukocytes to the area
41
heparin
inhibits clot formation that would impede leukocyte mobility
42
mast cells
secrete histamine and heparin like basophils but in connective tissues
43
lymphocytes include
- B cells
- T cells
- NK cells
44
T cells and B cells are apart of ___ immunity
adaptive
45
NK cells participate in ____ immunity
innate
46
monocytes
emigrate from blood into connective tissues and transform into macrophages
47
macrophage system
all the body's avidly phagocytic cells except leukocytes
48
what is included in the macrophgae system
- monocytes
- macrophages
- dendritic cells
49
some macrophages are ____ while others are _____
- wandering
- fixed
50
examples of specialized forms of macrophages in specific locations (3)
- microglia (CNS)
- alveolar macrophages (lungs)
- stellate macrophages (liver)
51
blood-borne antimicrobial proteins
- interferons
- complement system
52
interferons
proteins secreted by virally infected cells and immune cells
53
interferons serve as
alarm to nearby cells
54
interferons bind to receptors on nearby cells and do what?
stim their synthesis of defensive antiviral proteins to prevent their infection
55
interferons activate ____ to do what?
- NK cells and macrophages
- better destroy infected cells or cancer cells
56
complement system
group of 30 or more globular proteins that contribute to both innate immunity and adaptive immunity
57
complement system synthesized mainly by
liver
58
complement system circulate in the blood in ___ form
inactive
59
what do activated complements participate in?
- inflammation (C3a)
- immune clearance (C3b)
- phagocytosis (C3b)
- cytosis (C3b)
60
three pathways of complement system activation
- classical pathway
- alternative pathway
- lectin pathway
61
classical complement activation pathway is ___ than alternative pathway
faster
62
classical complement activation pathway requires
antibody binding to microbe
63
what happens in the classical pathway when the antibody binds to the microbe?
changes the antibody shape and exposes complement-binding sites on the antibody
64
binding of the ____ to the antibody sets off reaction cascade
complement C1
65
complement fixation
complement C1 binding on the antibody that sets off a reaction cascade
66
alternative complement activation pathway
complement C3b binds to microbe surface activating reaction cascade
67
lectins
plasma proteins that bind to carbohydrates on the pathogen's surface activating reaction cascade
68
lectin complement activation cascade is dependent on
lectins
69
four outcomes of complement activation
- inflammation
- immune clearance
- phagocytosis
- cytolysis
70
inflammation as an outcome of complement activation
C3a stims mast cells and basophils to secrete histamine and other inflammatory chem which activate and attracts neutrophils and macrophages
71
immune clearance as an outcome of complement activation
C3b binds the antigen-antibody complexes to red blood cells that then circulate to the liver and spleen where macrophages strip off and destroy the Ag-Ab complexes leaving RBC unharmed
72
phagocytosis as an outcome of complement activation
C3b coats microbial cells and serves as binding sites for phagocyte attachment
73
what is it called when the microbial cell gets coated by C3b in phagocytosis after complement activation?
opsonization
74
cytolysis as an outcome of complement activation
- complement C3b initiates formation C5b
- C5b aggregates with other complement proteins within plasma membrane of microbe which forms the membrane attack complex
75
membrane attack complex
a hole in the target cell membrane
76
what does the membrane attack complex do
- electrolytes leak out
- water flows in rapidly
- target cell ruptures
77
natural killer cells continually
patrol body looking for pathogens and diseased host cells
78
immunological surveillance
continually being on patrol for pathogens and diseased cells
79
what do NK cells do?
attack and destroy microbes, transplanted cells, cells infected with viruses, and cancer cells
80
how do NK cells destroy microbes
recognize infected cell and bind to it and release perforins
81
perforins
polymerize to form a ring to create a hole in the target's plasma membrane
82
granzymes
group of protein-degrading enzymes
83
granzymes function
enter through pore and degrade intracellular enzymes and induce apoptosis
84
apoptosis
programmed cells death
85
cancer cells exhibit
tumor specific antigens
86
where are tumor-specific antigens located?
cell's plasma membrane
87
cancer cells are identified as abnormal by
NK cells
88
immunological escape
cancer cells that destroy NK cells that detect them or avoid detection by not displaying tumor-specific antigens or masking them
89
in viral infections cells infected with virus present
abnormal proteins on their plasma membrane which allows NK cells to identify and destroy them
90
fever aka
pyrexia
91
fever
abnormal elevation of body temp
92
fever results from
- trauma
- infections
- drug reactions
- brain tumors
93
what does a fever do? (3)
- promote interferon activity
- elevates metabolic rate and accelerates tissue repair
- inhibits reproduction of bacteria and viruses
94
recovery from fever is faster when
you let the fever take its course
95
antipyretics
fever reducing medications
96
stages of fever (3)
- onset
- stadium
- defervescence
97
what the six steps of the course of a fever?
- infection and pyrogen secretion
- hypothalamic thermostat is reset to higher set point
- onset
- stadium
- infection ends, set point returns to normal
- defervescence
98
onset of fever
body temp rises
99
stadium of fever
body temp oscillates around set point
100
defervescence of fever
body temp returns to normal
101
reye syndrome
serious disorder in children younger than 15 following an acute viral infection such as chickenpox or flu
102
what can trigger reye syndrome
use of aspirin to control fever
103
what happens in reye syndrome
- swelling of brain neurons
- pressure of swelling brain
- fatty infiltration of liver and other viscera
104
what are the symptoms of pressure of swelling brain (5)
- nausea
- vomiting
- disorientation
- seizures
- coma
105
____ die of reye syndrome
30%
106
what happens to most survivors of reye syndrome
suffer intellectual disabilities
107
inflammation
local defensive response to tissue injury, trauma, or injury
108
general purposes of inflammation
- limit spread of pathogens and destroy them
- remove debris from damaged tissue and initiate tissue repair
109
four cardinal symptoms/signs of inflammation
- redness
- swelling
- heat
- pain
110
inflammation involves numerous
cytokines
111
cytokines
small proteins that function in chemical communication between cells
112
cytokines do what during inflammation
alter physiology of receiving cell
113
cytokines include
- interferon
- interleukins
- tumor necrosis factor
- chemotactic factors
114
most immediate requirement after tissue injury is
get defensive leukocytes to the site quickly
115
how are leukocytes moved to injury spot quickly?
local hyperemia
116
hyperemia
increased blood flow
117
what chemicals cause hyperemia?
- histamine
- leukotrienes
- cytokines
118
what are vasodilators secreted by?
- basophils
- mast cells
- cell damaged by trauma, toxins, or organisms triggering inflammation
119
hyperemia other function
washes toxins and metabolic waste from the site more rapidly
120
vasoactive chemicals stim
endothelial cells to contract
121
what happens when endothelial cells contract
widens gaps between them
122
what happens when gaps widen between endothelial cells?
- increase capillary permeability
- fluid, leukocytes, and plasma proteins leave bloodstream
123
cell adhesion molecules are made by
endothelial cells
124
what do cell adhesion molecules aid in
recruitment of leukocytes
125
how do cell adhesion molecules aid in recruitment of leukocytes
make membranes sticky so leukocytes adhere to vessel wall
126
margination
leukocytes adhering to vessel walls
127
diapedesis
- emigration
- leukocytes crawl through gaps in the endothelial cells and enter tissue fluid
128
extravasated
term for cells and chemicals that have left the bloodstream
129
what is the heat of inflammation caused by
hyperemia
130
what is the redness of inflammation caused by
- hyperemia
- extravasated RBCs in the tissue
131
what is swelling in inflammation caused by?
increased fluid filtration from the capillaries
132
what is pain in inflammation caused by?
- direct injury to the nerves
- pressure on the nerves from edema
- stim of pain receptors by prostaglandins
- bacterial toxins
- bradykinin
133
other priority of inflammation
prevent pathogens from spreading throughout body
134
____ filters into tissue fluid and clots to form stick mesh that walls off microbes
fibrinogen
135
heparin prevents
clotting at site of injury
136
pathogens are in fluid pocket surrounded by
clot
137
pathogens are attacked by
antibodies, phagocytes, and other defenses
138
neutrophils accumulate at the injury site within
an hour
139
after leaving bloodstream neutrophils exhibit
chemotaxis
140
chemotaxis
attraction to chemicals that guide them to injury site
141
____ quickly respond to and kill bacteria
neutrophils
142
how do neutrophils kill bacteria
phagocytosis
143
respiratory burst
neutrophils absorb O2 to form H2O2 an release hypochlorite
144
hypochlorite
highly toxic and forms killing zone around cell
145
neutrophils secrete ____ for what function?
- cytokines
- recruitment of macrophages and additional neutrophils
146
____ and ___ secrete colony-stimulating factor
macrophages and T cells
147
what do colony-stimulating factors from macrophages and t cells do
stim leukopoiesis and raise WBC count
148
neutrophilia
5000 cells/uL to 25000 cells/uL in bacterial infection
149
eosinophilia
elevated eosinophil count in allergy or parasitic infection
150
tissue cleanup and repair primarily involves
monocytes
151
monocytes arrive in ____ and become macrophages
8-12 hours
152
how do macrophages assist in tissue cleanup and repair
engulf and destroy bacteria, damages host cells, and dead and dying neutrophils
153
____ contributes to tissue cleanup
edema
154
how does edema contribute to tissue cleanup?
swelling compresses veins and reduces venous drainage
155
forces of edema open valves of lymphatic capillaries, promoting
lymphatic drainage of bacteria, dead cells, and debris
156
pus
yellow accumulation of dead neutrophils, bacteria, cellular debris, and tissue fluid
157
abscess
accumulation of pus in a tissue cavity
158
platelet-derived growth factor
secreted by blood platelets and endothelial cells in injured areas
159
platelet-derived growth factor stims ___ to multiply and ____
- fibroblasts
- synthesize collagen
160
hyperemia delivers oxygen, amino acids, and other necessities for ___
protein synthesis
161
increased heat
- increases metabolic rate
- speeds mitosis
- tissue repair
162
_____ forms a scaffold for tissue reconstruction
fibrin clot
163
pain does what for tissue repair
makes us limit the use of body part so it has chance to rest and heal
164
_____ serves as the third line of defense
adaptive immunity
165
what are the three characteristics that distinguish adaptive immunity and innate immunity?
- systemic affect
- specificity
- memory
166
systemic effect in adaptive immunity
acts throughout the body
167
specificity in adaptive immunity
generates protection and immunity to specific pathogens on an individual basis
168
memory in adaptive immunity
- when re-exposed to the same pathogen
- the body reacts so quickly that there is no noticeable illness
169
two types of adaptive immunity
- cellular
- humoral
170
what happens in cellular immunity
T lymphocytes directly attack and destroy foreign cells or diseased host cells
171
cellular immunity aka
cell mediated
172
what is the function of cellular immunity
rids the body of pathogens that reside in human cells where they are inaccessible to antibodies
173
what does cellular immunity work against other than pathogens in cells?
- parasitic worms
- cancer cells
- transplanted cells
174
humoral immunity aka
antibody mediated
175
what happens in humoral immunity
mediated by B cells that become plasma cells that release antibodies that do not directly destroy a pathogen but tag it for destruction
176
humoral immunity is effective against
- extracellular viruses
- bacteria
- yeasts
- protozoans
- molecular diseases agents
177
what are molecular disease agents
- toxins
- venoms
- allergens
178
other forms of classifying immunity
- natural active immunity
- artificial active immunity
- natural passive immunity
- artificial passive immunity
179
natural active immunity
production of one's own antibodies or T cells as a result of infection or natural exposure to antigen
180
example of natural active immunity
catching the flu and gaining immunity to that strain
181
artificial active immunity
production of one's own antibodies or T cells as a result of vaccination against disease
182
vaccine
consists of dead or attenuated pathogens that stim the immune response without causing the disease
183
booster shots
may be given to re-stim immune memory to maintain a high level of protection
184
example of artificial active immunity
shots
185
natural passive immunity
temporary immunity that results from antibodies produced by another person
186
example of natural passive immunity (2)
- fetus acquires antibodies from mother through placenta
- baby acquires them during breast feeding
187
artificial passive immunity
temporary immunity that results from the injection of immune serum from another person or animal
188
immune serum
antibodies
189
example of artificial passive immunity
emergency treatment for snakebite, botulism, tetanus, rabies, and other diseases
190
antigen
any molecule that can bind an antibody
191
most antigens have ___ MW
high
192
what are antigens usually composed of?
- proteins
- polysaccharides
- glycoproteins
- glycolipids
193
characteristics enable body to distinguish between
self and non self
194
epitopes
certain regions of an antigen molecule that stim immune responses
195
epitopes aka
antigenic determinants
196
haptens
too small to be antigenic in themselves
197
hapten aka
incomplete antigens
198
haptens may trigger immune responses by
combining with a host molecule, creating a complex that the body recognizes as foreign
199
examples of haptens
- cosmetics
- detergents
- industrial chemical
- poison ivy
- animal dander
- penicillin
200
antibodies aka
immunoglobulins
201
antibodies
defensive proteins that play a variety of defensive roles
202
human immune system capable of ____ different antibodies
1 trillion
203
soluble antibodies are dissolvable in what? (8)
- blood plasma
- tissue fluids
- lymph
- mucus
- saliva
- intestinal secretions
- tears
- breast milk
204
antibody monomer
basic structural unit of an antibody
205
antibody monomer composed of
four polypeptide chains linked by disulfide bonds
206
what are the four polypeptide chains in antibody monomers called?
two heavy and two light chains
207
all four polypeptide chains have ___ that give antibody its uniqueness
variable region
208
antigen binding site formed from
the V regions of the heavy and light chain on each arm
209
where does the antigen binding site attach
the epitope of an antigen molecule
210
constant region has the ___ amino acid sequence as variable region
same
211
what does the constant region determine
mechanism of antibody action
212
antigen classes (5)
- IgM
- IgG
- IgD
- IgA
- IgE
213
IgA as monomer in
plasma
214
IgA as dimer in
- mucus
- saliva
- tears
- breast milk
- intestinal secretions
215
IgA prevent
pathogen adherence to epithelia and penetrating underlying tissues
216
IgA provides ____ immunity to newborns
passive
217
IgD
- monomer
- B cell transmembrane antigen receptor
218
IgD functions in
B cell activation by antigens
219
IgE
- monomer
- bound to receptors on basophils and mast cells
220
IgE stims what two things
- release of histamine and other chemical mediators of inflammation and allergy
- eosinophil defensive actions against parasites
221
IgG
- monomer
- constitutes 80% of circulating antibodies
222
IgG is the predominant antibody in ___
secondary immune response
223
IgG is capable of
- complement fixation
- crossing placenta to fetus
224
IgM
pentamer in plasma and lymph
225
IgM is predominant antibody in ____
primary immune response
226
IgM is capable of
- strong agglutinating
- complement fixing abilities
227
three types of lymphocytes
- NK cells
- T cells
- B cells
228
NK cells are a part of ___ immunity
innate
229
T and B cells are part of ___ immunity
adaptive
230
T cell production
produced in red bone marrow but migrate to thymus to complete their maturation process
231
positive selection
cortical epithelial cells test developing T cells to ensure they have the proper receptors
232
what happens when positive selection does not occur
T cells die
233
T cells can fail by
reacting to self antigen
234
what happens to T cells that react to self antigen
they're eliminated to ensure the immune system is self tolerant
235
self tolerant
will not attack one's own tissues
236
anergy
self reactive T cells remain alive but unresponsive
237
with proper receptors T cells become _____
immunocompetent
238
immunocompetent
capable of recognizing antigens presented to them
239
B cells development
develop entirely in red bone marrow
240
what happens to B cells that react to self anitgens
undergo either anergy or clonal deletion
241
self tolerant B cells do what?
synthesize antigen surface receptors, divide rapidly, produce immunocompetent clones
242
B cells leave bone marrow and do what?
colonize lymphoid tissues and organs as T cells
243
T cells can only recognize antigens presented by
antigen presenting cells
244
APCs include
dendritic cells, macrophages, and B cells
245
function of APCs depend on
MHC proteins
246
MHC proteins are encoded by
major histocompatibility complex genes
247
MHC proteins act as
cell identification tags
248
cell identification tags
label every cell of your body as belonging to you
249
what is the only instance that MHC proteins are not structurally unique
identical twins
250
MHCs are displayed on ___ of APCs along with ___
- surface
- fragment of presented antigen
251
antigen processing
APC encounters antigen, internalizes it by endocytosis, digests it into fragments, and attaches it to the MHC protein
252
what happens after antigen processing
cell displays MHC protein with the antigen in its plasma membrane
253
if APC displays a self antigen to a T cell
the T cell disregard it
254
if an APC displays a non-self antigen to a T cells
the appropriate T cell will initiate an immune response against the source of that antigen
255
APCs and lymphocytes communicate to cytokines called
interleukins
256
cellular immunity
form of specific defense in which the T lymphocytes directly attack and destroy diseased or foreign cells
257
classes of T cells
- cytotoxic T cells
- helper T cells
- memory T cells
258
cytotoxic T cells
carry out attack
259
helper T cells
promote activities of other immune cells
260
memory T cells
responsible for memory in cellular immunity
261
what happens when APC encounters and processes an antigen
migrates to the hearest lymph node and displays it to the T cells
262
when T cells encounter a displayed antigen on the MHC protein
they initiate an immune response
263
what are the two classes of MHC T cells respond to
- MHC-I
- MHC-II
264
MHC-I proteins
- occur on all nucleated cells
- internal peptides are presented on cell surface including virus-infected cells
- cancer cells
265
MH-II proteins
- occur on APCs
- external antigens are presented on cell surface
266
cytotoxic T cells respond only to
MHC-I proteins
267
helper T cells respond only to
MHC-II
268
T cell activation begins when
Tc or Th cell binds to an MHC protein displaying an epitope that the T cell is programmed to recognize
269
costimulation
additional signaling processes required for T cell activation
270
in addition to MHC and antigen binding T cells must also bind
signaling proteins on surface of APCs in damaged/infected tissues
271
what is the purpose of T cells binding to signaling proteins?
helps to ensure the immune system doesn't launch an attack in the absence of an enemy
272
what happens if T cells don't bind to the signaling proteins
autoimmune disorders
273
successful T cell activation will trigger
clonal selection
274
activated T cell undergoes
repeated mitosis
275
repeated mitosis of activated T cells gives rise to
clone of identical T cells programmed against the same epitope
276
what do the clones of T cells become?
- effector cells
- cytotoxic cells
- memory cells
- helper cells
277
T cell recall response
immune memory follows the primary response in cellular immunity
278
why does the T cell recall response occur?
- memory cells are long-lived
- memory cells are more numerous than naive T cells
- memory cells have fewer steps to be activated
279
what are the four main steps of T cell activation?
- antigen recognition
- costimulation
- clonal selection
- attack
280
____ play central role in coordinating both cellular and humoral immunity
helper T cells
281
what are the three effects that occur when helper T cells secrete interleukins
- attract neutrophils and NK cells
- attract macrophages, stim their phagocytic activity, and inhibit them from leaving area
- stim T and B cell nitosis and maturation
282
what happens when T cell recognizes MHC-II
secrete interleukins
283
_____ only T cells that directly attack other cells
cytotoxic T cells
284
when cytotoxic T cells recognize complex of an antigen and MHC-I what happens
it docks on those cells
285
after cytotoxic T cells dicks what happens?
cell delivers a lethal hit of chemicals
286
what are the chemicals in a lethal hit?
- perforins and granzymes
- interferons
- tumor necrosis factor
287
perforins and granzymes
kill cells in the same manner as NK cells
288
interferons
inhibit viral replication and recruit and activate macrophages
289
tumor necrosis factor
aids in macrophage activation and kills cancer cells
290
what happens after a cytotoxic T cell delivers lethal hit?
cell goes off in search of another enemy cell while chemicals do their work
291
B cell activation begins when
an antigen binds to B cell receptors
292
___ has thousands of surface receptors for one antigen
immunocompetent B cells
293
receptor mediated endocytosis
antigen binds to several receptors, links them together, and is taken into the cell
294
What do B cell processes do after the antigen is taken into the cell
B cell processes digests the antigen then displays antigen fragments with MHC-II on surface
295
what happens after MHC-II is displayed on surface of B cell
secretes interleukins that activate the B cell
296
____ triggers clonal selection
B cell activation
297
B cell mitosis gives rise to
clones of identical B cells programmed against the same antigen
298
most clonal B cells differentiate into
plasma cells
299
what else can B cells become other than plasma cells
memory B cells
300
plasma cells secrete
antibodies at a rate of 2000 molecules per second
301
what is the lifespan of a plasma cell
4-5 days
302
antibodies travel through body in
blood and other body fluids
303
first exposure of a plasma cell to antigen triggers
production to IgM and a slower production of IgG
304
later exposure of a plasma cell to the same antigen does what?
rapid production of IgG
305
antibody assist the immune response in four ways
- neutralization
- complement fixation
- agglutination
- precipitation
306
neutralization as an immune response
masking active regions of an antigen
307
complement fixation as immune response
activating complement by the classical pathway
308
agglutination as immune response
clumping of enemy cells to immobile them
309
agglutination and precipitation cleared by
phagocytes
310
precipitation assisting in immune responses
antigen molecules are clumped by antibodies
311
primary response
immune reaction brought about by the first exposure to an antigen
312
protective antibodies are delayed for ____. Why?
- 3-5 days
- naive B cells multiply and differentiate into plasma cells
313
as plasma cells produce antibodies what happens?
antibody titer rises
314
antibody titer
level in the blood plasma
315
what happens to the antibody titer when IgM appears
peaks in about 10 days and then soon declines
316
___ levels rise as ___ declines in the primary response
- IgG
- IgM
317
how long does it take for the IgG level to drop to a low level
within a month
318
primary response leaves one with
immune memory of the antigen
319
during clonal selection some B cells become
memory B cells
320
secondary response
immune response when re-exposed to the same antigen
321
memory B cells become plasma cells within hours of
reexposure
322
IgG titer does what in secondary response
rises sharply an dpeaks in a few days
323
are there symptoms for a secondary response? why?
no because response is to rapid that the antigen has little chance to exert noticeable effect on the body
324
IgG remian elevated for how long after secondary response
for weeks to years
325
why do IgG remain elevated for so long?
long-lasting protection
326
autoimmune diseases
- failure to self tolerance
- immune system does not correctly distinguish self sntigens from foreign ones and produces auto-antobodies that attack body's own tissues
327
reasons for failure of self tolerance
- cross-reactivity
- abnormal exposure of self anitgens to the blood
- changes in structure of self antigens
328
cross reactivity as a reason for failure to self tolerance
some antibodies against foreign antigens react to similar self antigense
329
example of cross reactivity as a reason for failure to self tolerance
rheumatic fever where strep antibodies attack the heart valves
330
abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance
some of our native antigens are not normally exposed to the blood
331
what is an exmaple of abnormal exposure to slef antigen in the blood as reason fro failure of self tolerance
blood testes barrier keep sperm from getting in to the blood
332
changes in structure of self-antigens as reason for failure of self tolerance
viruses and drugs may change the structure of self antigens or cause the immune system to perceive them as foreign
333
immunodeficienies are characterized by
an immune system that fails to react vigorously enough
334
severe combined immunodificiency disease
hereditary lack of T and B cells
335
SCID leaves people vulnerable to
oppotunistsic infection
336
aquired immunideficiency syndrome
non-hereditary diseases contracted after birth caused by HIV
337
hwo does HIV cause AIDS
HIV invades helper T cells, macrophages, and dendritic cells by tricking them to internalize viurses by receptor mediated endocytosis
338
HIV is a
retrovius
339
retrovirus
uses the viral enzyme reverse transcriptase to convert its viral RNA genome into DNA which can then insert into host cell DNA
340
HIV cripples entire immune system by
destorying helper T cellsh
341
host with HIV is most volnerable to
opportunistic infections
342
early signs and symptoms of AIDS
flu-like symptoms of chills and fever
343
signs and symptoms of AIDS progress into
- night sweats
- fatigue
- headache
- extreme weight loss
- lymphadenitis
344
what is the normal T helper cell count
600-1200 cells/uL
345
what is the T helper cell count in AIDS
200 cells/uL
346
what are some opportnistic infections people with AIDS are susceptible to?
- toxoplasma
- pneumocystis
- herpes simplex virus
- cytomegalovirus
- TB
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HIV transmitted through
- blood
- semen
- veginal secretions
- breast milk
- across placenta
348
is there a cure for AIDS
no but there is antiretroviral therapy that maintains near normal life expectancy
349
COVID 19
global pandemic oc 2020-2021 caused bu SARS-CoV-2
350
viral structure of COVID 19
single strand of RNA stabilized by RNA-binding nucleocapsid protein surrounded outer lipid envelope studded with spike proteins
351
how many genes are in the RNA strand of COVID 19
14
352
infection cycle of COVID 19
- virus inhaled and invades lung cells
- virus replicated within host cell
- new virus released to infect new cells
353
what cells do COVID 19 cells infect and how
great (type II) alveolar cells by invading their ACE2 receptors
354
mechanism of COVID 19
- other vody cells with ACE2 receptors also infected
- cytokines released by immune cells activate inflammation
355
what other body cells have ACE2 receptors
- heart
- kidneys
- digestive tract
- blood vessels
- brain
356
COVID 19 has the potential to induce a
cytokine storm
357
cytokine storm
produces excessive hyperinflammatory response
358
common symptoms of COVID 19
- flu-like symptoms
- loss of smell and taste
- possible breathing difficulty and low blood oxygen
359
some patients infected by COVID 19 experience
- respiratory failure
- shock
- multiorgan dysfunction
360
____ most effective way to prevet critial illness and helt spread fo COVID 19
vaccination
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