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Phase 2a Sam > ICS - IMMUNOLOGY > Flashcards

ICS - IMMUNOLOGY Flashcards

1
Q

What is haematopoiesis?

A

Formation of red and white blood cells

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2
Q

What types of barriers make up the innate immune response - give examples of this

A

Physical barriers - Skin, gut lining, Ciliated Epithelia of airways

Chemical - Stomach and Vaginal low pH, and lysozymes in tears - break down bacteria cell walls

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3
Q

What are the 2 branches of the immune system?

A

Innate and adaptive

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4
Q

Give some features of the innate immune system

A
  • Non - specific
  • Resistance is not improved by repeat infections
  • Instinctive
  • Short lasted (days)
  • No memory
  • Involves Myeloblasts (Basophil Neutrophil and Eosinophil) and Macrophages
  • Present from birth
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5
Q

Give some features of the adaptive immune system

A

Specific ‘Acquired’ immunity
* Requires lymphocytes
* Antibodies involved
* Resistance is improved by repeat infection
* Slower response (days-weeks)
* B lymphocytes & T lymphocytes

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6
Q

What is the cell from which all WBCs and RBCs are made from?

A

Haematocytoblast

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7
Q

What is the function of lysozyme?

A

It destroys bacterial cell walls.

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8
Q

Give examples of 3 polymorphonuclear leukocytes.

A
  1. Neutrophils.
  2. Basophils.
  3. Eosinophils.
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9
Q

Give examples of 3 mononuclear leukocytes.

A
  1. Monocytes.
  2. B lymphocytes.
  3. T lymphocytes.
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10
Q

What are the two cells that a Haematocytoblast gives rise to?

A

Common Myeloid Progenitor
Common Lymphoid Progenitor

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11
Q

What cells do Common Myeloid Progenitors give rise to?

A

Erythrocyte (RBC)
Mast Cell
Megakaryocyte
Myeloblast

EMMM

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12
Q

What cells do Myeloblasts give rise to?

A
  • Neutrophil
  • Basophil
  • Eoisinophil
  • Monocytes
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13
Q

What do Monocytes give rise to?

A

Macrophages and Dendritic cells

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14
Q

What cells do common lymphoid progenitor cells give rise to?

A

Natural killer cells
B Lymphocyte
T Lymphocyte

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15
Q

What cell does a B lymphocyte give rise to? What does this cell do?

A

Plasma cells, that release antibodies

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16
Q

In which primary lymphoid tissue do T cells mature?

A

Thymus.

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17
Q

In which primary lymphoid tissue do B cells mature?

A

Bone marrow.

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18
Q

What do neutrophils do in innate immunity

A

They Phagocytose
Can either use cytoplasmic granules, or
Oxidative Burst, where Neutrophil produces lots of ROS - Destroy themselves and engulfed pathogens

Make up 70% of WBC

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19
Q

What is serum?

A

The clear liquid part of the blood that remains after blood cells and clotting proteins have been removed.

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20
Q

Describe the role of eosinophils

A

Make up 5% of blood
Lifespan: 8-12 days

Stain Pink with Eosin
Phagocytic
Known for fighting Parasites
Larger than neutrophils

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21
Q

What is the difference between a macrophage and a monocyte?

A

Monocytes are found in the blood and then differentiate into macrophages or dendritic cells in tissue

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22
Q

Describe the neutrophil innate immune response

A

Engulf pathogens using phagocytosis, FORMING PHAGOSOME

Granules in neutrophil FUSE TO FORM PHAGOLYSOSOME, causes it to become acidic (kills 2% of pathogens)

Neutrophil continues to engulf more pathogens

Once neutrophil is full, an oxidative burst occurs

These highly reactive oxygen species kill neutrophil but also the pathogens engulfed

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23
Q

Describe the role of basophils

A

Make up 2% of blood
Lifespan: 2 days
Similar to mast cells involved in allergic reactions

High affinity for IgE, when IgE binds, they DEGRANULATE, RELEASSING HISTAMINE

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24
Q

How are basophils involved in allergic reactions?

A

They have high affinity IgE receptors
Binding of IgE to receptor results in de-granulation releasing histamine

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25
Q

What is the difference between mast cells and basophils?

A

Mast cells are in fixed tissue, whereas basophils are able to circulate around the body

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26
Q

What are the 3 categories of Soluble factors

A

Complement factors

Antibodies

Cytokines, Chemokines

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27
Q

What are complement factors? What do they do?

A

Group of ~20 serum proteins secreted by the liver that need to be activated to be functional.

They are activated only as part of the immune response – 3 activation pathways

Modes of action:

  • Direct lysis - via MACs
  • Attract more Leukocytes to site of infection (C3a and C5a, chemotaxis)
  • Coat invading organism (make them easier to eat by phagocytes, C3b) ==> opsonization
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28
Q

Where do antibodies come from? What are they, effectively?

A

Antibodies - Immunoglobulins, act as adapter that links a microbe to a phagocyte. - or , A blood protein produced in response to and counteracting a specific antigen

Antigen is presented to them, often by T Helper cell, links to a B cell receptor - this turns into a plasma cell, that secrete antibodies, which can bind to the specific antigen it was presented with

Basically just B cell receptor in secreted form

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29
Q

What do antibodies do?

A

Circulate in the serum (noncellular part of the blood) and MARK PATHOGENS FOR DESTRUCTION
They act as an adapter that links a microbe to a phagocyte

SO ANTIBODIES AREN’T BOUND TO CELLS AND FLOAT FREELY IN THE BLOOD

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30
Q

What are cytokines? What do they do? Name some key ones

A

Cytokines - proteins secreted by immune and non-immune cells, signal immune cells to move to the site of inflammation

Interferons
Interleukins
Colony Stimulating factors
Tumour Necrosis Factors
Chemoknies

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31
Q

specific cytokines: What do interferons do?

A

Inducer a state of antiviral resistance in uninfected cells

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32
Q

What do colony stimulating factors do?

A

Involved in directing the division and differentiation of bone marrow stem cells – precursors of leukocytes

aka specific CSF will stimulate/signal the growth of specific leukocytes

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33
Q

What do chemokines do?

A

attract Leukocytes, that travel along chemokine concentration gradient

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34
Q

What are interleukins

A

Can cause cells to divide, to differentiate and to secrete factors
Can be pro-inflammatory (eg. IL1) or anti-inflammatory (eg. IL-10)

DDS - Divide, Differentiate, Secrete

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35
Q

What substance causes endothelial cells to become sticky? What secretes this substance?

A

TNFa, secreted by macrophages in the infected tissue.

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36
Q

How does the body recognise bacteria that is foreign?

A

PAMPs = Pathogenic Assocaited Molecular Patterns - Patterns on microbes that are different to ours

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37
Q

What senses microbes in
a) Blood
b) Tissues?

A

In blood – Monocytes, Neutrophils
In tissues – Macrophages, Dendritic cells

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38
Q

What links the innate and adpative immune systems together?

A

The displaying of antigens by phagosomes on MHCs, can then present the antigen to the lymphocytes

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39
Q

Name the 3 antigen presenting cells

A

Macrophages
Dendritic Cell
B cells

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40
Q

Why can’t T cells recognise your own cells?

A

T cells that recognise self are killed in the foetal thymus as they mature (called T cell selection)

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41
Q

What are the 2 types of antigens?

A

Intrinsic/Intracellular (in the cells eg Virus)
or
Extrinsic/Extracellular

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42
Q

For extrinsic antigens, what is do they use class I or II MHC? Do they need Antigen Presenting cells or can they use any? What T Cells do they use?

A

Class II MHC, Uses APCs only. Uses T helper cell (CD4)

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43
Q

For intrinsic antigens, do they use class I or II MHC? Do they need Antigen Presenting cells or can they use any? What T Cells do they use?

A

Class I MHC, presented on all cells. Uses T Cytotoxic CD8 Cells

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44
Q

Describe the role of T lymphocytes
Can they recognise soluble antigens?

A

Make up 10% of blood
Lifespan: hours-years
In charge of cell mediated immunity - antigen specific
Can’t recognise soluable antigens

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45
Q

Where do T lymphocytes originate and mature

A

They originate in bone marrow and mature in the thymus

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46
Q

What are B cells?

What do they do?
What MHC do they contain?

Do they need an MHC?

A

Have receptors on surface but don’t need MHC
Can bind to any antigen that has shape specific to their receptors
Contain MHC II

Can also:

  • Perform phagocytosis
  • Can be an antigen presenting cell
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47
Q

What happens when a T cell gets activated

A

It helps a B cell to transform into a plasma cell

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48
Q

How do T cells recognise antigens?

A

For T cells to recognise antigens they must be displayed by an antigen presenting cell and bound to MHC1/2.

T cells can’t recognise soluble antigens.

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49
Q

What is the function of T helper 1 (CD4)?

A

It helps the immune response against intracellular pathogens.

Secretes cytokines.

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50
Q

What is the function of T helper 2 (CD4)?

A

It helps produce antibodies against extracellular pathogens. Secretes cytokines.

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51
Q

What is the function of Cytotoxic T cell (CD8)?

A

It can kill cells directly by binding to antigens; they induce apoptosis.

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52
Q

What is the function of T reg (FoxP3)?

A

They regulate the immune response.

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53
Q

Which cells express MHC1?

A

All nucleated cells express MHC1. e.g. a virus infected or cancer cell would express MHC1.

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54
Q

Which cells express MHC2?

A

Antigen presenting cells ONLY e.g. macrophages, B cells, dendritic cells.

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55
Q

Which MHC would an extracellular antigen (exogenous) lead to the expression of?

A

MHC2.

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56
Q

Which MHC would an intracellular antigen (endogenous) lead to the expression of?

A

MHC1.

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57
Q

What does a helper T cell bind to?

A

The T cell receptor binds to an antigen epitope which is bound to MHC2 on an APC.

See left hand picture

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58
Q

Which interleukin is secreted when a helper T cell is bound to a T cell receptor?

A

IL-2. This then binds to an IL-2 receptor on the T cell and produces a positive feedback mechanism leading to division and differentiation.

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59
Q

Describe the process of a T helper cell binding to a B cell.

A

So B cells - pick up an antigen form a pathogen and display it on MHC 2 ===> T helper 2 cells bind to the B - cells via this, and release cytokines that induces B cell Clonal expansion

  • so they differentiate into plasma cells and memory B cells
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60
Q

What do plasma cells secrete

A

Antibodies

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61
Q

Give 3 functions of antibodies.

A

Neutralise toxins.
Opsonisation.
Activate classical complement system.

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62
Q

What are the two main types of T cell

A

CD4+ (Helper)
CD8+ (Cytotoxic)

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63
Q

What CD are all T cells positive for?

A

CD3

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64
Q

What are CD4+ cells called and what do they do?

What MHC do they see

A

-They are called helper T cells
- They secrete cytokines that coordinate immune response
- Can only see antigens presented on an MHC II molecule

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65
Q

What are CD8+ cells called and what do they do?

A

They are called cytotoxic T cells
They kill target cells
Very specific killing (only kill cells with antigen presented on MHC I molecule)

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66
Q

What do antibodies consist of?

A

Two heavy chains, and two light chains

These form two regions that are joined together by a disulphide bond

see picture

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67
Q

What are the two different regions of an antibody?

A

Fragment antigen binding (Fab) (A variable region)
Constant fragment (fc) (stays the same)

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68
Q

What makes up the two different regions on an antibody?

A

The fab regions is made up of 1 of the light chains, and a part of one of the heavy chains.

The Constant fragment is made of the remainder of the heavy chain

There are two fab regions and two constant fragments

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69
Q

What chains determine the class of antibody?

A

Heavy chain

70
Q

What are the 5 classes of antibodies?

A

IgG
IgA
IgM
IgE
IgD
GAMED

71
Q

What are Natural Killer Cells? What do they do?

A

Large lymphocytes with granules
They target cells infected with intracellular organisms e.g., virus
They also target cancer cells

72
Q

Describe how dendritic cells are involved in the immune response to a pathogen

A

They are excellent at phagocytosis
Once they are mature, they break up pathogens into small amino acid chains
Will move through lymph to nearest node and perform antigen presentation to T cells - they are the best at this

73
Q

How do NKC’s kill target cells?

A

They punch holes in cell membranes creating pores or they enter cells and cause apoptosis

74
Q

What is the only way that CD4+ Helper T Cell see antigens?

A

Only if the antigen is presented on MHC II

75
Q

What is the only way that CD8+ Cytotoxic T Cell KILL antigens?

A

It can only KILLs cells with anitgen presented on MHC I

76
Q

Name 3 receptors that make up the PRR family

A

Toll-like receptors (TLR).
2. Nod-like receptors (NLR).
3. Rig-like receptors (RLR)

TLRs are the main ones

77
Q

What is the main function of TLR’s?

A

TLR’s send signals to the nucleus to secrete cytokines and interferons.

These signals initiate tissue repair. Enhanced TLR signalling = improved immune response

78
Q

What are PRR’s a receptor for?

A

PAMPs

79
Q

TLR’s are adapted to recognise damaged molecules. What characteristic do these damaged molecules often have in common?

A

They are often hydrophobic

80
Q

Where are circulating PRR secreted from?

A

Epithelia, phagocytes and the liver. They can activate the complement cascade and induce phagocytosis

81
Q

What happens when a PAMP binds to a PRR?

A

The innate immune response and inflammatory response is triggered.

82
Q

What is extravasation? What causes it?

A

Leukocyte (WBC) migration across the endothelium.

It is caused by the secretion of TNF alpha, from the macrophages ast tissues

83
Q

Describe the process of extravasation

A
  1. Macrophages at tissues release TNF alpha.
  2. The endothelium is stimulated to express adhesion molecules and to stimulate chemokines.
  3. Neutrophils bind to adhesion molecules; they roll, slow down and become stuck to the endothelium.
  4. Neutrophils are activated by chemokines.
  5. Neutrophils pass through the endothelium to the tissue to help fight infection.
84
Q

What are TLRs? Where are they found?

A

Found on macrophages, dendritic cells & neutrophils
- They are proteins that recognise and bind to PAMPs; eg lipopolysaccharide, viral and bacterial nucleic acids

When binding happens, second messengers are
generated within the immune cell which lead to the
secretion of inflammatory mediators such as IL-1, IL-12
& TNF-alpha

They are PLASMA MEMBRANE BOUND AND BIND TO EXTRACELLULAR LIGAND

85
Q

Specific TLRs: What does TLR 2 bind to?

A

Gram Positive Bacteria
Fungi

Specifically - binds lipoteichoic acid, part of peptidoglycan on gram positive bacteria (note there is a thin peptidoglycan cell wall on gram negative bacteria)

86
Q

Specific TLRs: What does TLR 5 bind to?

A

Flagellin is detected by TLR5, 5 begins with F as does flagellin is a good
way to remember

Eg E.Coli flagellated, so TLR 5 can detect it

87
Q

Specific TLRs: What does TLR 4 bind to?

A

Gram Negative Bacteria

Specifically - lipopolysaccharide, part of the bacterial cell wal

88
Q

Describe the role monocytes

A

Make up 5% of blood
Lifespan: months
Play an important role in innate (phagocytosis) and adaptive (antigen presentation) immunity

89
Q

What role do macrophages play in the immune response?

3 THINGS

A

The first line of non-self-recognition
Main role is to remove foreign (microbes) and self (dead/tumour cells)
Present antigens to T cells
Release cytokines to attract other immune cells

90
Q

What do eosinophil granules contain? What does this do?

A

Contains Major Basic Protein, which

Activates neutrophils
Induces histamine release from mast cells
Provokes bronchospasm

91
Q

What cells is known as the professional antigen presenting cells

A

Dendritic cells

92
Q

What is IgM

A

Makes up 4% of antibody population
1st antibody response made
Can be made without T cell response
Most effective at activating complement pathway

93
Q

What is IgG?

A

Most abundant antibody in serum makes up 75%
Serves as an opsonin: helps phagocytes bind to pathogen and makes it easier for phagocytosis to occur
Activates the common complement pathway
Helps NKC’s to kill viruses

94
Q

What is IgA?

A

Makes up 20% of antibody population in serum
Serves as an opsonin
Main antibody found in mucosal sites and prevents pathogens entering the body
Forms IgA1 and IgA2
Babies receive lots if IgA in breastmilk

95
Q

What is IgE?

A

Makes up 0.004% of antibody population in serum
Associated with allergic and anti-parasitic responses
Triggers granule release when binding to basophils, Eosinophils and mast cells
Triggers inappropriate release of histamine granules in allergic reactions

96
Q

What is IgD?

A

Makes up 1% of the serum antibody population
Found with IgM

Helps mature B cells leave the Bone marrow

97
Q

Specific TLRs: What does TLR 7 and 8 bind to?

A

Viruses

98
Q

Specific TLRs: What does TLR 9 bind to?

A

Bacteria and DNA viruses

TLR 9 is an intracellular PAMPS

99
Q

What are the 5 main classes of antibody?

What is the main type? What one is made first?

A

5 distinct classes

IgG
IgA
IgM
IgD
IgE

But IgG is the main type
IgM is made first

100
Q

What is the basic structure of antibodies?

A

Has a four-chain structure; two identical heavy (H) chains and two
identical light (L) chains

101
Q

Where are the complement proteins produced?

A

The Liver

102
Q

What are the 3 complement pathways:

A

The classical pathway (discovered first)
The alternative pathway (always at work)
Lectin Binding pathway

103
Q

What does C1 do? (Classical pathway)

A

C1 proteins bind two or more antibodies, leading to activation
.
Activated C1 then cleaves C4 and C2, which combine to from C3 Convertase, on the surface of the Pathogen

C3 convertase activates C3, making C3a and C3b

104
Q

The classical pathway: What does C3b do?

A

C3b is an opsonin - They bind to the antiphagocytic capsule around the pathogen, making it easier and quicker to be phagocytosed

It also cleaves and activate C5, producing C5b

105
Q

The classical pathway: What does C5b do?

A

Reacts with C6,7,8,9 to form the membrane attack complex (MAC)

106
Q

Lectin Binding pathway: How is it triggered? What is mannose

A

By Mannose binding lectin protein
Mannose is a sugar that is very commonly found in the cell walls of pathogens

107
Q

Lectin Binding pathway: What does Mannose binding protein do?

A

It activates C2 and C4 into C3 convertase, like C1 does in the classical pathway.

108
Q

Outline how the alternative pathway is activated, and what happens in it

A

Usually activated by bacterial endotoxin, a lipopolysaccharide present on the outer membrane of gram negative bacteria.

This results in spontaneous hydrolysis of C3 into small amounts of factor C3b, which combines with other factors to produce C3 convertase.

C1 inhibits it

109
Q

Outline the two main roles of
C3a, C4a, and C5a

A
  1. promote synthesis of pro-inflammatory cytokines.
  2. They bind to mast cells and basophils to cause degranulation, and The histamine and serotonin released increase vascular permeability

They are complement components responsible for causing inflammation

110
Q

What are the 3 main outcomes that can be brought about by the complement pathway?

A
  1. Formation of MACs - (C5b - activating MACS with C6 C7, C8, C9)
  2. Opsonisation of pathogens - (C3b)
  3. Lead to the Formation of chemokines, for Chemotaxis (C3a, C4a, C5a,)
111
Q

What are MACs? How are they harmful to bacteria

A

Membrane attack complex, formed by the joining of C5-9 on the cell membrane of bacteria

MAC is a leaky pore like channel. Ions and water pass through the channel and disrupt the intracellular microbe environment -> microbe lysis.

112
Q

Which complement plasma proteins are pro-inflammatory and cause chemotaxis and activation of neutrophils and monocytes etc?

A

C3a and C5a.

113
Q

Which complement plasma proteins have opsonic properties when bound to a pathogen?

A

C3b

114
Q

Outline the main complement proteins - what activates what?

A

C1 –> C2 +C4 –> C3 CONVERTASE – C3A (CHEMOTAXIS) AND C3B (OPSONIN)

C3B OPSONISATION, AND CLEAVES C5 —-> C5A AND C5B C5A (CHEMOTAXIS) C5B —. REACTS WITH C6,7,8,9 TO FORM MACS

115
Q

Define Opsonisation

A

Opsonisation - the process where molecules bind to a pathogen, making it more palatable to the phagocyte, for easier phagocytosis

C3b binds to the pathogen, easier for phagocytes to grab

116
Q

Outline what hypersensitivity is

A

The over-reaction by the immune system to things you don’t need to react to
* Refers to diseases in which immune responses to the environmental antigens
cause inflammation and damage to the body itself

117
Q

What is a cytokine?

A

Soluble proteins secreted by lymphocytes or macrophages/monocytes
that act as stimulatory or inhibitory signals between cells

118
Q

Give some specific examples of PAMPs that macrophages may recognise

A
  • Peptidoglycan
  • Lipopolysaccharide
  • Lipoteichoic Acid

^^^ All in bacteria cell walls

or
- Flagella proteins
- Mannan

^^ in Fungal wall

  • Viral RNA or DNA
119
Q

Name some cells with PRRs

(5)

A

Macrophages
Neutrophils
Eosinophils
Basophils
Mast Cells

120
Q

What are the two types of PRRs

A

Phagocytic PRRs - Bind and eat pathogen (do not release cytokines)
Signalling PRRs - Release Cytokines - to send reinforcements, but don’t phagocytose

121
Q

Where are TLRs found?

A

Found on all Leukocytes, as well as Endothelial cells and epithelial cells

They pick up PAMPs and DAMPs

122
Q

Where would you find TLRs 1,2,4,5 and 6? What do they bind to?

What do they lead to the release of?

A

Find them on the cell surface - Bind to PAMPs such as
- Peptidoglycan
- Lipopolysaccharide
- Flagella proteins
PLF

Secrete Interferon alpha and beta ===> Viral resistance

123
Q

Where would you find TLRs 3,7,8 and 9? What do they bind to?

What do they lead to the release of?

A

In the cell - bind to intracellular PAMPs - eg Viral RNA

secrete chemokines, to attract immune cells, eg TNF-a

124
Q

What happens when the TLRs within the cell get activated?

A

When activated they lead to the stimulation of pro inflammatory cytokines such as
TNF-a
Il-1b and IL-6

Which leads to Vasodilation, more leukocytes to the site and fever

125
Q

What happens with TLRs get activated? (Intracellular)

A

activate chemokines eg TNF-a

126
Q

What antibody is involved in a type 1 hypersensitivity reaction?

A

IgE

127
Q

In an allergic reaction what do the T-helper cells differentiate in to?

A

Th2 cells

128
Q

What does interleukin 1 do?
What about Interleukin 2?

A

IL-1 is mainly involved in acute inflammation and inducing fever, vasodilation, hypotension - (mainly comes from macrophages)

IL-2 - main functions include: stimulates growth and differentiation of T cell response (so would be decreased in HHIV/AIDS)

129
Q

What helps a T-helper cell to differentiate into a Th2 cell

A

interleukins: IL-4, IL5, IL-10

130
Q

What interleukin released by TH2 cells causes B-cells to release IgE antibodies?

A

IL-4

131
Q

What interleukin released by TH2 cells stimulates production of eoisnophils In a Type I hypersensitivity reaction?

A

IL-5

132
Q

What receptors do IgE antibodies bind to on mast cells?

A

Fc receptor

Its name is derived from its binding specificity for a part of an antibody known as the Fc (fragment crystallizable) region.

Fc receptors bind to antibodies that are attached to infected cells or invading pathogens.

133
Q

What happens when a sensitised mast cell (one that’s binded with IgE) binds to a previously seen antigen e.g., pollen

A

It degranulates and releases pro-inflammatory molecules e.g, histamine

134
Q

What receptors does histamine bind to? What does this lead to?

A

H1.
Bronchoconstriction
- Vasodilation
- Increased vascular permeability (which causes swelling and hives and redness)

135
Q

What happens 8-12 hours after an allergic reaction?

A

Leukotrienes LTB3, LTB4 are secreted by immune cells
Cause smooth muscle contraction
Causes signalling to other immune cells to aggregate in the area

136
Q

What cells are the primary cause of a type II hypersensitivity reaction?

A

B-cells

137
Q

What antibodies are secreted in type II hypersensitivity reaction?

A

IgG, IgM

138
Q

What are the two types of antigens attacked on cells by antibodies in a type II hypersensitivity?

A

Intrinsic (antigens normally produced)
## Extrinsic (things that have become attached to cells e.g., drugs)

139
Q

What is it called when an antibody binds to an antigen? When is this a problem?

A

Antigen-antibody complex, is an issue when this happens to host tissue

140
Q

Type I - what Interleukins are involved, and what do they do? What does IL-4 and IL-5 do, specifically?

A

IL-4, IL-5, IL-10, prime the niave T cells into becoming TH2 cells

IL-4 causes B cells to switch from making IgM to making IgE antibodies, that are specific to the antigen that triggered the reaction

IL-5 causes the activation and degranulation of Eosinophils

141
Q

Type I hypersensitivity - what does the secreted IgE do?

A

Binds of FCe receptors on mast cells activating them so they can recognise the allergen again next time it comes in, and degranulate

142
Q

Type I hypersensitivity - When mast cells degranulate and release proinflammatory mediators, what does this cause?

What do Leukotrienes do?

A

The release of Histamine that binds to H1 receptor leads to:
- Bronchi Smooth muscle contraction ==> Leads to difficulty breathing
-Blood vessel dilation => Leads to more vasclar perembaility, so oedma and hives

Leukotrienes (specifically LTB4 and LTC4) facilitate communication that causes smooth muscle contraction and attracts more immune cells

143
Q

What is a feature of type II hypersensitivity?

A

Tissue specific antibodies lead to the destruction of SPECIFIC ORGANS

In General it is Cytotoxic
Antibody mediated

144
Q

Type II Hypersensitivity: What is central tolerance?

A

When immune cells that are self-reactive to your body cells get destroyed

145
Q

Type II Hypersensitivity: What happens, because central tolerance isnt perfect?

A

Imperfect central tolerance means that escpated self reactve B cells become activated and secrete IgM or (with the help of T helper cells) secrete IgG

146
Q

Type II Hypersensitivity: What does the IgM and IgG do when it is released from self reactive immune cells? What does it go on to form?

A

Binds to antigens on your own normal cells, Either on:

Intrinsic Antigens: Antigens normally made by host
Extrinsici Antigens: Antigens that are attached on self-cells from outside the body (eg penicillin medication that binds to the surface of a RBC)

Which creates a Antigen-Antibody Complex. This is normal in infection , but problematic when this happens on a host tissue, like in Type II reactions

147
Q

What specific disease can occur when specific cells are targeted in type II hypersensitivity?

A

==> The attacking of certain cells can lead to Haemolytic Anaemia, Thrombocytopaenia, or Neutropoenia. Or, antibodies binding to basement membrane can lead to Goodpasture’s Syndrome , seen in the Kidney or Lung

148
Q

Type II Hypersensitivity: Now a Antigen-Antibody Complex has formed on a host tissue, cytotoxic mechanisms become activated - What will the complement pathway cause?

A

The 3 Complement things

Complement System C1 binds to the Fc portion of the antibody. The 3 outcomes of Compliment system happens

149
Q

Type II Hypersensitivity: If you suspect Haemolytic anaemia, what test can you use?

A

Coombs test: RBCs are mixed with Coombs reagent.

If Agglutinates, then antibodies are present

(Agglutinates - the formation of clumps of cells)

150
Q

Type II Hypersensitivity: What do Natural killer cells do?

A

They recognise the Fc tail of the antibodies that have tagged the bodies own cell, and destroy this cell by punching holes in it and releasing granzymes

151
Q

Type III Hypersensitivity: What are Immune complexes

A

They are a molecule formed from the binding of multiple SOLUBALE antigens to antibodies.[1]

The bound antigen and antibody act as a unitary object

152
Q

Type III Hypersensitivity: Using Lupus as an example, what happens to the DNA, and what forms?

A

Escaped Self B cells take DNA that has come from an old body cell, and takes a bit of it, forming an AUTOANTIGEN (an antigen that has come from the body)

Triggers B cells to make specific IgG autoantigen to the DNA

153
Q

Type III Hypersensitivity: Because the autoantigens are small and soluble in the blood, what do they end up doing?

A

They float and get stuck in the basement membrane of vessels, which activates the compliment system.

Leads to increased Vascular permeability, leading to oedema
C5a,4a,3a cause chemotaxis, causing macrophages to try and phagocytose vessel wall with autoantigen - LEADING TO VASCULITIS, leading to more leakage of DNA for example, so the process starts again

154
Q

Type III Hypersensitivity: Where in the body does Vasculitis seen in Type III Hypersensitivity most often occur?

A

Basement membranes in the Kidney - Glomerulonephritis
Joints, in synovial fluid - Arthritis

155
Q

What makes a T cell naive?

A

The fact that their T cell receptor hasn’t bound to a specific antigen yet.

156
Q

Type IV Hypersensitivity: What do T helpers do when they become activated?

A

T Helper cells become activated by an antigen (eg poison ivy molecule)

Th1 cells release IL-2 which proliferate/duplicate, and then release interferons that lead to macrophages that:

release proinflammatory cytokines, (TNF, IL-1, IL-6) leading to leaky endothelial membranes –> More immune cells at the site ==> oedema, redness, fever

ROS, lysosomes that attack the site

Th17 cells triggered neutrophil recruitment

157
Q

Type IV Hypersensitivity: What do T Cytotoxic do when they become activated?

A

Attack the target self cells that present the specific antigen - eg in Type 1 diabetes, where immune cells attack islet cells in the pancreas

158
Q

Outline Type I Hypersensitivity, in an essence. Give an example of it and the reactant involved.

A

Mast-cell activation releases histamines and other mediators, IgE,

Anaphylaxis

159
Q

Outline Type II Hypersensitivity, in an essence. Give an example of it and the reactant involved.

A

Antigen EMBEDDED IN HOST CELLS cause complement activation and destruction by MAC.
IgG,

Acute Transfusion reactions

160
Q

Outline Type III Hypersensitivity, in an essence. Give an example of it and the reactant involved.

A

Antibody BINDS TO SOLUABLE ANTIGEN, forming a circulating immune complex lodges in a vessel wall and causes a local inflammatory response.

IgG,
Rheumatoid Arthritis, Vasculitis, Glomerulonephritis

161
Q

Outline Type IV Hypersensitivity, in an essence. Give an example of it and the reactant involved.

A

Antigen presenting cells activates Th1/Cytoxic T cells. T cells activation macrophages and cause an inflammatory response.

T Cells

Contact Dermatitis (to Nickel/Poison Ivy), Mantoux tuberculin test, T1DM, Hashimotos Thyroiditis

162
Q

What test can diagnose contact delayed Type IV hypersensitivity reactions, to things such Nickel??

A

The patch test

163
Q

Talk through the Pathophysiology of immune anaphylaxis, 1st exposure

A

1st exposure to allergen: Th2 cells are primed, and the release of IL-4 causes B cells to switch their production of IgM to IgE antibodies.

IgE antibodies bind to mast cells and basophils. The cells are now sensitised to the allergen.

164
Q

Talk through the Pathophysiology of immune anaphylaxis, 2nd exposure

A

On the Second exposure, : Cross linkage of the antigen-specific IgE antibody bound to the sensitised cells causes mast cell degranulation and release of various mediators (leukotrienes, histamine and prostaglandins).

This causes widespread vasodilation, bronchoconstriction and increased permeability of vascular endothelium

165
Q

What happens in non immune anaphylaxis?

A

Not caused by any IgE antibodies

  • Due to direct mast cell degranulation
  • Some drugs/food are recognised to cause this
  • No prior exposure needed
  • Clinically identical to immune anaphylaxis
166
Q

Anaphylaxis - how do you treat it?

A

Commence basic life support ; A (airway), B (breathing), C (circulation)

Specific treatment:
- STOP DRUG if infusion
- Adrenaline 1mg (10mls of 1:10,000 (IV)) 1ml IV increments -
note: if cardiac arrest then may need to give cardiac massage in
order to get drugs circulating
- IV Anti histamine (Chlorphenamine 10mg)
- IV Hydrocortisone (100 to 200mg) - note: unlikely to cause harm
in excess so can’t really give too much
* Effect of adrenaline:
- Vasoconstriction, bronchodilation & increased cardiac output

167
Q

What is the precise dose of adrenaline that you give in anaphylaxis?

What is the MOA of adrenaline here?

A

Adrenaline IM / 0.5mg / 1 in 1,000

Stimulation / agonist of beta adrenergic receptors

168
Q

Name some physiological responses in the body to the mediators of anaphylaxis

A

Vasodilation,
Increased vascular
permeability
tachycardia
hypotension
maximise blood glucose levels in brain

All of these responses occur due to stimulation of beta-adrenergic receptors

169
Q

What are some risk factor for anaphylaxis?

A

<30 years old
Having a history of anaphylaxis
Having allergies/asthma

Atopy - the genetic tendency to develop allergies

Being female

170
Q

What blood test would you use to look for anaphylaxis?

A

Serum mast-cell tryptase

Tryptase - can show mast-cell degranulation (histamine elevation, only lasts a short amount of time).

Levels of serum tryptase, which is a mast-cell specific protease, peak at one hour after an anaphylactic reaction, remaining elevated for approximately six hours.

Elevated serum tryptase levels imply either massive mast-cell degranulation, as occurs in anaphylaxis, or a condition such as mastocytosis.

However, not every case of anaphylaxis causes a rise in tryptase - both the sensitivity and specificity are around 95%.

171
Q

Recap - name the toll like receptors that are found on the cell surface.

A

TLRs 1,2,4,5,6

172
Q

Recap - name the toll like receptors that are intracellular

A

TLRs 3,7,8,9

Phase 2a Sam (18 decks)

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