Chapter 21 - The Immune System - Innate and Adaptive Body Defenses Flashcards Preview

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Flashcards in Chapter 21 - The Immune System - Innate and Adaptive Body Defenses Deck (468)
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1
Q

The immune system’s two intrinsic systems are:

A
  1. 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
  1. innate defenses have specific pathways for certain substances
  2. 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
  1. 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
  1. they are a physical barrier to most microorganisms
  2. they are keratin resistant to weak acids and bases, bacterial enzymes, and toxins
  3. 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
  1. the acidity of skin and secretions–acid mantle
  2. enzymes
  3. defensins
  4. 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
  1. lysozome of saliva
  2. respiratory mucus
  3. 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
  1. mucus-coated hairs in nose
  2. cilia of upper respiratory tract that sweep dust
  3. 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
  1. phagocytes
  2. natural killer (NK) cells
  3. antimicrobial proteins
  4. fever
  5. 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
  1. macrophages
  2. mast cells
  3. WBCs
  4. inflammatory chemicals
25
Q

The phagocytes that participate in internal defenses are:

A
  • neutrophils

- macrophages

26
Q

These are the most abundant phagocytes but die fighting.

A

neutrophils

27
Q

_____ become phagocytic on exposure to infectious material.

A

neutrophils

28
Q

____ develop from monocytes.

A

macrophages

29
Q

The chief phagocytic cells are:

A

macrophages

30
Q

____ macrophages wander through tissue spaces, e.g. alveolar macrophages.

A

free

31
Q

___ macrophages are permanent residents of some organs, e.g. Kupffer cells (liver) and microglia (brain).

A

fixed

32
Q

In order for phagocytosis to take place, the phagocyte must

A

adhere to particle

33
Q

Some microorganisms evade phagocytic adherence with ____.

A

capsule

34
Q

____ marks pathogens—coating by complement proteins or antibodies.

A

opsonisation

35
Q

In phagocytosis, cytoplasmic extensions bind to and engulf the particle in a vesicle called ____.

A

phagosome

36
Q

In phagocytosis, the phagosome fuses with lysosome, which creates ____.

A

phagolysosome

37
Q

Pathogens are killed during phagocytosis due to acidifying and digesting with _____.

A

lysosomal enzymes

38
Q

If lysosomal enzymes are unable to kill pathogens, helper T cells cause a release of enzymes of _____, which kill pathogens.

A

respiratory burst

39
Q

What are the three ways that helper T cells kill pathogens that are resistant to lysosomal enzymes?

A
  1. release cell-killing free radicals
  2. produce oxidising chemicals (e.g. H2O2)
  3. increase pH and osmolarity of phagolysosome
40
Q

In phagocytosis, defensins in neutrophils pierce ____.

A

membrane

41
Q

nonphagocytic large granular lymphocytes

A

natural killer (NK) cells

42
Q

NK cells attack cells that lack

A

“self” cell-surface receptors

43
Q

NK cells induce ___ in cancer cells and virus-infected cells.

A

apoptosis

44
Q

NK cells secrete potent chemicals that enhance:

A

inflammatory response

45
Q

This is triggered whenever body tissues are injured.

A

inflammatory response

46
Q

This prevents the spread of damaging agents.

A

inflammation

47
Q

The cardinal signs of acute inflammation are:

A
  • redness
  • swelling
  • heat
  • pain
  • sometimes impairment of function
48
Q

When inflammation is triggered, it disposes of what?

A

cell debris and pathogens

49
Q

When inflammation is triggered, it alerts which system?

A

adaptive immune system

50
Q

When inflammation is triggered, it sets the stage for what?

A

repair

51
Q

The inflammatory response begins with chemicals released into _____ by injured tissues, immune cells, blood proteins.

A

ECF

52
Q

Macrophages and epithelial cells of boundary tissues have ____ receptors.

A

Toll-like (TLR)

53
Q

11 types of toll-like receptors (TLR) recognise specific classes of:

A

infecting microbes

54
Q

Activated TLRs trigger release of _____ that promote inflammation.

A

cytokines

55
Q

The three inflammatory mediators are:

A
  • kinins
  • prostaglandins
  • complement
56
Q

Inflammatory mediators dilate _____.

A

local arterioles

57
Q

When inflammatory mediators dilate local arterioles, this is known as:

A

hyperemia

58
Q

When inflammatory mediators dilate local arterioles, this causes:

A

redness and heat of inflamed region

59
Q

Inflammatory mediators make capillaries ____.

A

leaky

60
Q

Inflammatory mediators attract ____ to area.

A

leukocytes

61
Q

Does edema increase capillary permeability or decrease it? What does this cause?

A

increase; exudate goes to tissues

62
Q

Exudate is fluid containing ___ and ___.

A

clotting factors; antibodies

63
Q

Exudate causes:

A

local swelling (edema)

64
Q

When swelling occurs, it pushes on nerve endings which causes:

A

pain

65
Q

Pain can also occur from:

A
  • bacterial toxins
  • prostaglandins
  • kinins
66
Q

Exudate moves foreign material into ____.

A

lymphatic vessels

67
Q

Exudate delivers ____ and ____ to area of inflammation.

A

clotting proteins; complement

68
Q

The clotting factors that exudate delivers to area of inflammation form _____.

A

fibrin mesh

69
Q

The fibrin mesh formed by clotting factors at areas of inflammation is the scaffold for ____.

A

repair

70
Q

The fibrin mesh formed by clotting factors at areas of inflammation isolates the injured area so that:

A

invaders can’t spread

71
Q

In phagocyte mobilisation, ___ lead, and ___ follow.

A

neutrophils; macrophages

72
Q

As phagocyte attack continues, ___ arrive.

A

monocytes

73
Q

12 hours after leaving bloodstream, monocytes become ____. These are called ___.

A

macrophages; “late-arrivers”

74
Q

“Late-arrivers” replace ____ and remain for ____.

A

dying neutrophils; clean up prior to repair

75
Q

If inflammation is due to pathogens, ____ is activated and ____ arrive.

A

complement; adaptive immunity elements

76
Q

The steps for phagocyte mobilisation are:

A
  1. leukocytosis
  2. margination
  3. diapedesis of neutropils
  4. chemotaxis
77
Q

the release of neutrophils from bone marrow in response to ____-inducing factors from injured cells

A

leukocytosis

78
Q

neutrophils cling to walls of capillaries in inflamed area in response to CAMs

A

margination

79
Q

inflammatory chemicals promote positive ___ of neutrophils

A

chemotaxis

80
Q

inflammatory chemicals that promote chemotaxis are known as

A

chemotactic agents

81
Q

Two different antimicrobial proteins are:

A
  • interferons (IFNs)

- complement proteins

82
Q

Antimicrobial proteins attack microorganisms directly or indirectly?

A

directly

83
Q

Antimicrobial proteins hinder the microorganisms’ ability to ____.

A

reproduce

84
Q

The family of immune-modulating proteins are known as:

A

interferons

85
Q

Viral-infected cells secrete interferons to:

A

warn neighbouring cells

86
Q

After viral-infected cells secrete IFNs, they enter neighbouring cells and cause the cell to do what?

A

produce proteins that block viral reproduction and degrade viral RNA

87
Q

IFN alpha and beta also activate ____.

A

NK cells

88
Q

IFN ____ is secreted by lymphocytes.

A

gamma (immune interferon)

89
Q

IFN gamma activates ____.

A

macrophages

90
Q

IFN gamma has widespread ____ effects.

A

immune-mobilising

91
Q

Since IFN activates NK cells and macrophages, it indirectly fights ____.

A

cancer

92
Q

Artificial IFNs are used to treat:

A
  • hepatitis C
  • genital warts
  • MS
  • hairy cell leukaemia
93
Q

The complementary system is composed of ~20 blood proteins that circulate in ___ form.

A

inactive

94
Q

The complement system includes which blood proteins?

A
  • C1-C9
  • factors B, D, and P
  • other regulatory proteins
95
Q

Complement is the major mechanism for destroying:

A

foreign substances

96
Q

Our cells contain complement activation ____.

A

inhibitors

97
Q

Complement unleashes inflammatory chemicals that:

A

amplify all aspects of inflammatory response

98
Q

Complement kills bacteria and certain other cell types by ____.

A

cell lysis

99
Q

Complement enhances which defense?

A

both innate and adaptive

100
Q

There are three pathways to complement activation, which are:

A
  • classical pathway
  • lectin pathway
  • alternative pathway
101
Q

In the classical pathway, antibodies bind to ____ and ____. This is called _____.

A

invading organisms; complement components; complement fixation

102
Q

The classical pathway is the ___ step in complement activation.

A

first

103
Q

____ are produced by the innate system to recognise foreign invaders.

A

lectins

104
Q

When lectins are bound to foreign invaders they can also bind and activate ____.

A

complement

105
Q

Complement pathway that is triggered when activated C3, B, D, and P interact on the surface of microorganisms.

A

alternative pathway

106
Q

Each complement pathway involves activation of ___ and in an orderly sequence.

A

proteins

107
Q

In complement activation, each step ___ the next.

A

catalyses

108
Q

Each complement pathway converges on ___, which cleaves into __ and ___.

A

C3; C3a; C3b

109
Q

In complement activation, there is a common terminal pathway initiated that does three things, which are:

A
  • enhances inflammation
  • promotes phagocytosis
  • causes cell lysis
110
Q

Cell lysis begins when:

A

C3b binds to target cell

111
Q

After C3b binds to target cell, what happens?

A

insertion of complement proteins called [membrane attack complex (MAC)] into cell’s membrane

112
Q

After MAC is inserted into cell’s membrane, what happens?

A

MAC forms and stabilises a hole in the membrane surface

113
Q

After MAC forms a hole in the membrane surface, what happens?

A

Influx of water –> lysis of cell

114
Q

C3b also causes ____.

A

opsonisation

115
Q

C3a and other cleavage products amplify ___.

A

inflammation

116
Q

C3a stimulates mast cells and basophils to release ___.

A

histamine

117
Q

C3a attracts ___ and ____.

A

neutrophils; other inflammatory cells

118
Q

Fever is a systemic response to:

A

invading microorganisms

119
Q

Leukocytes and macrophages exposed to foreign substances secrete ___.

A

pyrogens

120
Q

Pyrogens act on:

A

body’s thermostat in the hypothalamus, raising body temperature

121
Q

The benefits of moderate fever are:

A
  • causing the liver and spleen to sequester zinc and iron (needed by microorganisms)
  • increasing metabolic rate –> faster repair
122
Q

this system must be primed by initial exposure to a specific foreign substance

A

adaptive (specific defense) immune system

123
Q

The adaptive immune system activates ___.

A

complement

124
Q

The adaptive immune system amplifies ____.

A

inflammatory response

125
Q

The adaptive immune system protects against ___ and ___.

A

infectious agents; abnormal body cells

126
Q

part of the adaptive immune system that recognises and targets specific antigens

A

specific

127
Q

part of the adaptive immune system that is not restricted to initial site

A

systemic

128
Q

the adaptive immune system has ____, which leads to stronger attacks to known anitgens

A

memory

129
Q

The two separate, overlapping arms of adaptive immune system are:

A
  • humoral (antibody-mediated) immunity

- cellular (cell-mediated) immunity

130
Q

humoral immunity is composed of ___, produced by lymphocytes, circulating freely in body fluids

A

antibodies

131
Q

in humoral immunity, antibodies bind temporarily to the target cell and do two things:

A
  • temporarily inactivate target cell

- mark the target cell for destruction by phagocytes or complement

132
Q

in cellular immunity ___ act against target cell.

A

lymphocytes

133
Q

lymphocytes that act against target cell act directly by

A

killing infected cells

134
Q

lymphocytes that act against target cell act indirectly by

A

releasing chemicals that enhance inflammatory response or activating other lymphocytes or macrophages

135
Q

substances that can mobilise adaptive defenses and provoke an immune response

A

antigens

136
Q

antigens are the targets of all ___ immune responses

A

adaptive

137
Q

Most antigens are large, complex molecules not normally found in

A

body (nonself)

138
Q

The two important functional properties of complete antigens are:

A
  • immunogenicity

- reactivity

139
Q

Examples of complete antigens are:

A
  • foreign protein
  • polysaccharides
  • lipids
  • nucleic acids
140
Q

ability to stimulate proliferation of specific lymphocytes

A

immunogenicity

141
Q

ability to react with activated lymphocytes and antibodies released by immunogenic reactions

A

reactivity

142
Q

incomplete antigens are known as

A

haptens

143
Q

incomplete antigens are not ___ by themselves

A

immunogenic

144
Q

Example of haptens:

A
  • peptides
  • nucleotides
  • some hormones
145
Q

haptens may be immunogenic if attached to ____ and combination is marked foreign

A

body proteins

146
Q

haptens cause the immune system to mount

A

harmful attack

147
Q

Examples of mounted harmful attack as a result of haptens:

A
  • poison ivy
  • animal dander
  • detergents
  • cosmetics
148
Q

antigenic determinants are also known as

A

epitopes

149
Q

Only certain parts (epitopes) of entire antigen are ___

A

immunogenic

150
Q

Antibodies and lymphocyte receptors bind to epitopes as enzyme binds ___.

A

substrate

151
Q

Most naturally occurring antigens have numerous antigenic determinants that

A
  • mobilise several different lymphocyte populations

- form different kinds of antibodies against it

152
Q

Large, chemically simple molecules (e.g. plastics) have little or no ___.

A

immunogenicity

153
Q

self-antigens are also known as

A

MHC proteins

154
Q

self-antigens are

A

protein molecules on the surface of cells that are not antigenic to self but antigenic to others in transfusions or grafts

155
Q

Example of self-antigens:

A

MHC glycoproteins

156
Q

MHC glycoproteins are coded by genes of ____ and are unique to the individual.

A

major histocompatibility complex

157
Q

MHC glycoproteins have a groove holding ___ or ___.

A

self-antigen; foreign antigen

158
Q

Lymphocytes only bind ___ on MHC proteins.

A

antigens

159
Q

The three types of cells of the adaptive immune system are:

A
  • B lymphocytes
  • T lymphocytes
  • Antigen-presenting cells (APCs)
160
Q

B lymphocytes participate in ___ immunity.

A

humoral

161
Q

T lymphocytes participate in ___ immunity.

A

cell-mediated

162
Q

these do not respond to specific antigens and play essential auxiliary roles in immunity

A

antigen-presenting cells (APCs)

163
Q

The five steps of lymphocyte development, maturation, and activation are:

A
  • origin (all originate in red bone marrow)
  • maturation
  • seeding secondary lymphoid organs and circulation
  • antigen encounter and activation
  • proliferation and differentiation
164
Q

Lymphocytes are educated as they mature, and become B cells in ___ or T cells in ___.

A

bone marrow; thymus

165
Q

a lymphocyte can recognise one specific antigen by binding to it is known as

A

immunocompetence

166
Q

lymphocytes unresponsive to own antigens is known as

A

self-tolerance

167
Q

Thanks to immunocompetence, B or T cells display a unique receptor on their surface when they achieve maturity, so they can bind

A

only one antigen

168
Q

T cells mature in the thymus under ___ and ___ pressures.

A
  • positive selection

- negative selection

169
Q

selects T cells capable of regonising self-MHC proteins; failures are destroyed by apoptosis

A

positive selection

170
Q

T cells capable of recognising self-MHC proteins is known as

A

MHC restriction

171
Q

prompts apoptosis of T cells that bind to self-antigens displayed by self-MHC; ensures self tolerance

A

negative selection

172
Q

B cells are positively selected if they successfully make

A

antigen receptors

173
Q

B cells that are self-reactive are handled by

A

elimination by apoptosis (clonal deletion)

174
Q

Immunocompetent B and T cells that are not yet exposed to antigen are called

A

naive

175
Q

Naive B/T cells are exported from ____ to ____.

A

primary lymphoid organs; “seed” secondary lymphoid organs

176
Q

Exportation of naive B/T cells increases the chance of:

A

encounter with antigen

177
Q

examples of primary lymphoid organs

A
  • bone marrow

- thymus

178
Q

examples of secondary lymphoid organs

A
  • lymph nodes

- spleen

179
Q

naive lymphocyte’s first encounter with antigen leads to selection for further development. this is known as

A

clonal selection

180
Q

If the correct signals are present in clonal selection,

A

lymphocyte will complete its differentiation

181
Q

An activated lymphocyte ____.

A

proliferates

182
Q

Due to lymphocyte proliferation, this leads to

A

exact clones

183
Q

Most lymphocyte clones become

A

effector cells that fight infections

184
Q

Few lymphocyte clones remain as

A

memory cells

185
Q

Memory cells are able to respond to the same antigen

A

more quickly the second time

186
Q

B and T memory cells and effector T cells circulate ___.

A

continuously

187
Q

____ determine which foreign substances the immune system will recognise.

A

genes (not antigens)

188
Q

Immune cell receptors are the result of

A

acquired knowledge of microbes (likely in environment)

189
Q

Lymphocytes make how many different types of antigen receptors?

A

up to a billion

190
Q

Lymphocytes are coded for by ~____ genes.

A

25,000

191
Q

Gene segments are shuffled by ____.

A

somatic recombination

192
Q

these engulf antigens

A

antigen-presenting cells (APCs)

193
Q

APCs present fragments of antigens to ___ for recognition.

A

T cells

194
Q

The three major types of APCs are:

A
  • dendritic cells
  • macrophages
  • B cells
195
Q

dendritic cells are located in

A

connective tissues and epidermis

196
Q

macrophages are located in

A

connective tissues and lymphoid organs

197
Q

dendritic cells phagocytise ___

A

pathogens

198
Q

dendritic cells enter ___ to present antigens to ___ in lymph node

A

lymphatics; T cells

199
Q

the most effective antigen-presenter known is

A

dendritic cell

200
Q

dendritic cells are the key link between

A

innate and adaptive immunity

201
Q

macrophages are widespread in ___ and ___

A

lymphoid organs; connective tissues

202
Q

macrophages can activate

A

naive T cells

203
Q

macrophages present antigens to T cells to

A

activate themselves into voracious phagocytes that secrete bactericidal chemicals

204
Q

these do not activate naive T cells

A

B cells

205
Q

B cells present antigens to ___ to assist own activation

A

helper T cell

206
Q

B cells are activated when

A

antigens bind to its surface receptors and cross-link them

207
Q

After antigens cross-link surface receptors, what happens?

A

receptor-mediated endocytosis of cross-linked antigen-receptor complexes (clonal selection)

208
Q

After receptor-mediated endocytosis of cross-linked antigen-receptor complexes takes place, what happens?

A

proliferation and differentiation into effector cells

209
Q

Most clone cells become ____ cells.

A

plasma

210
Q

Plasma cells secrete ___ at a rate of ___ for how long?

A

specific antibodies; 2000 molecules/sec; four to five days, then die

211
Q

Antibodies circulate in ___ or ___.

A

blood; lymph

212
Q

Antibodies bind to ___ and mark for

A

free antigens; destruction by innate or adaptive mechanisms

213
Q

Clone cells that do not become plasma cells become ____.

A

memory cells

214
Q

Memory cells provide ____ memory and mount ___ response to future exposures of same antigen.

A

immunological; immediate

215
Q

In immunological memory—primary immune response, upon first antigen exposure, what takes place?

A

cell proliferation and differentiation

216
Q

The lag period for cell proliferation and differentiation in the primary immune response is:

A

three to six days

217
Q

In the primary immune response, peak levels of plasma antibody are reached in ___ days.

A

10

218
Q

After peak level of plasma antibodies in primary immune response of immunological memory, what happens?

A

antibody levels decline

219
Q

Re-exposure to the same antigen gives ____ response. (Part of secondary immune response)

A

faster, more prolonged, more effective

220
Q

(part of secondary immune response) Sensitised memory cells respond within:

A

hours

221
Q

(part of secondary immune response) Antibody levels peak in ___ days at much higher levels.

A

two to three

222
Q

(part of secondary immune response) Antibodies bind with ___ affinity.

A

greater

223
Q

(part of secondary immune response) Antibody level can remain high for

A

weeks to months

224
Q

when B cells encounter antigens and produce specific antibodies against them, this is known as

A

active humoral immunity

225
Q

The two types of active humoral immunity are

A
  • naturally acquired

- artificially acquired

226
Q

response to bacterial or viral infection

A

naturally acquired humoral immunity

227
Q

response to vaccine of dead or attenuated pathogens

A

artificially acquired humoral immunity

228
Q

most of dead or attenuated pathogens are

A

vaccines

229
Q

Vaccines spare us symptoms of

A

primary response

230
Q

Vaccines provide

A

antigenic determinants that are immunogenic and reactive

231
Q

Vaccines can cause

A
  • illness trying to vaccine against

- allergic responses

232
Q

___ and ___ help prevent illness or allergic responses induced by vaccines.

A
  • “naked DNA”

- oral vaccines

233
Q

In ____ immunity, readymade antibodies are introduced into body.

A

passive humoral

234
Q

In passive humoral immunity, B cells are ___ by antigens.

A

not challenged

235
Q

Does immunological memory occur in passive humoral immunity?

A

no

236
Q

In passive humoral immunity, protection ends when

A

antibodies degrade

237
Q

Two types of passive humoral immunity

A
  • naturally acquired

- artificially acquired

238
Q

antibodies are delivered to fetus via placenta or to infant through milk. this is known as

A

naturally acquired passive humoral immunity

239
Q

injection of serum, such as gamma globulin, is known as

A

artificially acquired passive humoral immunity

240
Q

In artifically acquired passive humoral immunity, protection is immediate but ends when

A

antibodies naturally degrade in body

241
Q

the gamma globulin portion of blood is known as

A

immunoglobulins

242
Q

proteins secreted by plasma cells are

A

antibodies

243
Q

Antibodies are capable of binding specifically with antigen detected by ___.

A

B cells

244
Q

Antibodies are grouped into one of ___ Ig classes.

A

five

245
Q

four looping polypeptide chains linked by disulfide bonds

A

antibody monomer

246
Q

Antibodies have T- or Y- shaped ____.

A

antibody monomer

247
Q

Overall antibody shape/structure:

A
  • 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
Q

Variable regions at one end of each antibody arm combine to form two identical ____.

A

antigen-binding sites

249
Q

Constant regions of antibody stem determine

A

antibody class

250
Q

Constant regions of antibody stem serve common functions in all antibodies by dictating:

A
  • cells and chemicals that antibody can bind

- how antibody class functions to eliminate antigens

251
Q

The different classes of antibodies are:

A
  • IgM
  • IgA
  • IgD
  • IgG
  • IgE
252
Q

Characteristics of IgM antibodies:

A
  • pentamer (larger than others)
  • first antibody released
  • potent agglutinating agent
  • readily fixes and activates complement
253
Q

Characteristics of IgA antibodies:

A
  • monomer or dimer
  • in mucus and other secretions
  • helps prevent entry of pathogens
254
Q

Characteristics of IgD antibodies:

A
  • monomer attached to surface of B cells

- functions as B cell receptor

255
Q

Characteristics of IgG antibodies:

A
  • monomer; 75-85% of antibodies in plasma
  • from secondary and late primary responses
  • crosses placental barrier
256
Q

Characteristics of IgE antibodies:

A
  • monomer active in some allergies and parasitic infections

- causes mast cells and basophils to release histamine

257
Q

B cells can switch antibody classes but retain ____.

A

antigen specificity

258
Q

B cells can switch from ___ at first; then ___.

A

IgM; IgG

259
Q

Almost all secondary antibody responses are ___.

A

IgG

260
Q

How do antibodies affect antigens?

A

inactivate and tag antigens; do not destroy them

261
Q

When antibodies interact with antigens, they form:

A

antigen-antibody (immune) complexes

262
Q

The defensive mechanisms used by antibodies are

A
  • neutralisation and agglutination (two most important)

- precipitation and complement fixation

263
Q

the simplest defense mechanism is

A

neutralisation

264
Q

In neutralisation, antibodies block specific sites on ___ or ___.

A

viruses; bacterial exotoxins

265
Q

In neutralisation, antibodies that block sites prevent antigens from

A

binding to receptors on tissue cells

266
Q

In neutralisation ____ undergo phagocytosis.

A

antigen-antibody complexes

267
Q

antibodies bind same determinant on more than one cell-bound antigen

A

agglutination

268
Q

In agglutination, ____ agglutinate. An example is:

A

cross-linked antigen-antibody complexes; clumping of mismatched blood cells

269
Q

soluble molecules are cross-linked

A

precipitation

270
Q

When soluble molecules are cross-linked, what happens?

A

Complexes precipitate and are subject to phagocytosis.

271
Q

The main antibody defense against cellular antigens is:

A

complement fixation and activation

272
Q

In complement fixation, several antibodies bind close together on a cellular antigen. This leads to:

A

complement-binding sites on stem regions aligning

273
Q

When complement-binding sites on stem regions align, this triggers:

A

complement fixation into cell’s surface —> cell lysis

274
Q

Functions of activated complement are:

A
  • amplifies inflammatory response
  • promotes phagocytosis via opsonisation
  • –>positive feedback cycle that enlists more and more defensive elements
275
Q

A commercially prepared pure antibody (also known as ____) is specific for:

A

monoclonal antibody; single antigenic determinant

276
Q

Monoclonal antibodies are produced by:

A

hybridomas

277
Q

cell hybrids; fusion of tumor cell and B cell

A

hybridomas

278
Q

Monoclonal antibodies proliferate indefinitely and have ability to produce:

A

single type of antibody

279
Q

monoclonal antibodies are used in

A
  • research
  • clinical testing
  • cancer treatment
280
Q

What do antigen-antibody complexes do to antigens?

A

do not destroy; prepare them for destruction by innate defenses

281
Q

Antibodies do not invade solid tissue unless:

A

there is a lesion present

282
Q

Antibodies can act intracellularly if:

A

attached to virus before it enters cell

–>activate mechanisms that destroy virus

283
Q

In the cellular immune response, T cells provide defense against ____.

A

intracellular antigens

284
Q

Some T cells ___ cells; others release chemicals that:

A

directly kill; regulate immune response

285
Q

In cell-mediated immune response, there are two populations of T cells based on which glycoprotein surface receptors are displayed. These are:

A
  • CD4 cells

- CD8 cells

286
Q

CD4 cells usually become ____ cells.

A

helper T

287
Q

Helper T (CD4) cells activate:

A
  • B cells
  • other T cells
  • macrophages
  • direct adaptive immune response
288
Q

Some CD4 cells become ____.

A

regulatory T cells

289
Q

Regulatory T cells moderate ____.

A

immune response

290
Q

CD4 cells can also become ____.

A

memory T cells

291
Q

CD8 cells become ____.

A

cytotoxic T cells

292
Q

Cytotoxic T cells (CD8) destroy cells that are

A

harboring foreign antigens

293
Q

CD8 cells can also become ___

A

memory T cells

294
Q

Helper, cytotoxic, and regulatory T cells are ____ T cells.

A

activated

295
Q

CD4 or CD8 cells are also known as

A

naive T cells

296
Q

T cells only respond to processed fragments of antigens displayed on

A

surfaces of cells

297
Q

Antigen presentation is vital for activation of ___ and normal functioning of ___.

A

naive T cells; effector T cells

298
Q

The two types of MHC proteins important to T cell activation are:

A
  • Class I MHC proteins

- Class II MHC proteins

299
Q

Both types of MHC proteins are synthesised at __ and bind to ____.

A

endoplasmic reticulum; peptide fragments

300
Q

proteins that are displayed by all cells except RBCs

A

class I MHC proteins

301
Q

proteins that are displayed by APCs (dendritic cells, macrophages, B cells)

A

class II MHC proteins

302
Q

Class I MHC proteins bind with fragment of protein synthesised

A

in the cell

303
Q

a fragment of protein synthesised in the cell is known as

A

endogenous antigen

304
Q

In a normal cell, an endogenous antigen is ___. In an infected or abnormal cell it is ___.

A

self-antigen; nonself antigen

305
Q

Class I MHC proteins are crucial for

A

CD8 cell activation

306
Q

Class I MHC proteins inform cytotoxic T cells of

A

microorganisms hiding in cells (cytotoxic T cells ignore displayed self-antigens)

307
Q

Class I MHC proteins act as

A

antigen holders; form “self” part that T cells recognise

308
Q

Class II MHC proteins bind with fragments of ____ that have been engulfed and broken down in a phagolysosome.

A

exogenous antigens

309
Q

Class II MHC proteins are recognised by ____.

A

helper T cells

310
Q

Class II MHC proteins signal ___ cells that help is required.

A

CD4

311
Q

CD4 and CD8 cells have different requirements for MHC protein that presents antigens to them. CD4 cells that become Th bind only:

A

class II MHC proteins typically on APC surfaces

312
Q

CD4 and CD8 cells have different requirements for MHC protein that presents antigens to them. CD8 cells that become cytotoxic T cell bind only:

A

class I MHC proteins on APC surfaces

313
Q

Once (CD8 cells that become) cytotoxic T cells are activated, they seek:

A

same antigen on class I MHC proteins on any cell

314
Q

CD8 cells are activated by class __ MHC proteins.

A

I

315
Q

How do APCs get endogenous antigens from another cell and display them on class I MHCs?

A

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
Q

The two-step process of T cell activation:

A
  • Antigen binding

- Co-stimulation

317
Q

Both steps of T cell activation occur on surface of:

A

same APC

318
Q

Both steps of T cell activation are required for ___.

A

clonal selection

319
Q

T cell antigen receptors (TCRs) bind to ____ on APC surface.

A

antigen-MHC complex

320
Q

TCR that recognises the nonself-self complex is linked to:

A

multiple intracellular signaling pathways

321
Q

Other T cell surface proteins are involved in ____. (Ex. ___)

A

T cell activation; CD4 and CD8 help maintain coupling during antigen recognition

322
Q

T cell activation–co-stimulation–requires T cell binding to:

A

other surface receptors on an APC (co-stimulatory signals)

323
Q

Cytokines (interleukin 1 and 2 from APCs or T cells) trigger ___ and ___ of activated T cell.

A

proliferation; differentiation

324
Q

Without co-stimulation of T cell activation, ___ occurs.

A

anergy

325
Q

In anergy, T cells become:

A

tolerant to that antigen

326
Q

In anergy, T cells are unable to:

A

divide

327
Q

In anergy, T cells do not:

A

secrete cytokines

328
Q

T cells that are activated do what?

A
  • enlarge and proliferate in response to cytokines

- differentiate and perform functions according to their T cell class

329
Q

Primary T cell response peaks within:

A

a week

330
Q

T cell apoptosis occurs between days:

A

7 and 30

331
Q

The benefit of T cell apoptosis:

A

activated T cells are a hazard–produce large amount of inflammatory cytokines
–>hyperplasia, cancer

332
Q

Effector activity wanes as amount of:

A

antigen declines

333
Q

Memory T cells remain and mediate:

A

secondary responses

334
Q

chemical messengers of the immune system are:

A

cytokines

335
Q

Cytokines mediate:

A
  • cell development
  • differentiation
  • responses in immune system
336
Q

Cytokines include ___ and ___.

A

interferons; interleukins

337
Q

____ is released by macrophages which co-stimulates bound T cells.

A

Interleukin 1 (IL-1)

338
Q

Interleukin 1 co-stimulates bound T cells to:

A
  • release interleukin 2 (IL-2)

- synthesise more IL-2 receptors

339
Q

IL-2 is a key growth factor, acting on cells that:

A

release it and other T cells

340
Q

IL-2 encourages activated ____ to divide rapidly.

A

T cells

341
Q

Other cytokines amplify and regulate:

A

innate and adaptive responses

342
Q

Examples of cytokines that amplify and regulate innate and adaptive responses:

A
  • tumor necrosis factor – cell toxin

- gamma interferon – enhances killing power of macrophages

343
Q

Helper T (Th) cells play a central role in:

A

adaptive immune response

344
Q

Helper T cells activate both:

A

humoral and cellular arms

345
Q

Once primed by APC presentation of antigen, helper T cells do what?

A
  • help activate T and B cells
  • induce T and B cell proliferation
  • their cytokines recruit other immune cells
346
Q

Without helper T cells, there is no:

A

immune response

347
Q

Helper T cells interact directly with B cells displaying:

A

antigen fragments bound to MHC II receptors

348
Q

Helper T cells stimulate B cells to ___ and ___.

A

divide more rapidly; being antibody formation

349
Q

B cells may be activated by helper T cells by binding to _____. Reponse is:

A

T cell-independent antigens; weak and short-lived

350
Q

Most antigens require Th co-stimulation to activate B-cells, these are called:

A

T cell-dependent antigens

351
Q

CD8 cells require helper T cell activation into:

A

destructive cytotoxic T cells

352
Q

Helper T cell activation of CD8 cells cause dendritic cells to express ____ required for CD8 cell activation.

A

co-stimulatory molecules

353
Q

Helper T cells amplify responses of:

A

innate immmune system

354
Q

Helper T cells activate ___, which leads to:

A

macrophages; more potent killers

355
Q

Helper T cells mobilise _____ and ____ and attract other types of ___.

A

lymphocytes; macropages; WBCs

356
Q

Helper T cells are divided into these subsets of helper T cells:

A
  • Th1
  • Th2
  • Th17
357
Q

Subset helper T cells that mediate most aspects of cellular immunity:

A

Th1

358
Q

Subset helper T cells that defend against parasitic worms; mobilise eosinophils, promote allergies:

A

Th2

359
Q

Subset helper T cells that link adaptive and innate immunity by releasing IL-17; may play role in autoimmune disease:

A

Th17

360
Q

these cells directly attack and kill other cells

A

cytotoxic T cells (Tc)

361
Q

activated cytotoxic cells circulate in blood and lymph and lymphoid organs in search of:

A

body cells displaying antigen they recognise

362
Q

Cytotoxic (Tc) cell targets are:

A
  • virus-infected cells
  • cells with intracellular bacteria or parasites
  • cancer cells
  • foreign cells (transfusions or transplants)
363
Q

Cytotoxic T cells bind to a ___ complex.

A

self-nonself

364
Q

Cytotoxic T cells can destroy all:

A

infected or abnormal cells

365
Q

Lethal hit of cytotoxic cells–two methods:

A
  • Tc cell releases perforins and granzymes by exocytosis

- Tc cell binds specific membrane receptor on target cell, and stimulates apoptosis

366
Q

Perforins create pores through which:

A

granzymes can enter target cell

367
Q

Granzymes stimulate ____.

A

apoptosis

368
Q

Regulatory T cells dampen immune response by:

A

direct contact or by inhibitory cytokines such as IL-10 and TGF-beta

369
Q

Regulatory T cells are important in preventing:

A

autoimmune reactions

370
Q

By preventing autoimmune reactions, regulatory T cells do (two) things:

A
  • suppress self-reactive lymphocytes in periphery (outside lymphoid organs)
  • research into using them to induce tolerance to transplanted tissue
371
Q

Natural killer cells recognise other (3) signs of abnormality:

A
  • lack of class I MHC
  • antibody coating target cell
  • different surface markers of stressed cells
372
Q

NK cells use same key mechanisms as ___ cells for killing their target cells.

A

cytotoxic T cells

373
Q

In ___, NK and cytotoxic T cells prowl for markers they recognise.

A

immune surveillance

374
Q

The four varieties of organ transplants are:

A
  • autografts
  • isografts
  • allografts
  • xenografts
375
Q

graft from one body site to another in same person

A

autograft

376
Q

graft between identical twins

A

isograft

377
Q

graft between individuals who are not identical twins

A

allograft

378
Q

graft from another animal species

A

xenograft

379
Q

Sucess of graft depends on similarity of __.

A

tissues

380
Q

Autografts and isografts have ideal donor tissues which are almost always successful if:

A

there is a good blood supply and no infection

381
Q

There has been research into ___grafts from genetically engineered animals.

A

xenografts

382
Q

The most common graft is:

A

allograft

383
Q

In allograft, ___, ___, and ___ are mached as closely as possible.

A

ABO; other blood antigens; MHC antigens

384
Q

In immunosuppressive therapy problems, the patient’s ___ is supressed.

A

immune system

385
Q

After the immune system is suppressed, it cannot:

A

protect from foreign agents

386
Q

After the immune system is suppressed, bacterial and viral infections lead to:

A

death

387
Q

After the immune system is suppressed, it must balance drugs for ____ but no toxicity.

A

graft

388
Q

After the immune system is suppressed, it uses ___ to control infections.

A

antibiotics

389
Q

After the immune system is suppressed, undr best circumstances, rejection is after ____ in __% of patients.

A

10 years; 50%

390
Q

congenital or acquired condition that impairs function or production of immune cells or molecules such as complement or antibodies

A

immunodeficiency

391
Q

Severe combined immunodeficiency syndrome (SCID) is a ___ defect.

A

genetic

392
Q

In SCID, there is a marked deficit in ___ and ___ cells.

A

B; T

393
Q

In SCID, there is a defective ___ enzyme.

A

adenosine deaminase (ADA)

394
Q

SCID is fatal if untreated; it is treated with ___ transplants.

A

bone marrow

395
Q

Lymphoma is an acquired ____.

A

immunodeficiency

396
Q

Lymphoma is cancer of ____.

A

lymphocytes

397
Q

Lymphoma leads to immunodeficiency by depressing:

A

lymph node cells

398
Q

Acquired immune deficiency syndrome (AIDS) cripples the immune system by:

A

interfering with activity of helper T cells

399
Q

AIDS is characterised by:

A
  • severe weight loss
  • night sweats
  • swollen lymph nodes
400
Q

With AIDS, opportunistic infections occur, such as:

A
  • pneumocystis pneumonia

- Kaposi’s sarcoma

401
Q

AIDS is caused by ____ transmitted by bodily fluids–blood, semen, and vaginal secretions

A

human immunodeficiency virus (HIV)

402
Q

HIV enters body via:

A
  • blood transfusions
  • blood-contaminated needles
  • sexual intercouse and oral sex
  • vaginal secretions
403
Q

HIV destroys ___ cells, which leads to:

A

helper T cells; depression of cell-mediated immunity

404
Q

HIV multiplies in lymph nodes throughout ___ period, ~10 years if untreated

A

asymptomatic

405
Q

There are symptoms of HIV when ___ collapses:

A

immune system

406
Q

HIV also invades brain, which leads to:

A

dementia

407
Q

HIV-coated glycoprotein complex attaches to:

A

CD4 receptor

408
Q

Acquired Immune Deficiency Synrome (AIDS) arises from:

A

HIV reverse transcriptase

409
Q

HIV reverse transcriptase leads to:

A

frequent errors; high mutation rate and resistance to drugs

410
Q

AIDS can be treated with these antiviral drugs:

A
  • fusion inhibitors
  • integrase inhibitors
  • reverse transcriptase and protease inhibitors
  • antiretroviral vaginal gel
411
Q

____ block HIV’s entry into cell.

A

fusion inhibitors

412
Q

____ block viral RNA integration into host’s DNA.

A

integrase inhibitors

413
Q

_____ inhibit viral replication enzymes.

A

reverse transcriptase and protease inhibitors

414
Q

antiretroviral vaginal gel reduces AIDS risk by ___%.

A

50

415
Q

immune system loses ability to distinguish self from foreign

A

autoimmune disease

416
Q

in autoimmune disease, there is production of ____ and ____ that destroy body tissues.

A

autoantibodies; sensitised Tc cells

417
Q

Examples of autoimmune diseases:

A
  • MS
  • myasthenia gravis
  • Graves’ disease
  • type I diabetes mellitus
  • systemic lupus erythmatosus
  • glomerulonephritis
  • rheumatoid arthritis
418
Q

Autoimmune diseases are treated by suppressing the entire immune system by:

A
  • anti-inflammatory drugs (e.g. corticosteroids)
  • blocking cytokine action
  • blocking co-stimulatory molecules
419
Q

Research into autoimmune disease treatment includes:

A
  • activating regulatory T cells
  • inducing self-tolerance using vaccines
  • directing antiboies against self-reactive immune cells
420
Q

In autoimmune disease, weakly self-reactive lymphocytes may be activated by:

A
  • foreign antigens that may resemble self-antigens

- new self-antigens may appear

421
Q

When foreign antigens that may resemble self-antigens appear, antibodies against foreign antigen may:

A

cross-react with self-antigen

422
Q

In autoimmune disease, new self-antigens may appear, generated by:

A
  • gene mutations
  • changes in self-antigens by hapten attachment or infectious damage
  • release of novel self-antigens by trauma to barrier
423
Q

immune responses to perceived (otherwise harmless) threat cause tissue damage

A

hypersensitivities

424
Q

different types of hypersensitivities are distinguished by:

A
  1. their time course

2. whether antibodies or T cells are involved

425
Q

Antibodies cause ___ and ___ hypersensitivities.

A

immediate; subacute

426
Q

T cells cause ___ hypersensitivity.

A

delayed

427
Q

_____ hypersensitivities begin in seconds after contact with allergen.

A

acute (type I) [allergies]

428
Q

Initial contact with allergen is ____ but sensitises person.

A

asymptomatic

429
Q

Allergy reaction may be ___ or ___.

A

local; systemic

430
Q

Allergy reaction involves ___ secrete by ___ cells.

A

IL-4; Th2

431
Q

Secreted IL-4 stimulates ____ to produce ___.

A

B cells; IgE

432
Q

Produce IgE binds to ___ and ___, which leads to:

A

mast cells; basophils; flood of histamine release and induced inflammatory response

433
Q

A later encounter with same allergen leads to:

A

allergic reaction

434
Q

mast cells of skin and respiratory and gastrointestinal mucosa react to allergen

A

local reaction

435
Q

allergic systemic response is ____.

A

anaphylactic shock

436
Q

in allergic reaction, histamine release leads to

A

blood vessels dilated and leaky –> runny nose, hives, watery eyes
-asthma if allergen is inhaled

437
Q

allergic reaction histamine release is controlle by

A

antihistamines

438
Q

systemic response to allergen that directly enters blood and circulates rapidly

A

anaphylactic shock

439
Q

in anaphylactic shock, ___ and ___ are enliste throughout the body

A

basophils; mast cells

440
Q

Systemic histamine release may cause:

A
  • constriction of bronchioles; tongue may swell
  • sudden vasodilation and fluid loss from bloodstream that may cause
  • > circulatory collapse (hypotensive shock) and death
441
Q

anaphylactic shock is treate by

A

epinephrine

442
Q

subacute hypersensitivities are caused by ___ and ___ transferred via blood plasma or serum

A

IgM and IgG

443
Q

subacute hypersensitivities have a ___ onset and ___ duration

A

slow; long

444
Q

two subacute hypersensitivities are:

A
  • cytotoxic (type II reactions)

- immune complex (type III) hypersensitivity

445
Q

an example of cytotoxic (type II) reaction

A

mismatched blood transfusion reaction

446
Q

an example of immune complex (type III) hypersensitivity

A

systemic lupus erythematosus

447
Q

antibodies bind to antigens on specific body cells, stimulate phagocytosis and complement-mediated lysis of cellular antigens

A

cytotoxic (type II) reactions

448
Q

in immune complex (type III) hypersensitivity, ___ are widely distributed in body or blood

A

antigens

449
Q

in immune complex (type III) hypersensitivity, once antigens are distributed in the body, ____ form.

A

insoluble antigen-antibody complexes

450
Q

in immune complex (type III) hypersensitivity, complexes cannot be cleared from:

A

particular area of body

451
Q

in immune complex (type III) hypersensitivity, complex buildup leads to:

A
  • intense inflammation
  • local cell lysis
  • cell killing by neutrophils
452
Q

delayed hypersensitivities (type IV) have a ___ onset.

A

slow

453
Q

delayed hypersensitivities (type IV) mechanism depends on _____ cells.

A

helper T

454
Q

in delayed hypersensitivities (type IV), ____ and ___ cause damage.

A

cytokine-activated macrophages; cytotoxic T cells

455
Q

an example of delayed hypersensitivity (type IV) is

A

allergic contact dermatitis (e.g. poison ivy)

456
Q

type IV hypersensitivity agents act as ____.

A

haptens

457
Q

___ test depends on type IV hypersensitivity reaction.

A

TB skin

458
Q

immune system stem cells develop in liver and spleen in weeks ____.

A

1-9

459
Q

bone marrow becomes primary source of stem cells when?

A

later and through adult life

460
Q

lymphocyte development continues in ___ and ___.

A

bone marrow; thymus

461
Q

___ lymphocytes preominate in newborn; ___ system educated as person encounters antigens

A

Th2; Th1

462
Q

depression, emotional stress, and grief do what do the immune response?

A

impair

463
Q

vitamin ____ is required for activation of CD8 cells to produce Tc cells

A

D

464
Q

vitamin D supplements reduce _____.

A

influenza

465
Q

vitamin D deficiency is linked to ____.

A

MS

466
Q

with age, immune system begins to ___.

A

wane

467
Q

as a person ages, there is greater susceptibility to:

A

immunodeficiency and autoimmune diseases

468
Q

as a person ages, there is greater incidence of:

A

cancer