CHAPTER II – IMMUNITY Flashcards

1
Q

It is the study of: discriminating self from non-self

A

IMMUNOLOGY

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2
Q

IMMUNOLOGY PURPOSE:

A

eliminate non-self components such as infectious agents

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3
Q

Responsible for the surveillance and destruction of substances that are foreign to the body

A

IMMUNE SYSTEM

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4
Q

Attack microorganism that exists outside the host’s cell or used to attack microorganisms that infect cells

A

IMMUNE SYSTEM

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5
Q

Defending the body against the development of tumors

A

IMMUNE SYSTEM

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6
Q

IMMUNE SYSTEM Divided into two main categories based on:

A

(a) the manner in which the interaction with the foreign substance,
(b) and whether it causes a more efficient response towards a subsequent infection

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7
Q

: silent gene; needs stimulus to develop into cancer

A

ONCOGENE

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8
Q

: chronic smoking

A

Oral, mouth, lung cancer

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9
Q

: unhealthy foods, reheating

A

Colon cancer

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10
Q

(scavenger organ; cleans senescent/old RBCs)

A

spleen

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11
Q

TYPES OF IMMUNITY

A
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12
Q

Non-specific immunity

A

INNATE IMMUNITY

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13
Q

Refers primarily to anatomical, cellular, and humoral defenses that functions in the early stages of host defense

A

INNATE IMMUNITY

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14
Q

Physical

A

Barriers; skin, mucus, cilia
Flushing Action: Blinking of eyelids, Peristalsis and Urination

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15
Q

Chemical

A

Salts: Cerumen and Sebum
Acids: Low pH of Stomach and Vagina
Lipids: Fatty acids in the sebaceous glands and gallbladder

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16
Q

Normal flora

A

Non pathogenic bacteria in:
oGIT
oVagina
oNasopharynx

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17
Q

Non pathogenic bacteria in:
oGIT –
oVagina –
oNasopharynx –

A

Citrobacter, Bacteroides, E. coli (passed in stool)

Lactobacillus acidophilus: maintains acidic pH

Streptococcus, Neisseria

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18
Q

Physiologic process

A

Sneezing
Coughing
Vomiting, Gag reflex
Perspiration
Shivering
Crying
Urinatio
 Defacation

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19
Q

Sweat maintains skin pH at

A

5.6 (acidic)

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20
Q

Acids: Low pH of Stomach and Vagina
oDue to

A

HCl or Pepsin

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21
Q

Resistant to stomach acid
Causes peptic ulcer
Produces UREASE (alkaline)

A

Helicobacter pylori

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22
Q

– through ingestion

A

Vomiting, Gag reflex

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23
Q

Maintenance of normal temperature

A

Perspiration

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24
Q

– to prevent hypothermia

A

Shivering

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25
Q

Crying– tears contain

(antibacterial; has IgA)

A

lysozymes

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26
Q

Others

A

Body temperature
Oxygen Tension

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27
Q

 - < 37oC

A

Body temperature

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28
Q

 – thin air; increased hemoglobin

A

Oxygen Tension

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29
Q

SECOND LINE OF DEFENSE

CELLULAR FACTORS

NON-CELLULAR/SOLUBLE SUBSTANCES IN BLOOD (HUMORAL FACTORS)

A

1.Phagocytes
2.Basophil and Mast Cells
3.NK Cells
4.APCs

1.Complement System
2.Cytokines
3.Interferons
4.Inflammatory Reaction
5.Acute reactants

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30
Q

Secretion of factors primarily involve in the second line of defense

A

CYTOKINES

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31
Q

Promotes inflammatory response

A

Interleukin-1

Hydrolytic enzymes

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32
Q

Promotes innate immunity

A

Interleukin-6

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33
Q

Promotes elimination of pathogens through cell lysis

A

Complement

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34
Q

Kills tumor cells

A

Tumor Necrosis Factor

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35
Q

Able to interfere with viral replication

A

INTERFERON

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36
Q

Prevent viruses to reach target cells

A

INTERFERON

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37
Q

IFN-alpha Other name

A

Leukocyte IFN

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38
Q

IFN-beta Other name

A
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39
Q

IFN-gamma Other name

A
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40
Q

IFN-alpha Primary producers

A

Null Lymphocytes

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41
Q

IFN-beta Primary producers

A

Fibroblasts, Epithelial Cells, MACs (macrophages)

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42
Q

IFN-gamma Primary producers

A

T Helper 1 Cells (CD4), T
Cytotoxic Cells (CD8)

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43
Q

IFN-alpha IFN-beta IFN-gamma Function

A

Anti - Viral

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44
Q

Sensitive indicators of inflammatory response

A

ACUTE PHASE REACTANTS

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45
Q

Non-specific test for bacterial infection (comes w/ culture)

A

ACUTE PHASE REACTANTS

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46
Q

increase rapidly due to infection, injury, or trauma to the tissues

A

ACUTE PHASE REACTANTS

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47
Q

produced primarily by hepatocytes (liver parenchymal cells) within 12 to 24 hours in response to an increase in certain intercellular signaling polypeptides called cytokines

A

ACUTE PHASE REACTANTS

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48
Q

– can stimulate APR

A

IL-1 and hydrolytic enzymes

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49
Q

6-10 (fastest response time)

A

C-reactive protein

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50
Q

24

A

Serum amyloid A

Alpha1 - antitrypsin

Haptoglobin

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51
Q

23

A

Fibrinogen

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52
Q

48-72

A

Ceruloplasmin

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53
Q

49-72

A

Complement C3

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54
Q

(carrier protein)

A

Alpha1 - antitrypsin
Haptoglobin

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55
Q

(coagulation factor I)

A

Fibrinogen

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56
Q

0.5

A

C-reactive
protein

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57
Q

3.0

A

Serum
amyloid A

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58
Q

200-400

A

Alpha1 -
antitrypsin (carrier protein)

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59
Q

11-400

A

Fibrinogen (coagulation factor I)

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60
Q

11-400

A

Fibrinogen (coagulation factor I)

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61
Q

40-200

A

Haptoglobin (carrier protein)

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62
Q

20-40

A

Ceruloplasmin

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63
Q

60-140

A

Complement
C3

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64
Q

0.15.1.0

A

Mannose-binding protein

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65
Q

1000x

A

C-reactive
protein

Serum
amyloid A

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66
Q

2-5x

A

Alpha1 - antitrypsin (carrier protein)

Fibrinogen (coagulation factor I)

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67
Q

2-10x

A

Haptoglobin (carrier protein)

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68
Q

2x

A

Ceruloplasmin

Complement C3

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69
Q

Opsonization, Complement activation

A

C-reactive
protein

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70
Q

(enhancement of phagocytosis; opsonins coat Ag for easy phagocytic recognition

A

Opsonization

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71
Q

(leads to lysis)

A

Complement activation

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72
Q

Removal of cholesterol

A

Serum
amyloid A

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73
Q

Protease inhibitor

A

Alpha1 -
antitrypsin (carrier protein)

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74
Q

Clot formation

A

Fibrinogen (coagulation factor I)

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75
Q

Binds hemoglobin

A

Haptoglobin (carrier protein)

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76
Q

Binds copper and oxidizes iron

A

Ceruloplasmin

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77
Q

Opsonization, lysis

A

Complement
C3

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78
Q

Complement activation

A

Mannose-binding protein

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79
Q

cell-eaters

A

phagocytes

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80
Q

Cells that engulf and digest foreign materials

A

phagocytes

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81
Q

Types of phagocytes

A

1.Neutrophils (Polymorphonuclear neutrophils)
2.Monocytes
3.Macrophages
4.Dendritic Cells
5.Fixed Phagocytes

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82
Q

– best Ag-presenting cell

A

Dendritic cells

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83
Q

oEngulfs, kills, and process Ag
oPresents fragment to T and B cell
oB cell creates Ab for Ag
oT cell processes and destroys Ag

A

Dendritic cells

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84
Q

Localized

A

Fixed phagocytes

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85
Q

Histiocytes

A

Connective tissue

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86
Q

Alveolar MACs

A

Lungs

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87
Q

Kupffer Cells

A

Liver

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88
Q

Littoral Cells

A

Spleen

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89
Q

Mesangial Cells

A

Kidneys

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90
Q

Microglia

A

Nerve cells/brain

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91
Q

Osteoclasts

A

Bone

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92
Q

Synovial A Cells

A

Synovial fluid

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93
Q

Hof-Bauer Cells

A

Placenta

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94
Q

Langerhans Cells

A

Skin/dermis/epidermis

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95
Q

– from circulating blood to tissues

A

Diapedesis

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96
Q

– towards Ag due to a chemical messenger called CHEMOTAXIN

A

Chemotaxis

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97
Q

Indirect interaction:
Direct interaction:

A

Opsonization

Pattern Recognition Receptors (PRRS)

98
Q

– enhancement of phagocytosis (C3b, IgG1 and IgG3)

A

Opsonization

99
Q

– phagocytes use their PRRS to recognize and adhere to Pathogen Associated Molecular Patterns (PAMPS)

A

Pattern Recognition Receptors (PRRS)

100
Q

(Attachment and Recognition)

A
  1. Adhesion
101
Q

(Engulfment)

A
  1. Ingestion
102
Q

Vacuole + Pathogen = (?) (Ag inside the phagocyte)

A

PHAGOSOME

103
Q

Occurs in the Phagolysosomes

A
  1. Digestion or Killing
104
Q

Phagosome + Granules = (?) (granules released)

A

PHAGOLYSOSOME

105
Q

Modes of killing:

A

oNitric Oxide
oOxygen Independent Mechanism
oOxygen Dependent Mechanisms

106
Q

aka respiratory burst – consumption oxygen followed by release of toxic products

A

oOxygen Dependent Mechanisms

107
Q

1.Toxic Reactive Oxygen Intermediates

A

Superoxide anion
Hydrogen peroxide
Hydroxyl Radical

108
Q

MProduces Hypochlorite (bleach), highly toxic substance

A

2.Myeloperoxidase

109
Q

: antibiotic like peptides made by Phagocytes

A

Defensins

110
Q

Digestive enzymes:

A

Lysozymes and Lactoferrin

111
Q

1.Large granular lymphocytes (LGL)

A

NATURAL KILLER CELLS

112
Q

2.Nonspecific immunity
Exist in the body at birth
Not produced by immunologic insult – can act w/o a stimulus

A

NATURAL KILLER CELLS

113
Q

3.ADCC (Antibiotic Dependent Cellular Cytotoxicity)

A

NATURAL KILLER CELLS

114
Q

4.Non-phagocytic

A

NK

115
Q

5.Form rosette in sheep RBC
oSmall flower/small rose

A

NK cell

116
Q
  1. oSurface marker – identity of different cells
    oCluster of differentiation
A

CD 56, CD16

117
Q

: NK cell exposed to IL-2 and IFN gamma

A

Lymphokine Activated Cell (LAK)

118
Q

8.Method of killing

A

Perforinsm
Apoptosism
Granzymes

119
Q

9.Target
Tumor cells – immortal cells
Virally infected cells – more effective killing if exposed to IFN-gamma
Transplant tissue (grafted cells and allogenic cells)

A
120
Q

NK needs low conc of (?) to act against an Ag

A

IgG

121
Q

– identity of different cells

A

oSurface marker

122
Q

o– T cell growth factor; strengthen cytotoxic activity of NK cells

A

IL-2

123
Q

o – interfere w/ viruses

A

IFN gamma

124
Q

(formation of pores causing lysis: ECF enters the cell or Ag → lyse/burst)

A

Perforins

125
Q

(programmed cell death)

A

Apoptosis

126
Q

(serine proteases that induces cell death)

A

Granzymes

127
Q

Overall reaction of the body to injury or invasion by an infectious agent

A

INFLAMMATION

128
Q

5 cardinal signs of inflammation:

A

oRubor – REDNESS
oCalor – HEAT
oTumor – SWELLING
oDolor – PAIN
oFunctio Laesa – LOSS OF FUNCTION

129
Q

Stages of inflammation:

A

1.Vascular response

2.Cellular response

130
Q

From injured cells

A

1.Vascular response

131
Q

Mast cells release histamine (recruit WBCs to areas w/ inflammation) and prostaglandin (recruit platelets during bleeding) which promotes vasodilation to promote:

A

a.Increased blood flow calor and rubor
b.Increased capillary permeability
c.Plasma leakage to tissue causing (tumor and dolor)

132
Q

2.Cellular response
1st Neutrophils –
2nd Monocytes and MACs –

A

acute inflammation

chronic inflammation

133
Q

oAPC
oIL-1
oPromote inflammatory response
ocauses fever
oincrease APR
ostimulate T cells to produce IL-2 for lymphocyte proliferation

A

Monocytes and MACs

134
Q

Directly killing infected host cells

A

1.T Lymphocytes

135
Q

Activating other immune cells, producing cytokines and regulating the immunes response

A

1.T Lymphocytes

136
Q

With surface receptors (like NK cells) – used to attach to Ags/immunogen

A

1.T Lymphocytes

137
Q

Participate in T cell activation

A

2.B Lymphocytes

138
Q

Bind to Ab via Ag-presentation

A

2.B Lymphocytes

139
Q

Needs Ag-presenting cell and T cell in order to be stimulated

A

2.B Lymphocytes

140
Q

Co-stimulation and cytokine production

A

2.B Lymphocytes

141
Q

Affects anti-microbial defenses and tissue inflammation

A

2.B Lymphocytes

142
Q

Serves as regulator cells that will modulate both cellular and humoral response

A

2.B Lymphocytes

143
Q

Major cells involed in humoral-mediated immunity

A

2.B Lymphocytes

144
Q

Capable of producing an Ab

A

3.Plasma cells

145
Q

Ab-producing B cell – has encountered an Ag that further matured to produce an Ab

A

3.Plasma cells

146
Q

Major humoral component

A

1.Antibodies

147
Q

THIRD LINE OF DEFENSE

CELLULAR COMPONENTS

HUMORAL COMPONENTS

A

T cell
B cell
Plasma cell

Abs
Cytokines

148
Q

Antibody mediated (noncellular)

A

Humoral-Mediated Immunity

149
Q

Cell mediated

A

Cell-Mediated Immunity

150
Q

B lymphocyte (able to interact w/ Ag and further matures into a plasma cell to produce Ab)

A

Humoral-Mediated Immunity

151
Q

T lymphocyte

A

Cell-Mediated Immunity

152
Q

Antibodies in serum

A

Humoral-Mediated Immunity

153
Q

Direct cell-to-cell contact or soluble products secreted (has corresponding receptors to bind to an antigen → stimulates reaction for B cells to go to the area → secretion of soluble products like Ab and cytokines)

A

Cell-Mediated Immunity

154
Q

Primary defense against bacterial infection

A

Humoral-Mediated Immunity

155
Q

Defense against viral and fungal infections, intracellular organisms, tumor antigens, and graft rejections (transplanted tissues or cells)

A

Cell-Mediated Immunity

156
Q

Extracellular microbes (acting on bacteria: can exist w/o a host cell)

A

Humoral-Mediated Immunity

157
Q

B lymphocyte (able to bind to EM)

A

Humoral-Mediated Immunity

158
Q

Secreted antibody

A

Humoral-Mediated Immunity

159
Q

Block infections and eliminate extracellular microbes

A

Humoral-Mediated Immunity

160
Q

Phagocytosed microbes in macrophage (will get a fragment from the phagocytosed Ag → present to B and T cell)

A

Cell-Mediated Immunity

161
Q

Intracellular microbes (e.g. viruses: requires host cell) replicating within infected cell

A

Cell-Mediated Immunity

162
Q

Helper T lymphocyte (has particular receptors to bind w/ PM in the macrophage)

A

Cell-Mediated Immunity

163
Q

Cytotoxic T lymphocyte

A

Cell-Mediated Immunity

164
Q

Activates macrophages to kill phagocytosed microbes

A

Cell-Mediated Immunity

165
Q

Kill infected cells and eliminate reservoirs of infection

A

Cell-Mediated Immunity

166
Q

Host: responsible for producing

A

Active Immunity

167
Q

Nonself: immunity is derived from the immune response another source’s Abs and are passively transferred to the host

A

Passive Immunity

168
Q

Ag (production of own Ab)

A

Active Immunity

169
Q

Ig, anti-sera

A

Passive Immunity

170
Q

Longer/Lifelong (Ex. Past exposure to chicken pox creates immunity)

A

Active Immunity

171
Q

Transient/Temporary (Ex. Booster dose)

A

Passive Immunity

172
Q

Less effective for Newborns (IS is not yet developed; rely on Abs from the mother; 0-3 mos old – fever can induce death)

A

Active Immunity

173
Q

More effective for newborns

A

Passive Immunity

174
Q

Effective in adults

A

Active Immunity

175
Q

Less effective in adults

A

Passive Immunity

176
Q

More prophylactic (prevention and protection)

A

Active Immunity

177
Q

More therapeutic or prophylactic (treatment)

A

Passive Immunity

178
Q

: experience infection (Ex. Past exposure to chicken pox creates immunity)

A

Natural Active

179
Q

: serum sickness (created from the lab; Ex. Serum sickness – type of allergic reaction leading to urticaria)

A

Artificial passive

180
Q

Long term immunity

A

Active Immunity

181
Q

Immediate reaction and protection

A

Passive Immunity

182
Q

Slow because Ag is detected then Ab is produced

A

Active Immunity

183
Q

Short term immunity

A

Passive Immunity

184
Q

Macromolecules that is capable triggering an adoptive immune response by inducing formation of antibodies or sensitized T cells of an immunocompetent host

A

Immunogen

185
Q

Substances that reacts with antibody or sensitized T cells but may not evoke an immune response

A

Antigen

186
Q

Is a foreign substance usually protein and polysaccharide

A

Antigen

187
Q

Triggers a specific immune response and induces the formation of a specific antibody or T cells response or both

A

Antigen

188
Q

Combines with an antibody

A

Antigen

189
Q

Active regions of an immunogen (that binds to antigen-specific receptors on lymphocytes or to secreted antibodies.

A

EPITOPE (antigenic determinant)

190
Q

Binds either on T-cell receptor and Antibodies

A

EPITOPE (antigenic determinant)

191
Q

Determinant site which are recognized by T cells or B cells

A

EPITOPE (antigenic determinant)

192
Q

The ability of antigen to react specifically with a free Ab or membrane coupled antibody (B Cell Receptor)

A

Antigenicity

193
Q

oSurface markers of B cells are Abs instead of CDs

A

Antigenicity

194
Q

The ability to induce a humoral or cell mediated immune response

A

Immunogenicity

195
Q

A specific protein that is produced in response to an immunogen and reacts with an antigen

A

Antibody (Ab)

196
Q

A substance that is non-immunogenic
oImmunogenic if a complete Ag
oAntigenetic but no immunogenic

A

HAPTEN

197
Q

But it can react with the products of a specific immune response with no Antibodies formation.

A

HAPTEN

198
Q

Non Protein and Low Molecular Weight (Less than 10,000) that could never induce an immune response when administered by themselves unless it coupled to a carrier molecule.

A

HAPTEN

199
Q

Has the property of antigenicity but not immunogenicity

A

HAPTEN

200
Q

FACTORS INFLUENCING IMMUNOGENECITY

A

Foreignness
Size
Chemical Composition and Complexity
Route dosage and timing
Adjuvants

201
Q

the more different the composition, the greater the response

A

Foreignness

202
Q

: derived from the same individual
: derived from the same species
: derived from different species (gives increased response)
: ag found in unrelated plants and animals, crossreact with Ab of another

A

Autoantigen

Alloantigen

Heteroantigen

Heterophile antigens

203
Q

oDonor:

A

alloantigen

204
Q

oPig heart:

A

heteroantigen

205
Q

The larger the (?), the more the immune response

A

MW

206
Q

Potent Ag :

A

> 10,000 Daltons

207
Q

Good immunogen

A

oAlbumin: 40, 000 D

208
Q

Excellent immunogen

A

oHemocyanin: 1M Daltons

209
Q

Chemical Composition and Complexity
Most immunogenic=
2nd:
Non immunogenic:

A

protein

Polysaccharide

lipids and nucleic acids

210
Q

Microbes:

A

Capsules, cell walls, toxins, viral capsids, flagella, etc.

211
Q

Nonmicrobes:

A

Pollen, egg white, red blood cell surface molecules, serum proteins, and surface molecules from transplanted tissue.

212
Q

are the most effective

A

Intravenous and intraperitoneal

213
Q

are stronger stimulus than subcutaneous or intramascular

A

Intradermal

214
Q

Smaller the (?), the less response

A

dose

215
Q

Substance added to vaccine and less immunogenic molecules (Hapten) to increase the immune response

A

Adjuvants

216
Q

Adjuvants Function:

A

oStimulate T cells : enhance cell mediated immunity
oStimulate B cells: enhance humoral response
oStimulate phagocytosis

217
Q

Adjuvants Examples:

A

oCFA: Complete Freund’s Adjuvant
oLPS: Lipopolysaccharide
oAlum adjuvant
oSqualene

218
Q

Water in oil emulsion of Mycobacterium/ Bordetella pertussis/MTB
Toxic to humans
Used for animal trial (mouse, guinea pigs)

A

CFA: Complete Freund’s Adjuvant

219
Q

Stimulate B cells

A

LPS: Lipopolysaccharide

220
Q

Stimulate phagocytosis
Used in human vaccines

A

Alum adjuvant

221
Q

From shark oil, for HIV vaccine

A

Squalene

222
Q

 are antigens which can directly stimulate the B cells to produce antibody without the requirement for T cell help.

A

T-independent antigens

223
Q

In general, polysaccharides are

A

T-independent antigens

224
Q

T-independent antigens Examples

A

oPneumococcal polysaccharide, lipopolysaccharide
oFlagella

225
Q

 are those that do not directly stimulate the production of antibody without the help of T cells.

A

T-dependent antigens

226
Q

Proteins are

A

T-dependent antigens

227
Q

T-dependent antigens Examples

A

oMicrobial proteins

228
Q

Typically polysaccharides with the ability to induce B-cell proliferation and antibody secretion in the absence of T cells

A

T-independent antigen

229
Q

An immunogen that requires T cell cooperation with B cells to synthesize specific antibodies

A

T-dependent antigen

230
Q

Do not require the help of T cells for the activation of B cells

A

T-independent antigen

231
Q

Require the help of T cells for the activation of B cells

A

T-dependent antigen

232
Q

Examples: Polymeric molecules with repeated antigenic determinants such as polysaccharides

A

T-independent antigen

233
Q

Examples: Protein antigens

A

T-dependent antigen

234
Q

Multivalent (higher chance to bind w/ B cell w/o T cell)

A

T-independent antigen

235
Q

Monovalent (only 1 epitope)

A

T-dependent antigen

236
Q

Slower and take several days to initiate a response

A

T-independent antigen

237
Q

Fast and require 1-2 days

A

T-dependent antigen

238
Q

React with all Ig isotypes

A

T-independent antigen

239
Q

React predominantly with IgM

A

T-dependent antigen

240
Q

Do not produce long-lasting antibody titers

A

T-independent antigen

241
Q

Produce long lasting serum antibody titer

A

T-dependent antigen