[DISCUSSION] MODULE 2 UNIT 1 Flashcards

1
Q

Innate immunity

A

NATURAL IMMUNITY

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2
Q

Ability of the individual to resist infection

A

NATURAL IMMUNITY

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3
Q

Normally present body functions

A

Ability of the individual to resist infection

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4
Q

NATURAL IMMUNITY is Considered:

A

• Non adaptive
• Nonspecific

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5
Q

Same for all pathogens or foreign substances

A

NATURAL IMMUNITY

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6
Q

• No prior exposure is required

A

NATURAL IMMUNITY

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7
Q

• No prior exposure is required
• Response does not change = same magnitude every time

A
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8
Q

NATURAL IMMUNITY CHARACTERISTICS:

A
  1. Components are preformed
  2. Standardized
  3. Without memory
  4. Nonspecific
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9
Q

NATURAL DEFENSE SYSTEM
• TWO PARTS:

A

• External defense system
• Internal defense system

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10
Q

EXTERNAL DEFENSE SYSTEM
• Composed of:

A
  1. Anatomic barriers
  2. Physiologic barriers
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11
Q

• Prevent most infectious agents from entering the body

A

Anatomic barriers

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12
Q

Anatomic barriers Examples:

A

• Intact skin
• Mucous membranes

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13
Q

Physiologic barriers

A

• Temperature
• Low pH
• Physiologic functions → coughing, sneezing, vomiting, diarrhea,
shedding of cells
• Oxygen tension
• Age
• Hormonal balance
• Chemical mediators → lysozyme, interferon, complement, toll-like
receptors, collectins

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14
Q

Physiologic functions

A

coughing, sneezing, vomiting, diarrhea,
shedding of cells

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15
Q

Chemical mediators

A

lysozyme, interferon, complement, toll-like
receptors, collectins

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16
Q

• Cleaves bacterial cell wall

A

• Lysozyme

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17
Q

• Induces antiviral state in uninfected cells

A

• Interferon

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18
Q

• Lyses microorganisms or facilitates phagocytosis

A

• Complement

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19
Q

• Recognize microbial molecules

A

• Toll-like receptors

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20
Q

• Signal cell to secrete immunostimulatory cytokines

A

• Toll-like receptors

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21
Q

→ disrupt cell wall of pathogen

A

• Collectins

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22
Q

• Second line of defense

A

INTERNAL DEFENSE SYSTEM

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23
Q

• Cells and soluble factors

A

INTERNAL DEFENSE SYSTEM

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24
Q

• Designed to recognize molecules that are unique to
infectious organisms

A

INTERNAL DEFENSE SYSTEM

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25
Q

• Phagocytosis

A

INTERNAL DEFENSE SYSTEM: Second line of defense

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26
Q

INTERNAL DEFENSE SYSTEM
Designed to recognize molecules that are unique to
infectious organisms

A

mannose found in microorganisms

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27
Q

enhanced by soluble factors called acute phase reactants

A

Phagocytosis

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28
Q

• Ability to recognize a given class of molecules

A

PATTERN RECOGNITION

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29
Q

• Ability to immediately recognize and combat invaders displaying such molecules is a strong feature of innate immunity

A

PATTERN RECOGNITION

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30
Q

Molecules with pattern recognition

A

PATTERN RECOGNITION

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31
Q

bind PAMPs

A

PRRs

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32
Q

• Molecules with pattern recognition
• May be soluble

A

complement, lysozyme

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33
Q

• Molecules with pattern recognition
• Cell-associated receptors

A

toll-like receptors (TLR’s)

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34
Q

• normal serum constituents

A

ACUTE PHASE REACTANTS

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35
Q

• increase rapidly by at least 25% due to infection, injury, or trauma to the tissues

A

ACUTE PHASE REACTANTS

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36
Q

• produced primarily by hepatocytes (liver parenchymal
cells)

A

ACUTE PHASE REACTANTS

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37
Q

• within 12 to 24 hours

A

ACUTE PHASE REACTANTS

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38
Q

• within 12 to 24 hours
• in response to an increase in certain intercellular signaling polypeptides called

A

cytokines

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39
Q

cytokines

A

IL-1β, IL-6, TNF-α

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40
Q

• most abundant of the coagulation factors in plasma

A

Fibrinogen

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41
Q

• forms the fibrin clot

A

Fibrinogen

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42
Q

• dimer with a molecular weight of 340,000 daltons

A

Fibrinogen

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43
Q

Fibrinogen Normal levels range from

A

100 to 400 mg/dL

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44
Q

• Promote healing process

A

Fibrinogen

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45
Q

• Prevents spread of microorganisms

A

Fibrinogen

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46
Q

• alpha2
-globulin with a molecular weight of 100,000 daltons

A

Haptoglobin

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47
Q

• bind irreversibly to free hemoglobin released by intravascular hemolysis

A

Haptoglobin

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48
Q

Preventing loss of free hemoglobin

A

Haptoglobin bind irreversibly to free hemoglobin released by intravascular
hemolysis

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49
Q

Haptoglobin
• Normal plasma concentrations range from

A

40 to 290 mg/dL

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50
Q

Haptoglobin plays an important role in:

A

• protecting the kidney from damage
• preventing the loss of iron by urinary excretion

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51
Q

Haptoglobin Most important function

A

to provide protection against oxidative
damage mediated by free hemoglobin

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52
Q

• single polypeptide chain with a MW of 132,000 daltons

A

Ceruloplasmin

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53
Q

• Principal copper transporting protein

A

Ceruloplasmin

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54
Q

• Essential to collagen formation & the extracellular cross-linking and
maturation of collagen and elastin

A

Ceruloplasmin

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55
Q

• Protect the matrix of healing tissue against superoxide ions

A

Ceruloplasmin

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56
Q

• Protease inhibitor

A

Alpha-2-macroglobulin

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57
Q

• Binds to proteolytic enzymes released from damaged tissues and
from phagocytic cells

A

Alpha-2-macroglobulin

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58
Q

• Scavenger protease inhibitor that binds excess molecules that
cannot be handled by the intended inhibitor

A

Alpha-2-macroglobulin

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59
Q

• homogeneous molecule with a MWof 118,000 daltons

A

C-Reactive protein (CRP)

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60
Q

• increases rapidly within 4 to 6 hours following infection, surgery, or
other trauma to the body

A

C-Reactive protein (CRP)

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61
Q

C-reactive protein (CRP)
• Capable of:

A
  1. Opsonization
  2. Agglutination
  3. Precipitation
  4. Activation of complement by the classical pathway
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62
Q

• Apolipoprotein synthesized in the liver (30mg/ml)

A

Serum amyloid A

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63
Q

• Precursor to amyloid deposition

A

Serum amyloid A

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64
Q

• Reported to cause adhesion and chemotaxis of phagocytic cells and
lymphocytes

A

Serum amyloid A

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65
Q

• Bind to lysosomal enzymes released during inflammation

A

Serum amyloid A

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66
Q

• Increased levels found to be a risk factor for heart attack in women

A

Serum amyloid A

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67
Q

• Can increase almost 1000-fold

A

Serum amyloid A

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68
Q

• Serum proteins that are normally present

A

Complement

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69
Q

• Mediation of inflammation

A

Complement

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70
Q

Complement Major functions:

A
  1. Opsonization
  2. Chemotaxis
  3. Lysis of cells
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71
Q

Trimer that acts as an opsonin that is Ca-dependent

A

Mannose-binding protein

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72
Q

Recognize foreign carbohydrates such as mannose and a number of
sugars

A

Mannose-binding protein

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73
Q

Mannose-binding protein
Recognize foreign carbohydrates such as mannose and a number of
sugars present in:

A

• Bacteria
• Some yeasts
• Viruses
• Several parasites

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74
Q

• Widely distributed in mucosal surfaces throughout the body

A

Mannose-binding protein

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75
Q

• Binding activates complement cascade and helps to promote phagocytosis

A

Mannose-binding protein

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76
Q

• High carbohydrate content and MW 44 kD

A

Alpha-1 acid glycoprotein

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77
Q

• Exact function not known

A

Alpha-1 acid glycoprotein

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78
Q

• Binds progesterone and may be important in its transport or metabolism

A

Alpha-1 acid glycoprotein

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79
Q

• Able to bind drugs such as lidocaine, keeping them in an inactive
circulating pool

A

Alpha-1 acid glycoprotein

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80
Q

CELLULAR DEFENSE MECHANISMS

A

• Neutrophils
• Eosinophils
• Basophils
• Mast cells
• Monocytes
• Tissue macrophages
• Dendritic cells

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81
Q

• Polymorphonuclear neutrophilic leukocyte (PMN)

A

NEUTROPHILS

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82
Q

• 50 – 70% of the total peripheral wbcs

A

NEUTROPHILS

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83
Q

• Diameter: 10 – 15 mm

A

NEUTROPHILS

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84
Q

• Nucleus: 2-5 segments

A

NEUTROPHILS

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85
Q

• Large number of neutral staining granules

A

NEUTROPHILS

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86
Q

NEUTROPHILS granules

A

• Primary granules
• Secondary granules

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87
Q

NEUTROPHILS
Primary granules (azurophilic) contain:

A

• Myeloperoxidase
• Lysozyme
• Proteinase 3
• Elastase
• Cathepsin G
• Lysosomal acid hydrolases
• Defensins

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88
Q

Small proteins that have antibacterial activity

A

Defensins

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89
Q

NEUTROPHILS
Secondary (specific) granules contain:

A

• Collagenase
• Lysozyme
• Lactoferrin
• Reduced NADPH oxidase
• Alkaline phosphatase

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90
Q

NEUTROPHILS
Tertiary granules contain:

A

gelatinase & plasminogen
activators

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91
Q

• Normally, half of the total neutrophil population is found in
a marginating pool on the walls of blood vessels

A

NEUTROPHILS

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92
Q

• The rest circulate freely for approx. 6 – 10 hours

A

NEUTROPHILS

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93
Q

• Capable of moving from the circulating blood to the
tissues

A

NEUTROPHILS

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94
Q

movement through blood vessel walls

A

DIAPEDESIS→

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95
Q

• Margination & adherence to the vessel wall

A

DIAPEDESIS

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96
Q

• Formation of pseudopods, squeeze through junctions of the endothelial
cells

A

DIAPEDESIS

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97
Q

• Wander randomly through the tissue or be attracted to a specific area by
chemotactic factors

A

DIAPEDESIS

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98
Q

chemical messengers that cause migration
of cells in a particular direction

A

Chemotaxins

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99
Q

Chemotaxins

A

5 days

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100
Q

Once in tissues, neutrophils’ life span: about

A

5 days

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101
Q

Once in tissues, neutrophils’ life span: about 5 days

A
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102
Q

12 to 16 mm

A

EOSINOPHILS

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103
Q

1 – 3%

A

EOSINOPHILS

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104
Q

EOSINOPHILS Numbers increased during:

A

• Allergic reaction
• Response to many parasitic infections

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105
Q

Eosinophils Nucleus

A

• Bilobed or ellipsoidal
• Eccentrically located

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106
Q

• Take up the acid eosin dye

A

EOSINOPHILS

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107
Q

Cytoplasm is filled with large orange to reddish-orange
granules

A

EOSINOPHILS

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108
Q

EOSINOPHILS granules

A

• Acid phosphatase
• b-glucuronidase
• Arylsulfatase
• Phospholipase
• Peroxidase
• Histaminase
• Aminopeptidase
• Ribonuclease

109
Q

Capable of phagocytosis but much less efficient than
neutrophils

A

EOSINOPHILS

110
Q

EOSINOPHIL phagocytosis

A

• Smaller numbers
• Lack of digestive enzymes

111
Q

EOSINOPHILS MOST IMPORTANT ROLE:

A

• Neutralizing basophil and mast cell products
• Killing of certain parasites

112
Q

ADCC

A

Eosinophils

113
Q

• Less than 1% of all circulating wbcs

A

BASOPHILS

114
Q

• Smallest of the granulocytes

A

BASOPHILS

115
Q

• 10 to 14 mm in diameter

A

BASOPHILS

116
Q

• Contain coarse densely staining deep bluish purple
granules that often obscure the nucleus

A

BASOPHILS

117
Q

• Constituents of granules: histamine, eosinophil
chemotactic factor of anaphylaxis (ECF-A), and a small
amount of heparin

A

BASOPHILS

118
Q

• Induce and maintain immediate hypersensitivity
reactions

A

BASOPHILS

119
Q

BASOPHILS

vasoactive amine that contracts smooth
muscle

A

HISTAMINE

120
Q

BASOPHILS anticoagulant

A

HEPARIN

121
Q

stream• Granules: lack hydrolytic enzymes although peroxidase
is present

A

BASOPHILS

122
Q

• Capable of phagocytosis

A

BASOPHILS

123
Q

• Only present for a few hours in the blood

A

BASOPHILS

124
Q

• Resemble basophils

A

MAST CELLS

125
Q

• May share a common stem cell precursor

A

MAST CELLS

126
Q

• Larger with a small round nucleus and more granules
than the basophil

A

MAST CELLS

127
Q

• Found in connective tissue, especially around blood and
lymphatic vessels

A

MAST CELLS

128
Q

• Long life span

A

MAST CELLS

129
Q

• May be capable of proliferation in the tissues

A

MAST CELLS

130
Q

• The enzyme content of the granules distinguish them from
basophils because they contain acid phosphatase,
alkaline phosphatase, protease & serotonin

A

MAST CELLS

131
Q

• Play a role in hypersensitivity reactions

A

MAST CELLS

132
Q

• Largest cells in the peripheral blood

A

MONOCYTES

133
Q

• Diameter: 12 to 22 mm, ave. 18 mm

A

MONOCYTES

134
Q

• Irregularly folded or horseshoe-shaped nucleus occupying
almost ½ of the entire cell’s volume

A

MONOCYTES

135
Q

• Abundant cytoplasm stains a
dull grayish-blue with a ground
glass appearance
(fine granules)

A

MONOCYTES

136
Q

One type of granules contain peroxidase, ACP,
arylsulfatase (similar to neutrophils)

A

MONOCYTES

137
Q

• Other type of granules contain b-glucuronidase,
lysozyme, lipase, but NO alkaline phosphatase

A

MONOCYTES

138
Q

• Make up 4 to 10% of total circulating wbc

A

MONOCYTES

139
Q

• Stay in the peripheral blood for up to 70 hours then
migrate to the tissue and become macrophages

A

MONOCYTES

140
Q

• All tissue macrophages arise from monocytes

A

TISSUE MACROPHAGES

141
Q

• Transition from monocyte to macrophage is characterized
by progressive cellular enlargement to between 25 and 50
mm

A

TISSUE MACROPHAGES

142
Q

• Increase in ER, lysosomes, & mitochondria

A

TISSUE MACROPHAGES

143
Q

• Unlike monocytes, macrophages contain NO
PEROXIDASE AT ALL

A

TISSUE MACROPHAGES

144
Q

Lung

A

Alveolar macrophages

145
Q

Liver

A

Kupffer cells

146
Q

Brain

A

Microglial cells

147
Q

Connective tissue

A

Histiocytes

148
Q

Kidney

A

Mesangial cells

149
Q

Bone

A

Osteoclast

150
Q

Spleen

A

Littoral cells

151
Q

Joints

A

Synovial A cells

152
Q

• Life span: months

A

TISSUE MACROPHAGES

153
Q

TISSUE MACROPHAGES Role →

A

initiating and regulating IR

154
Q

TISSUE MACROPHAGES Functions:

A
  1. Microbial killing
  2. Tumoricidal activity
  3. Killing of intracellular parasites
  4. Phagocytosis
  5. Secretion of cell mediators
  6. Antigen presentation
155
Q

• Covered with long membranous extensions making them
resemble nerve cell dendrites

A

DENDRITIC CELLS

156
Q

DENDRITIC CELLS Main function:

A

• Phagocytose antigen and present it to helper T lymphocytes
• Believed to be descendants of the myeloid line
• Classified according to tissue location
• E.g., Langerhans’ cells → skin and mucous

157
Q

DENDRITIC CELLS
skin and mucous membranes

A

Langerhans’ cells

158
Q

▪Interstitial dendritic cells

A

heart, lungs, kidney, GIT

159
Q

Toxins released via phagocytosis

A

Leukocidin
Listeriolysin
Streptolysin

160
Q

M. bacterium leptae and MBT contains this material that does not fuse with lysosome

A

Pristiophorus vacuole

161
Q

Catalase

A

Staphylococcus aureus

162
Q

▪Interdigitating dendritic cells

A

T lymphocyte areas
of the secondary lymphoid tissue and the thymus

163
Q

▪After capturing Ag in the tissue by
phagocytosis or endocytosis,

A

they
migrate to the blood or the lymphoid
organs & present Ag

164
Q

▪Most potent phagocytic cell in the tissue

A

DENDRITIC CELLS

165
Q

also known as large granular lymphocytes (LGL)

A

NK (Natural Killer) Cells

166
Q

identified by the presence of CD56 and CD16 and a lack of CD3
cell surface markers

A

NK (Natural Killer) Cells

167
Q

capable of killing virus-infected and malignant target cells

A

NK (Natural Killer) Cells

168
Q

upon exposure to IL-2 and IFN-gamma, NK cells become
lymphokine-activated killer (LAK) cells

A

NK (Natural Killer) Cells

169
Q

capable of killing malignant cells

A

lymphokine-activated killer (LAK) cells

170
Q

not a morphologically distinct type of cell

A

K (Killer cells)

171
Q

• any cell that mediates antibody-dependent cellular cytotoxicity (ADCC)

A

K (Killer cells)

172
Q

• have on their surface an Fc receptor for antibody and thus they can
recognize, bind and kill target cells coated with antibody

A

K (Killer cells)

173
Q

Killer cells which have Fc receptors include (?) which have an Fc receptor for IgG antibodies and
eosinophils which have an Fc receptor for IgE antibodies

A

NK, LAK, and macrophages

174
Q

Additional mechanism recently discovered on certain cells,
enhancing natural immunity

A

TOLL-LIKE RECEPTORS (TLRs)

175
Q

→ a protein originally discovered in the fruit fly

A

Toll

176
Q

Highest concentration occurs on monocytes, macrophages
and neutrophils

A

TOLL-LIKE RECEPTORS (TLRs)

177
Q

→ recognizes techoic acid and peptidoglycan in g+ bacteria

A

TLR2

178
Q

→ recognizes LPS

A

TLR4

179
Q

Monocytes, macrophages, endothelial cells, epithelial cells

A

Interleukin 1 (IL-1)

180
Q

Vasculature (inflammation); hypothalamus (fever); liver (induction of acute phase proteins)

A

Interleukin 1 (IL-1)

181
Q

Macrophages

A

Tumor Necrosis Factor-alpha (TNF-alpha) & Interferon alpha (IFN-alpha)

182
Q

Vasculature (inflammation); liver (induction of acute phase proteins); loss of muscle, body fat (cachexia); induction of death in many cell types; neutrophil activation

A

Tumor Necrosis Factor-alpha (TNF-alpha)

183
Q

Macrophages, dendritic cells

A

Interleukin 12 (IL-12)

184
Q

NK cells; influences adaptive inmmunity (promotes TH1 subset)

A

Interleukin 12 (IL-12)

185
Q

Macrophages, endothelial cells

A

Interleukin 6 (IL-6)

186
Q

Liver (induces acute phase proteins); influences adaptive immunity (proliferation and antibody secretion of B cell lineage

A

Interleukin 6 (IL-6)

187
Q

This is a family of molecules

A

Interferon alpha (IFN-alpha)

188
Q

Induces an antiviral state in most nucleated cells; increases MHC class I expression; activates NK cells

A

Interferon alpha (IFN-alpha) & Interferon beta (IFN-beta)

189
Q

Fibroblasts

A

Interferon beta (IFN-beta)

190
Q

Involves engulfment and destruction of pathogens and particulate matter by cells of the mononuclear phagocyte
system

A

PHAGOCYTOSIS

191
Q

Macrophages release monokines like (?)

A

IL-1, IL-6 and TNFa

192
Q

PHAGOCYTES:

A

• Fixed
• Wandering

193
Q

• CHARACTERISTICS OF PHAGOCYTIC PROCESS:

A
  1. AMOEBOID MOVEMENT
  2. CHEMOTAXIS
194
Q


Cell migration occurs in and out of blood vessels, and throughout the tissues

A

AMOEBOID MOVEMENT

195
Q

• Movement of cells or organisms toward objects in response to
chemical agents called CHEMOTAXINS

A

CHEMOTAXIS

196
Q

→ cell emigration from capillaries

A

Diapedesis

197
Q

modified a.a. present in the a.a. termini of proteins of most types of
bacteria

A

Microbial/ bacterial products: N-formylmethionine residues

198
Q

Attractants of phagocytes/chemotactic agents:

A

• Microbial/ bacterial products: N-formylmethionine residues
• Tissue components (leukotriene)
• Activated intermediates of the fibrinolysis, kallikrein, and
complement systems

199
Q

Once a particle is close enough to the target, the cells engulf it

A

PHAGOCYTOSIS

200
Q

STEPS IN PHAGOCYTOSIS

A
  1. Physical contact between the white cell and the foreign particle
  2. Formation of a phagosome
  3. Fusion with cytoplasmic granules to form a phagolysosome
  4. Digestion and release of debris to the outside
201
Q


Digestion of engulfed material inside the phagolysosome

A

CYTOPEPSIS

202
Q


Contents of the lysosome granules are important in breaking down
ingested material and in killing microorganisms

A

CYTOPEPSIS

203
Q

TWO MECHANISMS FOR DESTROYING FOREIGN PARTICLES

A
  1. Oxygen-independent mechanisms
  2. Oxygen-dependent mechanisms
204
Q

• Proteinases (hydrolytic enzymes)
• Cationic proteins
• Lysozyme
• Lactoferrin

A

OXYGEN INDEPENDENT MECHANISMS

205
Q

OXYGEN DEPENDENT MECHANISMS

A

• Myeloperoxidase
• Hydrogen peroxide (H2O2)
• Superoxide anion (O2– )

206
Q

→ toxic peroxidation of microorganisms

A

Myeloperoxidase

207
Q

→ oxygen in which one of the electrons has
moved to an orbit of higher energy

A

Singlet oxygen (‘O2
)

208
Q

→ a highly unstable oxidizing agent that
reacts with most organic molecules it encounters

A

Hydroxyl radical (OH–)

209
Q

increase in overall oxygen consumption by the neutrophil

A

RESPIRATORY BURST/ METABOLIC BURST

210
Q

• METABOLIC EVENTS DURING PHAGOCYTOSIS
• Accompanied by respiratory burst that involves the following:

A

1.
Increase in oxygen consumption
2.
Stimulation of HMP shunt activity
3.
Increase in production of hydrogen peroxide
4.
Superoxide anion production and singlet oxygen production

211
Q

→ extremely toxic to bacteria and tissue; very unstable; quickly converted to H2O2 by SOD → catalase

A

Superoxide anion

212
Q

The (?) combine and act synergistically

A

oxygen-dependent agents

213
Q

→ Hypochlorite

A

Myeloperoxidase + H2O2 + Halide (I- or Cl -)

214
Q

(?) is more antimicrobial than the three components alone

A

Hypochlorite

215
Q

LIMITATIONS OF PHAGOCYTOSIS

A
  1. Presence of capsules
  2. Opsonization inhibited
  3. Release of toxins
  4. Phagolysosome formation inhibited
  5. Able to escape into cytoplasm by lysing lysosomal
    membrane
  6. Resistance to killing by producing anti-oxidants
216
Q

PHAGOCYTOSIS
• IMPORTANCE:

A
  1. Destroy/ kill microorganisms
  2. Disposal of damaged and dying cells
  3. Suppression of the growth of spontaneously arising tumors
  4. Processing of antigens
  5. Removal of cancer cells
  6. Removal of debris from repairing wounds
  7. Removal of debris as embryonic tissues replace one another
217
Q

• Process of enhancing phagocytosis via the presence of opsonins

A

OPSONIZATION

218
Q

• Substances that promote phagocytosis

A

OPSONIZATION

219
Q

• OPSONINS:

A
  1. C3b split product of complement cascade
  2. C5a and C5b67 → chemotactic factors that also aid
    in the clearance of foreign materials
  3. Antibodies (phagocytes have a receptor for the Fc
    portion of IgG)
220
Q

→ chemotactic factors that also aid
in the clearance of foreign materials

A

C5a and C5b67

221
Q

Antibodies (phagocytes have a receptor for the Fc
portion of IgG)

A


IgG1 and IgG3

222
Q

→ gp that opsonizes & acts like glue to cause neutrophils and their targets to stick together

A

Fibronectin

223
Q

→ derivatives of arachidonic acid

A

Leukotrienes

224
Q

• Several kinds, not all act as opsonins

A

Leukotrienes

225
Q

• LTBy
is chemotactic

A

Leukotrienes

226
Q

→ tetrapeptide split product of IgG that stimulates chemotactic and phagocytic activities

A

Tuftsin

227
Q

• Complex series of non-specific soluble and cellular events

A

INFLAMMATION

228
Q

• Promotes elimination of the foreign entity

A

INFLAMMATION

229
Q

• Initiated by chemical mediators whenever phagocytosis
alone fails to prevent infection or when tissues are injured

A

INFLAMMATION

230
Q

INFLAMMATION Induced by:

A

pathogen attack, inert tissue injury, products of
complement activation, or by cytokines released by innate or
adaptive leukocytes that were activated elsewhere

231
Q

Five cardinal signs/clinical symptoms: (Celsus)

A
  1. Redness (rubor)
  2. Swelling (tumor)
  3. Heat (calor)
  4. Pain (dolor)
  5. Loss of function (functio laesa)(Galen)
232
Q

• Major Events associated with inflammation:

A
  1. Increased blood supply to the infected area
  2. Increased capillary permeability caused by retraction of
    endothelial cells lining the vessels
  3. Migration of white blood cells (mainly neutrophils) from the
    capillaries to the surrounding tissue
  4. Migration of macrophages to the injured area
233
Q

EVENTS OF INFLAMMATION

A
  • Histamine released from mast cells
  • Inreased permeability of the vessels
  • Soluble mediators
  • Amplification
  • Coagulation system and fibrinolytic system
234
Q

SIGNS OF INFLAMMATION

A
  • Redness and heat
  • Swelling and pain
235
Q

→ Cause dilation of the blood vessels & additional flow to affected area

A

Histamine released from mast cells

236
Q

→Fluids to leak out to the tissues

A

Inreased permeability of the vessels

237
Q

→Stimulation of the pain receptors (skin) by peptide mediators

A

Inreased permeability of the vessels

238
Q

initiate and control the response

A

Soluble mediators

239
Q

occurs through formation of clots

A

Amplification

240
Q

involvement

A

Coagulation system and fibrinolytic system

241
Q

→ vasodilation, increased vascular permeability, smooth muscle contraction, pain

A

Kinins (e.g., bradykinin)

242
Q

→ activates macrophages (from NK cells)

A

IFNg

243
Q

→ perpetuate the inflammatory
response

A

TNF, IL-1, IL-6

244
Q

→ from hepatocytes responding to TNF and IL-6; initiates complement cascade via C1 activation

A

CRP

245
Q

MEDIATORS OF INFLAMMATION

A
  1. Kinins (e.g., bradykinin)
  2. IFNg
  3. TNF, IL-1, IL-6
  4. CRP
  5. C3a & C5a → anaphylatoxin
  6. C3b
  7. Leukotrienes and prostaglandins
  8. Serotonin (5-hydroxytryptamine)
246
Q

→ provokes mast cell degranulation and consequent release of heparin and vasoactive amines (HISTAMINE) that induce
Vasodilation increases vascular permeability

A

C3a & C5a → anaphylatoxin

247
Q

opsonin

A

C3b

248
Q

→ increase vasodilation and promote neutrophil chemotaxis

A

Leukotrienes and prostaglandins

249
Q

→ vasodilation

A

Serotonin (5-hydroxytryptamine)

250
Q

• Neutrophils
• Macrophages

A

ACUTE INFLAMMATION

251
Q

• Mobilized within 30 to 60 minutes after the injury

A

Neutrophils

252
Q

• Neutrophil emigration lasts (?) hours

A

24 to 48

253
Q

• Proportional to the chemotactic factors present in the area

A

Neutrophils

254
Q

• Attempt to clear the area through phagocytosis

A

Macrophages

255
Q

• Most cases: healing process is completed with a return of normal
tissue structure

A

Macrophages

256
Q

Migration occurs several hours later and peaks at (?) hours

A

16 to 48

257
Q

• Prolonged inflammatory response

A

CHRONIC INFLAMMATION

258
Q

• Tissue damage and loss of function may result

A

CHRONIC INFLAMMATION

259
Q

• Often follows acute inflammation but can be the only inflammatory
response in certain viral infections and hypersensitivity reactions

A

CHRONIC INFLAMMATION

260
Q

• Characterized by infiltration of tissue with macrophages,
lymphocytes and plasma cells, or eosinophils

A

CHRONIC INFLAMMATION

261
Q

Infection: neutrophils. Macrophages
Allergy: eosinophils, mast cells

A

ACUTE

262
Q

Macrophages, lymphocytes

A

CHRONIC

263
Q

Complement, kinins, prostaglandins,
leukotrienes, acute phase cytokines,
chemokines

A

ACUTE

264
Q

Cytokines from macrophages and T cells

A

CHRONIC

265
Q

Rash, pus, abscess

A

ACUTE

266
Q

Rash, fibrosis, granuloma

A

CHRONIC

267
Q

Response to infection, hypersensitivity response

A

ACUTE

268
Q

Autoimmunity, response to intracellular bacterial infection

A

CHRONIC