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Foundations of health and disease > immunity > Flashcards

immunity Flashcards

1
Q

What is inflammation?

A

The body’s response to an irritant, an infectious pathogen, tissue damage etc.
Part of the innate immune response
Immediate and non-specific

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2
Q

what are the categories of inflammation

A

Acute inflammation (immediate response lasting a few days)
Chronic inflammation (lasting months or years)
Systemic inflammation (SI) – cytokine induced inflammatory response
Follows chronic inflammation.
Can lead to the development of conditions such as cardiovascular disease.

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3
Q

what are the signs of inflammation?

A

Localised signs of tissue inflammation:
Redness (Rubor)
Heat (Calor)
Swelling (Tumor)
Pain (Dolor)
Reduction or loss of tissue/organ function (functio laesa)
Whole body signs of inflammation:
Tiredness
General feeling of being unwell
Fever

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4
Q

how do you name a disease that is associated with inflammation

A

itis

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5
Q

what are the causes of acute inflammation

A

Infection (bacterial, viral)
Exposure to chemicals or radiation
Cell/tissue injury
Excessive immune reaction
Tissue necrosis due to restricted blood flow

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6
Q

what are the causes of chronic inflammation

A

A resistant infectious agent
Prolonged exposure to endogenous (necrotic tissue) or exogenous (chemicals) materials
Some diseases, e.g. chronic inflammatory bowel disease
Autoimmune disease

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7
Q

what are monocytes

A

precursors of macrophages

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8
Q

what are the steps in acute inflammation

A

Vessel dilation and increased blood flow
Vascular permeability
Leukocyte (neutrophil/monocyte) movement (migration)

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9
Q

what happens during acute inflammation

A

arterioles initially dilate and the opening of the sphincters leads to increased blood flow in the tissue capillary network.

In acute inflammation increased vascular permeability leads to the escape of fluid including blood cells and protein molecules to the extracellular space

  • exudation.
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10
Q

what happens during actue inflammation to the capillary hydrostatic pressure

A

it increases

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11
Q

what do histamines do during vasodilation

A

Histamine is released from granules in mast cells in response to tissue injury, heat, cold or antibody binding. It binds on G-protein coupled receptors on endothelial cells. It is also released by basophils and platelets. Fast and short-lived response.

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12
Q

what do bradykinin and leukotrienes do during vasodilation

A

Bradykinin (circulating in the blood plasma) and leukotrienes (produced by leukocytes and mast cells) also increase vascular permeability.

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13
Q

what are leukotrienes mode of action

A

act on the vascular smooth muscle tissue

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14
Q

what do kinins do

A

act on the vascular smooth muscle tissue causing contraction and vasodilation

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15
Q

what is the role of neutrophils in inflammation

A

Neutrophils accumulate near the endothelium (vascular wall).
Adhesion molecules (selectins) produced by the endothelial cells are detected by neutrophil receptors.
Integrin ligands bind strongly on neutrophil integrins, rolling stops and transmigration through the endothelium begins.

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16
Q

how are leukocytes activated in inflammation

A

via ligand-receptor binding

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17
Q

what does phagocytosis rely on

A

Phagocytosis relies on reactive oxygen species (ROS) and lysosomal enzymes.

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18
Q

where are ROS formed

A

ROS are formed in the membrane of the phagosomes in a phagocyte activated following pathogen recognition.

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19
Q

what is inside a phagosome

A

Inside a phagosome ROS and NO kill pathogens.

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20
Q

what are the steps to phagocytsosis

A
  1. microbes bind to phagocyte receptors
  2. phagocyte membrane zips up around the microbe
  3. phagosome forms with ingested microbe
  4. fusion of phagosome with lysosome
  5. degadation of microbes by lysosomal enzymes in phagolyosome
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21
Q

what is the source histamines

A

mast cells
basophils
platelets

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22
Q

what is the action of histamine

A

vasodilation
increased vascular permiability

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23
Q

what is the source of prostaglandins

A

mast cells
leukocytes

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24
Q

what is the action of prostaglandins

A

vasodilation
pain
fever

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25
Q

what is the source of cytokines

A

macrophages
endothelial cells
mast cells

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26
Q

what is the action of cytokines

A

endothelial activation
fever
hypertension

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27
Q

what is the source of chemokines

A

leukocytes
activated macrophages

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28
Q

what is the action of chemokines

A

chemotaxis
leukocyte activation

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29
Q

what is the source of complement factors

A

leukocyte chemotaxis and inflammation
pathogen killing
vasodilation

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30
Q

what is the most abundant complement factor

A

C3 which is cleaved to C3a and C3b

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31
Q

what does c3b do

A

C3b participates in the cleavage of C5 to C5a and C5b → signal amplification involving other complement factors.
it also stimulated phagocytosis

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32
Q

what do complement factors do

A

Complement factors circulate in the plasma in their inactive form.
Following cleavage they become active and function in histamine release, chemotaxis (recruitment of leucocytes) pathogen opsonisation (recognition of a pathogen by a phagocyte).

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33
Q

what does c3a do

A

stimulated inflammation

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34
Q

what do lipotoxins do

A

inhibit neutrophil recruitment (chemotaxis and adhesion to the vascular endothelium).

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35
Q

what type of molecules are produced in parallel with pro-inflammatory molecules

A

antiinflammitory molecules

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36
Q

when are mediator molecules expressed

A

in response to a stimulus

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37
Q

what are features of mediator molecules

A

short half-lives
quick decay

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38
Q

what happens when the inflammatory response is prolonged

A

Leukocytes can damage tissue when the inflammatory response is prolonged or when the leukocytes attack host tissues (autoimmune disease). Unchecked release of enzyme rich leukocyte granules can also cause tissue damage.

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39
Q

what are the local benefits of inflammation

A
  1. increased vascular permeability- assists transport of blood circulating antibodies and drugs to site of infection
  2. exudation and fluid release dilutes conc. of toxins
  3. vascular exudate includes fibrinogen wich coagulates blood
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40
Q

what happens at the end of an acute inflammatory response

A

complete resolution
healing by tissue replacement
progression to chronic inflammation

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41
Q

how does chronic inflammation form

A

repeated events of acute inflammaiton

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42
Q

what is chronic inflammation characterised by

A

increased numbers of lymphocytes plasma cells and macrophages

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43
Q

what are some features of chronic inflammation

A

Necrotic tissue can be present.
Inflammatory cells cause tissue damage.
Tissue repair mechanisms and angiogenesis are initiated.

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44
Q

What are the sources of TNF

A

Macrophages
Mast cells
T lymphocytes

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45
Q

What is the action of TNF in acute inflammation

A

Acute inflammation
Stimulates endothelial adhesion molecules
Secretion of other cytokines

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46
Q

What are the sources of IL-1

A

Macrophages
Ednothelial cells
Epithelial cells

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47
Q

What are the actions of IL-1 in acute inflammation

A

Stimulated endothelial adhesion molecules
Secretion of other cytokines
Acute inflammation

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48
Q

What are the sources of IL-6

A

Macrophages

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49
Q

What are the actions of IL-6 in acute inflammation

A

Systemic effects

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50
Q

What are the sources of chemokines

A

Macrophages
Endothelial cells
T lymphocytes

Mast cells

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51
Q

What is the action of chemokines in acute inflammation

A

Recruitment of leukocytes
Migration of cells in normal tissues

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52
Q

What are the source of IL-17

A

T lymphocytes

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53
Q

What is the action of IL-17 in acute inflammation

A

Recruitment of neutrophils and monocytes

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54
Q

What is the sources of IL-12

A

Dendritic cells
Macrophages

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55
Q

What is the action of IL-12 in chronic inflammation

A

Increased production of IFN-y

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56
Q

What is the source of IFN-y

A

T lymphocytes
NK cells

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57
Q

What is the action ofIFN-y in chronic inflammation

A

Activation of macrophage

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58
Q

What is the action of IL-17 in chronic inflammation

A

Recruitment of neutrophils and monocytes

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59
Q

Which diseases cause granulomatous inflammation

A

Tuberculosis
Leprosy
Syphilis
Crohn disease

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60
Q

What are systemic effects of acute inflammation caused by

A

Cytokine production in response to pathogen infection

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61
Q

What contributes to systemic effects on inflammation

A

TNF
IL-1
IL-6
Type 1 interferons

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62
Q

what cytokines and chemokines are used in endothelial cell local inflammation

A

TNF, IL-1-cytokines
IL-1 chemokines

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63
Q

what chemokines and cytokines are used in leucocyte activation

A

TNF, IL-1 cytokines
IL-1,IL-6 chemokines

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64
Q

what cytokines and chemokines are used within T-cell differentiation.

A

IL-1,IL6 cytokines
IL-17 chemokines

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65
Q

which cytokines cause fever within the brain

A

TNF IL-1 IL-6

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66
Q

which cytokines cause acute-phase proteins to exit the liver

A

Il-1 IL-6

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67
Q

which cytokines cause leukocyte production within the bone marrow

A

TNF IL-1 IL-6

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68
Q

Which cytokines cause low output of blood from the heart

A

TNF

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69
Q

which cytokines cause endothelial cells and blood vessels to have increased permeability

A

TNF

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70
Q

what induces fever

A

pyrogens

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71
Q

what stimulated the production of prostaglandins

A

TNF, IL-1 Il-6

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72
Q

what do prostaglandins do?

A

are molecules that act in the hypothalamus to release neurotransmitters that set the body temperature higher.

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73
Q

what is fever

A

Increase in body temperature between 1℃ to 4℃.

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74
Q

what is resolution

A

the restoration of tissue back to normal

75
Q

what conditions must be satisfied for resolution to proceed

A

Minimal cell death and tissue damage during the inflammatory phase.
Tissue or organ has regenerative capacity.
Quick destruction of infectious pathogens (macrophage/neutrophil phagocytosis).
Quick removal of cell debris (macrophage phagocytosis) and fluids (good vascular drainage).
End of vascular dilation.

76
Q

what do monocytes do

A

circulate the blood and migrate to tissues where they differentiate to mature macrophages

77
Q

what is the activity of macrophages

A

Chemotaxis: migration towards a damaged or infected area.

Phagocytosis: ingest cell debris.

Pinocytosis: ingest fluids.

78
Q

how is debris removed via phagocytosis

A

recognition
binding
signalling
phagocytosis

79
Q

label an antibody

A
80
Q

what are the 5 antibody istotypes

A
81
Q

Describe the lineage of CD4 and CD8 T cells

A
82
Q

what is immunity

A

the ability of an organisms to defend itself against: infectious agents, foreign cells, catastrophic cell destruction

83
Q

what is immunodeficiency

A

is the outcome of failed immunity caused either genetically or acquired through life

84
Q

what is allergy and hypersensitivity

A

result when the immune system responds inappropriately to antigens

85
Q

what is tolerance

A

state of immunological non-reactivity to an antigen

86
Q

what does red bone marrow produce

A

Site of production for all blood cells including b and T lymphocytes

87
Q

what do lymph nodes contain

A

resident lymphocytes and macrophages which neutralise pathogens and clear.

88
Q

what do spleens contain

A

act as an emergency blood store

89
Q

what does the thymus contain

A

site of maturation of t lymphocytes

90
Q

what is a leucocyte

A

white blood cell

91
Q

what are barrier systems for immunity

A
  • skin is impermeable to most infectious pathogens
  • Lysozymes in tear ducts nasal ducts and saliva breakdown black acidic bonds and assists the destruction of the bacterial cell wall
  • Mucus with in the Tokyo traps pathogens that are expelled by epithelial cell cilia
  • Lower stomach pH and digestive enzymes within the stomach make the environment uninhabitable for pathogens
  • Intestinal flora in the gut in vagina antagonise infection from external pathogens
92
Q

what is a macrophage

A

phagocytic, highly migratory, professional antigen presentation

93
Q

what is a neurtophil

A

highly abundant and migratory, coordinates inflammatory response

94
Q

what is an eosinophil

A

involved in host defence against nematodes and other parasites

95
Q

what is a basophil

A

involved in host defences against multicellular parasites

96
Q

what is a dendritic cell

A

the most adept of the family of antigen presenting cells (APC)

97
Q

what is B cell

A

adaptive, produce antibodies that bind to antigens on pathogens, exhibit immunological memory

98
Q

what is a t cell

A

adaptive, involved in killing virus infected cell, involved in coordinating immune responses, orchestrated of activation/termination

99
Q

what are pattern recognition receptors (PRR)

A

PRR in innate immunity detect antigens non-specifically using receptors for PAMPS

100
Q

what are PAMPs Pathogen Associated Molecular Patterns

A
  • PAMPS a molecular structures that occur in lower organisms
  • Signalling pathways are initiated when the signal binds its receptor
101
Q

Explain key immunological events that underlie inflammation and its resolution.

A
  • if you damage causes release of vasoactive and chemotactic factors that trigger local increase of blood flow and capillary permeability
  • Permeable capillaries allow an influx of fluid in cells
  • Phagocytes migrate to the site of inflammation (chemotaxis)
  • Phagocytes and antibacterial exudate destroy bacteria
102
Q

what to PRRR’s bind to

A

a limited array of PAMPS

103
Q

what do PRRs respond to

A

PAMPs that may be protein, carbohydrate or lipid based

104
Q

what are the PRR’s molecular memory

A

exhibits no molecular memory or ability to imrpove/adapt during an immune response

105
Q

what are the features of PRR genes

A

genes entirely germ-line encoded

106
Q

what to adaptive response receptors bind to

A

bind to a potentially infinite array of pathogen-associated peptides

107
Q

what are the antigens for ARRs

A

antigens are always protein peptides for t cells and occasionally carbohydrates or lipids for B cells

108
Q

what is the molecular memory like for ARR- adaptive response receptor

A

induces molecular memory and exhibits and ability to improve/adapt during the immune response

109
Q

what are the genes like for ARRs

A

gene editing results in a modification to the genome in somatic immune cells

110
Q

what is a complement in innate immunity

A
  • A family of plasma proteins that activate each other – the complement cascade
  • Capable of destabilising the membranes of invading bacteria
  • Coat invading bacteria, marking them for destruction by antibodies
  • Attracts phagocytes to the site of infection
111
Q

what are the soluble mediators in innate immunity

A

complements
lysozymes
cytokines

112
Q

how to leucocytes communicate

A
  • leucocytes communicate using cytokines and chemokines
  • They bind to receptors on the target cell to sugar signalling transduction cascades that ultimately lead to changes in gene expression and therefore cell function
113
Q

what are antibodies

A

glycoproteins which bind to a specific antigens.

114
Q

what is a epitope

A

The part of an antigen where the antibody binds to

115
Q

what determines the isotypes of an antibody

A

The variable (V) regions near the tip of the antibody can differ from molecule to molecule in countless ways, allowing it to specifically target an antigen

116
Q

what is antigenic specifity

A

the ability of the host cells to recognize an antigen specifically as a unique molecular entity and distinguish it from another with exquisite precision

117
Q

what is immunological memory

A

the ability of the immune system to respond more rapidly and effectively to pathogens that have been encountered previously

118
Q

what is somatic recombination

A

type of gene rearrangement by which cells of the adaptive immune system physically cut out small regions of DNA and then paste the remaining pieces of DNA back together in an error-prone way

119
Q

what is affinity maturation?

A

additional changes in the structure of the antibody can occur if it encounters an antigen to which the antibody can bind

120
Q

what is primary and secondary immune response

A

A primary (1°) immune response is the response that occurs following the first exposure to a foreign antigen. A secondary (2°)/anamnestic immune response occurs following subsequent exposures.

121
Q

how is diversity of an antibody created

A

The diversity of antibodies is created by the combination of variable regions of H chains and L chains.

122
Q

what is the primary and secondary response of a responding b cell

A

naive b cell
memory b cell

123
Q

what is the primary and secondary response of lag period following antigen administration

A

generally 4-7 days
generally 1-3 days

124
Q

what is the primary and secondary response of time of peak response

A

7-10 days
3-5 days

125
Q

what is the primary and secondary response of magnitude of peak antibody response

A

varies depending on the antigen
generally 100-1000 times higher than the primary response

126
Q

what is the primary and secondary response of isotype produced

A

IgM predominates early in response
igG predominates

127
Q

what is the primary and secondary response of antigens

A

thymus dependent and thymus independent
thymus dependent

128
Q

what is the primary and secondary response of antibody affinity

A

lower
higher

129
Q

what happens at first antigen exposure

A

lag period of 1-2 days before the first response begins with
the production of IgD and then IgM antibodies
pentameric structure of IgM leads to a high functional affinity
changes to the structure of the antibody constant region (class switching) and affinity maturation, IgG is produced.
- Once the antigen has been sufficiently neutralized, the levels of IgM and IgG deplete over time.

130
Q

what happens at second antigen exposure

A

the speed of the response is faster.
the bulk of the antibody synthesized is of the IgG isotype.
- The speed of the response depends on the memory B cells,
- When the antigen has been removed, the amount of antigen-specific IgG in blood circulation may or may not decrease,

131
Q

what are cytotoxic t cells

A

Search for and destroy target cells that bear non-self antigens presented in MHC class I context.

132
Q

what are t helper cells

A

Secrete cytokines that bind to receptors on B cells and T cells to stimulate their activity.

133
Q

what are t supressor cells

A

Secrete signaling molecules that bind to receptors on other immune cells to terminate their activity, thus suppressing immune responses that are no longer needed.

134
Q

what are t memory cells

A

Persist for life in a semi-dormant state, but rapidly re-activated on a second exposure to the antigen (pathogen) they are specific for. Bypass the need for the primary immune response on second infection.

135
Q

what does CD stand for

A

cluster of differentiation

136
Q

what do CD4+ mean

A

A cell that is CD4+ expresses CD4 and is therefore likely to be a T helper cell.

137
Q

what does CD8+ mean

A

A cell that is CD8+ expresses CD8 and is therefore likely to be a cytotoxic T cell.

138
Q

what does MHC do

A

to bind peptide fragments derived from pathogens and display them on the cell surface for recognition by the appropriate T cells.

139
Q

Explain how CD8 T cells recognise antigens

A
  • Once the peptide is loaded into the MHC class I complex it engages with cytotoxic CD8+ T cell.
    The CD8 molecule simultaneously “double checks” that the peptide is presented correctly
    The cytotoxic T cell will only kill the target cell once these engagements are complete.
140
Q

Explain how CD4 t cells recognise antigens

A

Once a peptide is loaded into the MHC class II complex and presented on a professional antigen-presenting cell (APC) surface, it engages with the T cell receptor on a passing CD4+ helper T cell. The helper T cell “double checks” the identity of the presenting cell before it becomes activated to secrete molecular messengers (cytokines) that further promote immune responses.

141
Q

How to CD4+ recognise antigens

A

recognise antigen presented in MHC class II context by professional APCs

142
Q

How do CD8+ recognise antigens?

A

recognise antigen presented in MHC class I context on infected body cells

143
Q

how are CD4+ activated

A

on activation secrete a variety of chemical messengers that stimulate immune responses

144
Q

how do CD8+ activated

A

on activation engange with and attack target cells by triggering apoptosis and damaging the cell membrane

145
Q

how does CD4+ receptors respond

A

t cell receptor typically responds to antigens derived from exogenous pathway

146
Q

how do CD8+ receptors respond

A

t cell receptor responds to antigens derived from the endogenous pathway

147
Q

how are CD4+ cells stimulated

A

requires stimulation from APC

148
Q

how are CD8+ cells stimulated

A

requires stimulation by an infected target cell and a CD4+ helper T cell

149
Q

where are MHC class I found

A

all nucleated cells

150
Q

where are MHC class II found

A

only on antigen-presentic cells

151
Q

what does MHC class I present antigens to

A

directly to CD8+ cytotoxic T cells

152
Q

what does MHC class II present antigens to

A

to CD4+ helper T cells

153
Q

what does MHC class I present peptide fragments derived from

A

derived from intracellular antigens

154
Q

what does MHC class II present peptide fragments derived from

A

extracellular antigens

155
Q

where is the peptide fragment of the MHC class I loaded in to

A

rough ER

156
Q

where is the peptide fragment of the MHC class II loaded in to

A

ENDOSOMAL VESICLES

157
Q

what is the endogenous pathway

A

deals with intracellular infections
most peptides presented in class I context are self-derived and will not trigger an immune response.

158
Q

what is the exogenous pathway

A

The exogenous pathway evolved to deal with extracellular infections. Only a select group of immune cells are capable of class II MHC presentation, including dendritic cells, macrophages, B cells

159
Q

where do B cells develop

A

develop and partially mature in the bone marrow then fully mature in the spleen

160
Q

where to T cells develop

A

originate in the bone marrow and develop in the thymus

161
Q

what do b cells recognise

A

intact protein antigen-soluble or pathogen associated

162
Q

what do t cells recognise

A

peptides derived from processed antigen and presented to them by another cell

163
Q

what are b cells subset

A

no major differences

164
Q

what are t cells subsets

A

CD4 and CD8

165
Q

what happens to b cell receptors during affinity maturation

A

mutate their receptor

166
Q

what happens to t cell receptors during affinity maturation

A

no affinity maturation takes place

167
Q

what is the response time for innate immunity

A

minutes/hours

168
Q

what is the response time for addaptive immunity

A

days

169
Q

what is the specificity of innate immunity

A

specific for molecules and molecular patterns associated with pathogens

170
Q

what is the specificity of adaptive immunity

A

highly specific
discriminates even minor differences in molecular structure
details of microbial or non-microbial structure recognised with high specificity

171
Q

what is the diversity of innate immunity

A

a limited number of germ line-encoded receptors

172
Q

what is the diversity of adaptive immunity

A

highly diverse
a very large number of receptors arising from genetic recombination of receptor genes

173
Q

what is the memory response of innate immunity

A

none

174
Q

what is the memory response of adaptive immunity

A

persistent memory with faster response of greater magnitude on subsequent infection

175
Q

what is the self/nonself discrimination of innate immunity

A

perfect
no microbe-specific patterns in host

176
Q

what is the self/nonself discrimination of adaptive immunity

A

very good
occasional failures of self/nonself discrimination result in autoimmune disease

177
Q

what are the soluble components of blood or tissue fluids of innate immunity

A

many antimicrobial peptides and proteins

178
Q

what are the soluble components of blood or tissue fluids of adaptive immunity

A

antibodies

179
Q

what are the major cell types of innate immunity

A

phagocytes
natural killer
dendtritic

180
Q

what are the major cell types of adaptive immunity

A

t cells
b cell
APCs

181
Q

how are t cells b cells and dendritic cells made

A

hematopoietic stem cells
lymphoid porgenitor

182
Q

how are most cells except b and t and nk cells made

A

hematopoietic stem cells
myeloid porgenitor

183
Q

what soluble molecules are in the innate immune response

A

lysozyme complement factors
cytokines
chemokines

184
Q

what soluble molecules are in the adaptive immune response

A

antibodies
cytokines

Foundations of health and disease (21 decks)

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