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Z Old Infection IGNORE > Innate and Adaptive Immunity > Flashcards

Innate and Adaptive Immunity Flashcards

1
Q

When are the bodies basic defences active?

A

At all times

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2
Q

What are the kind of basic defences of the body?

A
  • Mechanical
  • Chemical
  • Microbiological
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3
Q

Where are the main points of defence in the body?

A
  • Skin
  • Gut
  • Lungs
  • Eyes/nose
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4
Q

What are the mechanical defences of the body?

A
  • Epithelial cells joined by tight junctions at the skin, gut, lungs and eyes/nose
  • Longitudinal flow of air or fluid in the skin and gut
  • Movement of mucus by cells in the lungs
  • Tears and nasal cilia in the eyes/nose
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5
Q

What are the chemical defences of the body?

A
  • Fatty acids in skin
  • Low pH and enzymes (including pepsin) in the gut
  • Enzymes (lysozymes) in tears
  • Antibacterial peptides in the skin, gut, and lungs
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6
Q

What are the microbiological defences of the body?

A

Normal flora in the skin and gut

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7
Q

What are the three most important basic defences in the body?

A
  1. Epithelia
  2. Antibacterial peptides
  3. Enzymes
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8
Q

What is innate immunity?

A

The body’s first line of immune protection to infection after physical barriers such as the skin have been broken

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9
Q

What are the characteristics of innate immunity?

A
  • Rapid
  • Pre-existing
  • Lacks specificity and memory
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10
Q

What does innate immunity act in response to?

A

Pathogen Associated Molecular Patterns (PAMPs)

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11
Q

Is adaptive immunity fixed?

A

No, it adapts to different challenges it faces

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12
Q

What are the characteristics of adaptive immunity?

A
  • Slow
  • Specific
  • Has memory
  • Increases in intensity with subsequent exposure
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13
Q

What are the types of immunity?

A
  • Cellular
  • Humoral
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14
Q

What cells are involved in innate cellular immunity?

A
  • Neutrophils (or polymorphs)
  • Macrophages
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15
Q

What are macrophages called when in the blood?

A

Monocytes

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16
Q

What do the cells of the innate cellular immune response do?

A

Phagocytose microbes in order to destroy them via intracellular killing

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17
Q

What is involved in innate humoral immunity?

A
  • Complement system
  • Cytokines
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18
Q

What does the complement system involve?

A

A cascade of serum proteins

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19
Q

What happens in the process of phagocytosis?

A
  1. Initially, the cells migrate to the area via a chemotactic gradient of molecules
  2. Phagocytes recognise their targets by binding to their PAMPs
  3. The pathogen is then internalised via phagocytosis, and the phagosomes is fused with a lysosome, where the killing of microbes takes place
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20
Q

What molecules from the chemotactic gradient that causes phagocytes to migrate to the required area?

A
  • C5a
  • Leukotrienes
  • IL-8
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21
Q

What releases the chemotactic molecules that cause phagocytes to migrate to the required area?

A

Damaged cells, or the dendritic cells of the area

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22
Q

How is recognition of targets by phagocytes enhanced?

A

If the microbe has been opsonised

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23
Q

How are microbes opsonised?

A

Via IgG or C3b

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24
Q

Why is target recognition by phagocytes enhanced when the microbe has been opsonised?

A

As phagocytes have Fc and C3b receptors

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25
Q

How does the killing of microbes by phagocytes take place?

A

Using oxygen dependant or oxygen independant processes

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26
Q

What are the oxygen dependant processes of microbial killing?

A

Producing ROS via NAPH oxidase

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27
Q

What are the oxygen independant processes of microbial killing?

A

Lysosomal enzymes

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28
Q

How do the innate immune cells recognise various classes of microbe?

A

By Pathogen-Associated-Molecular-Patterns (PAMPs)

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29
Q

What are PAMPs?

A

Structures that groups of pathogens share

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30
Q

What are receptors that recognise PAMPs known as?

A

Pattern Recognition Receptors (PRRs)

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31
Q

Give two examples of PRRs

A
  1. Toll-like receptors
  2. Mannose receptors
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32
Q

Give 6 examples of Toll-Like Receptors (TLRs)

A
  1. TLR2
  2. TLR3
  3. TLR4
  4. TLR5
  5. TLR7
  6. TLR8
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33
Q

What is the PAMP for TLR2?

A

Peptioglycan

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34
Q

What is the PAMP group for TLR2?

A

Gram positive bacteria

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35
Q

What is the PAMP for TLR3?

A

dsRNA

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36
Q

What is the PAMP group for TLR3?

A

Viruses

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37
Q

What is the PAMP for TLR4?

A

LPS

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38
Q

What is the PAMP group for TLR4?

A

Gram negative bacteria

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39
Q

What is the PAMP for TLR5?

A

Flagellin

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40
Q

What is the PAMP group for TLR5?

A

Bacteria

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41
Q

What is the PAMP for TLR7?

A

ssDNA

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42
Q

What is the PAMP group for TLR7?

A

Viruses

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43
Q

What is the PAMP for TLR9?

A

dsDNA

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44
Q

What is the PAMP group for TLR9?

A

Viruses

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45
Q

What happens after the PRRs have responded to the PAMPs?

A

They will then go on to stimulate further innate and adaptive immune responses

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46
Q

What is the clinical significance of TLR-4?

A

It is responsible for septic shock seen in septicaemia of Gram negative bacteria

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47
Q

What is the complement system made up of?

A

A large number of different plasma proteins that interact with one another

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48
Q

What do the plasma proteins in the complement system interact with each other to do?

A
  • Opsonise pathogens
  • Induce a series of inflammatory responses that help to fight infection
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49
Q

What does the interaction of plasma proteins in the complement system cumulate in?

A

The Membrane Attack Complex (MAC)

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50
Q

What is a crucial feature of the complement system?

A

Several complement proteins are proteases that become activated only after cleavage

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51
Q

What is the result of the complement system being a proteolytic cleavage cascade?

A

There is an amplification effect that produces a large number of the effector molecules

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52
Q

How many pathways of complement activation are there?

A

3

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53
Q

What do the pathways of complement activation result in?

A

The formation of C3 convertase

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54
Q

What does C3 covertase do?

A

Activates the rest of the complement pathway

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55
Q

What are the pathways of complement activation?

A
  1. Classical pathway
  2. Lectin pathway
  3. Alternate pathway
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56
Q

What happens in the classical pathway of complement activation?

A
  1. IgM or IgG antibodies bind to antigens on microbial cellular surfaces, to form antigen-antibody complexes
  2. C1 binds to 2 of their Fc regions Cleavage of C2 and C4
  3. C3 convertase formed
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57
Q

What happens in the lectin pathway of complement activation?

A
  1. Plasma mannose binds to lectin on microbes
  2. Cleave of C2 and C4
  3. C3 convertase formed
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58
Q

What happens in the alternate pathway of complement activation?

A
  1. Small amount of C3b in serum deposits on the microbe surface
  2. Microbe bound C3b binds to another protein to form C3 convertase
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59
Q

What happens to C3 convertase once formed?

A

It is covalently bonded to the pathogen surface Here, they cleave C3 to generate large amounts of C3b and C3a

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60
Q

What is C3a?

A

A peptide mediator of inflammation

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61
Q

What is C3b?

A

The main effector molecule of the complement system

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62
Q

What does C3b do?

A
  • Acts as an opsonin, targeting the pathogen for destruction by phagocytes with C3b receptors
  • Removal of immune complexes
  • Binds to C3 convertase to form C5 convertase
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63
Q

What does C5 convertase do?

A

Produces C5a and C5b

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64
Q

What is C5a?

A

A potent inflammatory peptide

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65
Q

What does C5b do?

A

Leads to formation of the membrane attack complex (MAC)

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66
Q

What are the terminal complement components?

A

C5b, C6, C7, C8, C9

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67
Q

What do the terminal complement components do?

A
  • Form MAC
  • Lysis of certain pathogens and cells
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68
Q

What is required for production of the terminal complement components?

A

C3b

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69
Q

What complement components are involved in phagocyte recruitment?

A

C3a, C5a

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70
Q

What cells are involved in adaptive cellular immunity?

A
  • B cells
  • T cells
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71
Q

What are the types of B cells?

A
  • Plasma
  • Memory
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72
Q

What cells are involved in adaptive humoral immunity?

A

Antibodies

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73
Q

What does adaptive immunity utilise?

A

The antigen recognition arm of the immune system

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74
Q

What does adaptive immunity have to be able to do to utilise the antigen recognition arm of the immune response?

A

Distinguish self from non-self by means of specialised receptors

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75
Q

When can the immune system be particularly damaging?

A

If cells have specificity for self (autoimmunity)

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76
Q

Why is it important that adaptive immunity has memory of previously encountered infections?

A

It gives an accelerated and increased response on subsequent encounters

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77
Q

What is the accelerated and increased response on subsequent encounters due to the memory of adaptive immunity known as?

A

The secondary response

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78
Q

What does adaptive immunity show for individual pathogens?

A

A very high degree of specificity

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79
Q

What is the high degree of specificity of adaptive immunity to individual pathogens determined by?

A

The antigen-specific receptors that are expressed by individual clones of T and B lymphocytes

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80
Q

What is the problem with the rapid immunological response to a second encounter with measles virus?

A

It is of no value if cells and antibodies are rapidly mobilised, but have the wrong specificity

81
Q

What is the primary exposure?

A

When an antibody is encountered for the first time

82
Q

What is the lag phase?

A

The period of time before any antibody that has been encounter for the first time is detectable

83
Q

What has to happen during the lag phase?

A

The antigen has to be recognised, processed, and presented by APC’s to lymphocytes

84
Q

What do the events happening in the lag phase cumulate it?

A

The appearance of the primary antibody response

85
Q

What is the antibody of primary response?

A

IgM

86
Q

What happens after a while following the primary antibody response?

A

The serum concentration of IgM falls

87
Q

What happens if an antibody that a patient has previously been exposed to is administered again?

A

There is a rapid appearance of antibody with very little lag phase

88
Q

What is the second exposure to the same antibody called?

A

The secondary antibody response

89
Q

What is the antibody of secondary response?

A

IgG (usually)

90
Q

What is the secondary response due to?

A

The presence of memory cells

91
Q

What type of immunity is memory a function of?

A

Adaptive. It is not seen in innate immunity

92
Q

What is acute inflammation?

A

The response of living tissue to injury

93
Q

What is acute inflammation initiated to do?

A

Limit the tissue damage

94
Q

What is chronic inflammation?

A

Chronic response to injury with associated fibrosis

95
Q

What are the cardinal signs of inflammation?

A
  1. Heat
  2. Erythema (redness)
  3. Oedema (swelling)
  4. Pain
  5. Loss of function
96
Q

What are the 5 steps of acute inflammation?

A
  1. Vasodilation
  2. Gaps form in endothelium
  3. Exudation
  4. Margination and Emigration
  5. Macrophages and lymphocytes migrate
97
Q

What happens in the vasodilation stage of acute inflammation?

A

Small adjacent blood vessels dilate with increased blood flow

98
Q

What happens in the gap formation stage of acute inflammation?

A

Endothelial cells swell and retract, so there is no longer a completed intact internal lining

99
Q

What happens in the exudation stage of acute inflammation?

A

Vessels become leaky, and water, salts, and small plasma proteins leak through as exudate

100
Q

What happens in the margination and emigration stage of acute inflammation?

A
  1. Circulating neutrophils adhere to swollen endothelial cells in margination.
  2. Neutrophils then migrate through the vessel basement membrane in emigration
101
Q

How do macrophages and lymphocytes migrate?

A

In a similar way to neutrophils

102
Q

What are inflammatory cells attracted by?

A

Chemokines, such as leukotrienes, IL-8 and C5a

103
Q

How are cells involved in the immune response controlled and communicate?

A

Via cytokines

104
Q

What makes cytokines?

A

White blood cells

105
Q

What are cytokines commonly called?

A

Interleukins

106
Q

Give 3 pro-inflammatory cytokines

A
  1. IL-1
  2. IL-6
  3. TNF
107
Q

What are the chemical mediators for vasodilation?

A
  • Histamine
  • Prostaglandins
  • C3a
  • C5a
108
Q

What are the chemical mediators for increased vascular permeability?

A
  • Histamine
  • Prostaglandins
  • Kinins
109
Q

What are the chemical mediators for emigration of leukocytes?

A
  • Leukotrienes
  • IL-8
  • C5a
110
Q

What is meant by active immunisation?

A

Stimulating the patient’s own immune system with an appropriate antigen

111
Q

How can active immunisation be bought about?

A

Injecting an attenuated form of the live organism response for the disease in question, killed organisms, or a denatured toxin (toxoid)

112
Q

What happens in active immunisation?

A

There is a lag phase, followed by the appearance of antigen-specific immune cells and antibodies. Immunological memory is formed

113
Q

What must be true of a patient receiving active immunisation?

A

They must have an intact immune system

114
Q

What can happen if an immunocompromised patient is inoculated with a live vaccine?

A

It can be fatal

115
Q

What is meant by passive immunisation?

A

Administration of a serum containing antibodies against as a disease or toxin

116
Q

What is the advantage of passive immunisation?

A
  • It is quick, with no lag phase
  • Doesn’t require intact immune system
117
Q

What is the disadvantage of passive immunisation?

A
  • No immunological memory formed
  • Immune protection short lived
118
Q

What are malignancies of the immune system characterised by?

A

The proliferation and accumulation of malignant leukocytes blocked at different stages of development

119
Q

What happens in leukaemia?

A

There are increased number of white blood cells, which may dominate the peripheral blood picture

120
Q

When do lymphomas arise?

A

When the malignant cells are found within tissues, rather than blood e.g. lymph nodes, spleen

121
Q

What types of leukocytes can malignancies occur for?

A

Any

122
Q

What does malignancy of the immune system give rise to?

A

A dominant, non-functional population of immune cells

123
Q

What are malignancies of the immune system associated with?

A

Secondary immune deficiencies

124
Q

What are the origin cells of the immune system?

A

Pluripotent, haematopoietic stem cells in the bone marrow

125
Q

What are the stages of production of immune cells?

A

Proliferation and differentiation of haemopoietic stem cells

126
Q

What happens in proliferation of haemopoietic stem cells?

A

Starting with a stem cell, the cell divides into two. One replaces the original stem cell, and one that differentiates

127
Q

What is the process of the stem cell proliferating to provide one cell that replaces the original called?

A

Self-renewal

128
Q

What happens in differentiation of haemopoietic stem cells?

A

Haemopoietic progenitor will first differentiate to form either a myeloid blast or a lymphoid blast

129
Q

What forms from myeloid blast cells?

A

Either RBC, WBC or platelets

130
Q

What forms from lymphoid blast cells?

A

Immunoresponse cells

131
Q

What does the haemopoietic progenitor differentiate under the influence of?

A

A particular cytokine

132
Q

What causes differentiation to RBCs?

A

Erythropoietin

133
Q

What causes differentiation to platelets?

A

Thrombopoietin

134
Q

What is erythropoiesis controlled by?

A

Partial pressure of oxygen

135
Q

What does a low pO2 do?

A

Stimulates increased erythropoietin

136
Q

What cells are produced from the pluripotent haemopoietic stem cell in the bone marrow?

A
  • Common lymphoid progenitor
  • Common myeloid progenitor
  • Erythrocyte
137
Q

What is produced from the common lymphoid progenitor?

A
  • B cell
  • T cell
  • NK cell
  • Immature dendritic cell
138
Q

What is the effector cell from a B cell?

A

Plasma cell

139
Q

What is the effector cell from a T cell?

A

Activated T cell

140
Q

What is the effector cell from a NK cell?

A

Activated NK cell

141
Q

What route to B cells, T cells and NK cells take after production in the bone marrow?

A

They go into the blood, and then travel to lymph nodes

142
Q

What happens to immature dendritic cells once produced in the bone marrow?

A

They pass into the blood, and then the tissues, and then become mature dendritic cells in the lymph nodes

143
Q

What is produced from the common myeloid precursor?

A
  • Granulocyte/macrophage progenitor
  • Megakaryocyte/erythrocyte progenitor
144
Q

What is produce from the granulocyte/macrophage progenitor?

A

Granulocytes (or polymorphonuclear leukocytes)

145
Q

Where are granulocytes produced from granulocyte progenitors?

A

In the blood

146
Q

What cells are considered to be granulocytes?

A
  • Neutrophils
  • Eosinophils
  • Basophils
  • Unknown precursor of mast cells
  • Monocytes
147
Q

Where do unknown precursors of mast cells become mast cells?

A

In the tissues

148
Q

What do monocytes become?

A

Macrophages

149
Q

Where do monocytes become macrophages?

A

In tissues

150
Q

Where does the megakaryocyte progenitor produce megakaryocytes?

A

In the bone marrow

151
Q

What do megakaryocytes become?

A

Platelets

152
Q

Where do megakaryocytes become platelets?

A

In the blood

153
Q

What do erythroblasts become?

A

Erythrocytes

154
Q

How to lymphocytes appear microscopically?

A

Small cells with deeply basophilic nucleus and little cytoplasm

155
Q

What happens to lymphocytes when exposed to antigen?

A

They become larger, chromatin is less dense, and cytoplasm volume increases. It is then known as a lymphoblast

156
Q

What is the purpose of lympocytes?

A
  • Production of antibodies (B lymphocytes)
  • Cytotoxic and helper functions (T cells)
157
Q

What do B cells give rise to?

A

Plasma cells

158
Q

What do plasma cells do?

A

Produce antibodies

159
Q

Where are plasma cells found?

A

In spleen and lymph nodes

Rarely seen in blood

160
Q

Where do T cells undergo maturation?

A

In the thymus

161
Q

What are the types of T cells?

A
  • CD4+ helper
  • CD8+ cytotoxic
    *
162
Q

What do CD4+ helper cells do?

A

Secrete cytokines that act on other cells

163
Q

What do CD8+ cytotoxic cells do?

A

Cause lysis of infected cells

164
Q

How big are monocytes?

A

16-20µm in diameter

Largest nucleated cell of blood

165
Q

What shape of the monocyte nucleus?

A

Kidney shaped

166
Q

What happens when a monocyte migrates into tissues?

A

It develops into a macrophage

167
Q

What is the main role of the macrophage?

A

It is the principle resident phagocyte of the tissues

168
Q

What does the macrophage have?

A

Receptors for antibodies and complement

169
Q

What kind of macrophages are found in the CNS?

A

Microglia

170
Q

What kind of macrophages are found in the liver?

A

Kupffer cells

171
Q

What kind of macrophages are found in the lungs?

A

Alveolar macrophages

172
Q

What kind of macrophages are found in the bone?

A

Osteoclasts

173
Q

What are dendritic cells?

A

Progessional antigen presenting cells

174
Q

What is the apperance of dendritic cells characterised by?

A

Long, finger-like processes

175
Q

What do dendritic cells do?

A

Take up particulate matter by phagocytosis, and large amounts of extracellular fluid and it’s contents by macropinocytosis

176
Q

What is the most common type of leucocyte?

A

Neutrophils

177
Q

What kind of nucleus do neutrophils have?

A

Multi-lobed

178
Q

What kind of cells are neutrophils?

A

Short-lived phagocytic cells

179
Q

What do neutrophils have in their cytoplasm?

A

Granules contaning numerous bactericidal substances

180
Q

What do neutrophils do?

A

Avidly phagocytoses particles that are opsonised by IgG or complement

Function as an effector cell of humoral immunity

181
Q

What kind of nucleus do eosionphils have?

A

Bi-lobed

182
Q

What do eosinophils have in their cytoplasm?

A

Granules contain highly basic or ‘cationic’ proteins

183
Q

What are eosinophil granules important for?

A

Killing larger parasites, including worms

184
Q

What kind of nucleus do basophils have?

A

Bi- or tri-lobed nucleus

185
Q

What do basophils have in their cytoplasm?

A

Granules containing heparin, histamine and other vasoactive amines

186
Q

What do basophils have on their cell surface?

A

High affinity receptors for IgE

187
Q

When are basophil granules released?

A

At sites of inflammation/hypersensitivity

188
Q

What kind of nucleus do mast cells have?

A

Circular

189
Q

What kind of cell are mast cells?

A

Tissue cell

Not bone marrow derived

190
Q

What are mast cells similar to?

A

Basophils, in that they have granules of histamine

191
Q

What kind of cell is this?

A

Lymphocyte

192
Q

What kind of cell is this?

A

Plasma cell

193
Q

What kind of cell is this?

A

Monocyte

194
Q

What kind of cell is this?

A

Macrophage

195
Q

What kind of cell is this?

A

Dendritic cell

196
Q

What kind of cell is this?

A

Neutrophil

197
Q

What kind of cell is this?

A

Eosionphil

198
Q

What kind of cell is this?

A

Basophil

199
Q

What kind of cell is this?

A

Mast cell

Z Old Infection IGNORE (23 decks)

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