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Immunology Flashcards

1
Q

What are the 4 main factors that contribute towards inflammation

A
  • Dolor (pain)
  • Color (heat)
  • Tumor (swelling)
  • Rubor (redness)
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2
Q

WHat molecules do Mast cells secrete?

A
  • Histamines (mostly)
  • Leukotrienes
  • Prostaglandins
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3
Q

Describe how factor 12 is involved in the production of bradykinin?

A

XII is converted to prekalikiran which is then converted to kalikiren. Kalikiran then converts kininogen into bradykinins

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4
Q

What does PLA2 break down?

A

Phospholipids into arachadonic acid

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5
Q

What can arachadonic acid be converted into?

A
  • Leukotrienes (from lipooxygenase, LPO)

- Prostaglandins (from COX 1, 2)

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6
Q

What does lipoxygenase (LPO) convert arachadonic acid into?

A

Leukotrienes

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7
Q

What enzyme converts arachadonic acid into prostaglandins?

A

COX-1 and 2

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8
Q

What are the preformed granules found inside endothelial cells called?

A

weibel palade bodies (these are stimulated by local inflammatory cytokines and cause selectins to become active)

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9
Q

How can plasma leak out of the capillaries?

A

Local inflammatory cytokines bind to endothelial receptors causing them to contract, this creates spaces between the cells creating leaks

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10
Q

What causes nociceptor activation

A

Fluid pressing on them and bradykinin

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11
Q

What do white blood cells attach to on endothelial cells?

A

P selectins

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12
Q

What is the process called where WBCs roll along the endothelial cell surface on P selectins?

A

Margination

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13
Q

What do WBCs attach to during diapedesis?

A

P-CAMs?

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14
Q

What is positive chemotaxis?

A

When chemokines hit a specific point on WBCs which cause the WBCs to migrate to where the chemokines were coming from

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15
Q

What can cause the expression of E-selectins?

A

IL-1 and TNF-alpha, monocytes and neutrophils bind to it on the endothelium

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16
Q

What does IL-8 stimulate?

A
  • Activates cell to create ICAM and VCAM
  • Activates integrins on neutrophils - prefectly interacts with VCMA and ICAM on endothelium
  • Neutrophil undergoes diapedisis, and then positive chemotaxis
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17
Q

What do IL-1 and TNF-alpha cause the hypothalamus to produce?

A

PGE2 - initiating fever

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18
Q

What does IL-6 cause the production of?

A

Acute phase reactant proteins (C-reactive protein)

- Also Il-1 and TNF-a contribute

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19
Q

What does IL-1 and TNF-alpha cause in bone marrow?

A

Leukocytosis

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20
Q

What is a phagosome?

A

A vesicicle inside a phagocyte containing the actual bacteria

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21
Q

What do lysosomes contain?

A

Hydrolytic enzymes which break down the bacteria

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22
Q

What do the hydrolytic enzymes in phagolysosomes do to bacteria?

A

Break down cell wall and inner cell structures

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23
Q

What are the 3 types of antigen presenting cells?

A
  • B-cells
  • Macrophages
  • Dendritic cells
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24
Q

What does the neutrophil do with antigens inside the phagolysosome?

A
  • May exocytosis them into the interstitial fluid
  • Neutrophil may sacrifice itself with free radicals (oxidative burst)
  • May release DNA/chromatin which can bind onto foreign bacteria (NETS)
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25
Q

What condition can

Neutrophil extracellular traps (NETS) cause?

A

SLE

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26
Q

Give an example of an enzyme which may degrade bacteria in a
Neutrophil extracellular trap?

A

Cathepsin G

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27
Q

What cells contain MHC II?

A

Antigen Presenting Cells

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28
Q

What chromosome contains MHC-I?

A

Chromosome 6

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29
Q

What cells contain MHC-1?

A

All nuceated cells

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30
Q

What are NETS made up of?

A

Neutrophil chromatin

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31
Q

Through what mechanism can MHC molecules from macrophages be able to produce MHCs of different shapes?

A

Recombination

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32
Q

What is present on the surface of MHC-II?

A

Antigen

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33
Q

What do MHC-1 molecules have on them?

A

A self antigen

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34
Q

What are the 3 types of MHC 1 genes?

A

A B and C

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35
Q

What are the 3 types of MHC-2 genes?

A

DP, DQ, DR

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36
Q

Why are MHC genes clinically relevant?

A

When doing transplants there must be at least 6 MHC matches

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37
Q

What organ produces complement proteins?

A

Liver

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38
Q

What are the 3 pathways of the complement system?

A
  • Classical
  • Alternative
  • Lectin
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39
Q

What protein binds to the antibody on the bacteria in the classical pathway?

A

C1

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40
Q

What does C3 convertase split C3 into? What do they do?

A

C3a and C3b

  • C3a breaks off and acts as a chemotactic agent
  • C3b stays
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41
Q

What is the order of complement proteins?

A

C1, C4, C2, C3b, C5b, C6, C7, C8, C9

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42
Q

What 2 proteins act as chemotactic agents in the complement pathway?

A
  • C3a

- C5a

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43
Q

What do proteases released by the mast cell do to the complement system?

A

Activate C3a and C5a

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44
Q

What proteins in the complement system break off to create the MAC?

A

C5b, C6, C7, C8, C9

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45
Q

What shape is the Membrane Attack Complex?

A

Cylindrical pentameric protein

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46
Q

How does the MAC work?

A

Attaches to bacterial membrane - causes lysis through the influx of H2O, Na+ etc.

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47
Q

What does C3b act as?

A

An opsonin (makes phagocytosis of bacteria easier)

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48
Q

What is the receptor on the phagocyte called that interacts with C3b?

A

C3b receptor

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49
Q

What protein binds directly to the bacterial antigen in the alternative pathway?

A

C3b

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50
Q

What other protein is involved in the alternative pathway?

A

Factor B (technically joins C3b to C5b)

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51
Q

What does lectin bind to on the cell surface of bacteria?

A

Manose (antigen)

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52
Q

What complement protein binds to lectin in the lectin pathway?

A

C4 (C1 only classical protein not involved)

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53
Q

What are toll-like receptors?

A

Proteins on cell membrane or vesicles that respond to foreign pathogens (PAMPs) and elicit specific responses

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54
Q

What are interferons?

A

Signal nearby host cells to alert them of a virus signalling them to make anti-viral peptides, also can trigger NK cells and macrophages to become active and proliferate

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55
Q

What transcription factor can cells secrete when damaged by a virus?

A

IRF

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56
Q

What does the IRF transcription factor activate?

A

Interferons (IFN) (alpha, beta and gamma)

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57
Q

WHat are the 3 types of interferons (IFN)?

A
  • Alpha
  • Beta
  • Gamma
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58
Q

What interferon is not usually secreted by generalised tissue cells?

A

IFN-gamma (only in certain immune cells)

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59
Q

What do interferons activate?

A

Protein kinase R (in a cell beside it)

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60
Q

What does protein kinase R do?

A
  • Cleaves viruses and anti-viral peptides prohibiting the virus from entering other cells
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61
Q

What does IFN-gamma activate on other macrophages?

A

Proliferation (mitosis, and get bigger and MHC 1 and 2 molecules are expressed more)

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62
Q

What are the functions of IFN- alpha and Beta?

A
  • Activation of protein kinase R

- Activation of NK cells

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63
Q

Describe the mechanism of a NK cell?

A
  • NK cell can notice and kill cells with a downregulation of self-antigens (MHC-class Is) (this is usually due to viral infection or cancer)
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64
Q

What type of interferons can platelets produce?

A

IFN - Beta

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65
Q

What are the 3 mechanisms by which NK cells can notice a cell that needs to be killed?

A
  • Lack of MHC class I molecule
  • IgG bound
  • Has Mica
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66
Q

What common infections can be treated with interferons?

A
  • HSV
  • HPV
  • Multiple Sclerosis
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67
Q

How many toll-like receptors are there?

A

11 (function of 10 not really known)

68
Q

What can stimulate Toll-like receptors 1 and 2 to dimerise causing an intracellular cascade?

A
  • Lipoproteins

- Gp1 anchoring proteins -> Parasites

69
Q

What can stimulate TLR-2 and TLR-6?

A
  • Zymosin (from fungi)

- Lipoteichoic acid (gram +ve)

70
Q

What can stimulate TLR-4 dimerisation?

A

Lipopolysacharides on gram -ve

71
Q

What can stimulate TLR-5 dimerisation?

A

Flagellin (e.g E.coli)

72
Q

What can stimulate TLR-11?

A

Bacteria within urogenital system

73
Q

What TLRs are present on the cell membrane?

A
  • TLR-1 + 2
  • TLR-2 + 6
  • TLR-4
  • TLR-5
  • TLR-11
    1, 2, 4, 5, 6, 11
74
Q

What TLRs are present on the endosome inside the cell?

A
  • TLR-3
  • TLR-7
  • TLR-8
  • TLR-9
75
Q

What does TLR-3 respond to?

A

Double-stranded RNA

76
Q

What does TLR-9 respond to?

77
Q

What does TLR-7 respond to?

A

Single stranded RNA

78
Q

What does TLR-8 respond to?

A

single stranded RNA

79
Q

What do all the intracellular cascades from the TLRs result in?

A 
Activate transcription factors
- AP1 transcription factor 
- IRF 
- NFkB (nuclear factor kappa beta)
Stimulates production of proteins which ultimately enhance the immune response
80
Q

What does AP1 stimulation by TLRs result in?

A

Synthesis of protein signalling molecules

81
Q

What does IRF stimulation by TLRs result in?

A

Interferons (IFNs)

82
Q

What does NFkB stimulation by TLRs result in?

A

Synthesis of cytokines (TNF-alpha, IL-1B, IL-18), some may still need to be activated

83
Q

What antibodies lie on B cell receptors?

84
Q

How can B cell receptors be formed with different shapes to fit diferent antigens?

A

DNA recombination

85
Q

What is receptor mediated endocytosis?

A

The mechanism where a B lymphocyte makes pseudopodes and binds clatherins to create an endosome with the receptor and foreign antigen inside

86
Q

How does the B lymphocyte create an MHC-II molecule that fits perfectly to the endocytosed antigen?

A

Through recombination

87
Q

What is the difference between a naive and activated (antigen-presenting) B-lymphocyte?

A
  • Naive B lymphocyte contains B cell receptors (BCR)
  • Activated B-lymphocytes contain BCRs and an MHC-II molecule with an exposed antigen on the membrane surface being presented
88
Q

What does the dendritic cell (Antigen presenting cell) present its foreign antigen to?

A
  • Naive T helper (CD4+) cell
89
Q

What is the protein on the naive T helper cell called that binds to the antigen on the dendritic cell?

A

T cell receptor

90
Q

What is the protein on the naive T helper cell called that binds to the MHC-II on the dendritic cell?

A

Cluster of differentiation 4 (CD4) protein

91
Q

What protein does the B7 from the dendritic cell interact with on the T helper (CD4+) cell?

92
Q

What protein is activated by the binding of the foreign antigen and t cell receptor and also MHC-II and CD4+?

93
Q

What does CD3 do?

A

Primary signal

94
Q

What does the interaction of the B7 and CD28 cause?

A

Costimulation

95
Q

What does the macrophage produce after the primary and costimulation signals are triggered?

A

IL-1 - this binds on to another receptor causing a third signal

96
Q

What are the 3 signals which cause the T helper (CD4+) cell to become activated?

A
  • Primary signal
  • Costimulation signal
  • 3rd signal?
97
Q

What interleukin is produced by the T helper cell through the signals from the dendritic cell and binds on to a receptor on the same cell?

A

IL-2 (autocrine)

98
Q

What cytokines are produced by the T helper cells through the binding of the autocrine IL-2?

A
  • IL-5

- IL-4

99
Q

What can a naive T helper cell turn into?

A
  • T helper 1 cell

- T helper 2 cell

100
Q

What interleukin is required to turn a naive T helper cell into either Th1 or Th2 cell?

A
  • Th2 requires IL-4 (and IL-2)

- Th1 requires IL-12

101
Q

What proteins are produced by Th2?

A
  • IL-2
  • IL-4
  • IL-5
102
Q

What proteins are produced by Th1?

A
  • gamma-IFN

- TNF-alpha

103
Q

What do IL-4 and 5 do?

A

Clonal expansion -> Activates B lymphocytes

  • They have BCRs specific to the foreign antigen
  • Also MHC-II molecules with the foreign antigen

IL-5 activates the B cells causing them to differentiate into plasma cells or memory B cells (all have specific B cell receptors ready to respond to antigen)

104
Q

What are the different mechanisms of action of antibodies?

A
  • Neutralisation
  • Precipitation
  • Lysis (through MAC)
  • Agglutination (antigen antibody complex)
  • Opsonisation (directly or through complement)
105
Q

What is the humoral immunity response?

A

The process by which antibodies are made etc. (a branch of the selective immune system)
- Involves T helper cells which destroy external foriegn pathogens (freely circulating antigens)

106
Q

What do T-cytotoxic cells (CD8+) recognise?

A
  • MHC-I through CD8+

- Antigen through TCR (T cell receptor)

107
Q

How can T cytotoxic cells recognise a virally infected or cancerous T cell?

A
  • The virus can produce proteins inside a native cell which then get shown as a self-antigen on the MHC-I
  • The TCR recognises this and produces perforins and granzynes
108
Q

What do perforins do?

A

Produce holes in the cell membrane

109
Q

What do granzynes activate?

A

Activate pro-apoptotic genes

110
Q

Give an example of a pro-apoptopic protein?

111
Q

How does BAX function?

A

BAX binds on to BCL2 in the mitochondria - pulling it into the cytoplasm
- This allows cytochrome C to enter the cytoplasm from the mitochondria activating caspases which cause apoptosis

112
Q

What cell causes cell-mediated immunity?

A

Cytotoxic T cells (CD8+)

113
Q

What are the 3 ways by which NK cells can identify cells it needs to kill?

A
  • No MHC-I
  • MICA present
  • IgG
    Secretes perforins and granzymes (same mechanism as CD8+ cells)
114
Q

What components make up MHC molecules?

A

Alpha 1, 2 3 and Beta 2

115
Q

What do MICA molecues lack?

A

Beta 2 (otherwise identical to MHC)

116
Q

What are the different types of antibody?

A 
5 types 
- IgG
- IgA
- IgM
- IgE
- IgD 
GAMED
117
Q

What is the most abundent antibody?

A

IgG (65-70% found in blood plasma)

118
Q

What organelle is large in the plasma cell?

A

Rough endoplasmic reticulum

119
Q

When is IgG more abundent, in the primary or secondary immune response?

120
Q

What is neutralisation?

A

When antibodies (IgG) bind to a pathogen making it unable to bind to human cells

121
Q

What is it called when an antibody binds to a free antigen making phagocytosis easier?

A

Precipitation

122
Q

How can a baby get IgG antibodies from their mother?

A

Through the placenta

123
Q

In what structural form is IgA present?

A

Dimer (2 linked)

124
Q

In what areas are IgA antibodies abundant?

A
  • Saliva
  • Skin (sweat)
  • Mucosal lining of GI tract
  • Milk (lactation)
    Bodily fluids - the antibody can attach to 2 pathogens at once
125
Q

What are the 2 structural forms IgM can exist in?

A
  • Pentameric (5) form

- And monomeric form

126
Q

What protein connects the pentameric structure of IgM?

127
Q

When are IgM antibodies made?

A

During the primary immune response

128
Q

What antibody causes agglutination of erythrocytes?

A

IgM pentamer (type 2 hypersensitivity reaction)

129
Q

How many antigen binding sites do IgM pentamers have?

130
Q

Where can you find IgE?

A
  • Respiratory tract mucosa
  • Urogenital structures
  • Lamina propria and lymphatic tissue
  • Small amount in blood plasma
131
Q

What are the receptors on the mast cell called and what binds on to it?

A

FCER1 receptor IgE monomer binds to it (only form of IgE is a monomer)

132
Q

What antibody is involved in allergies?

A

IgE (binds to mast cell which releases Leukotrienes, prostaglandins, histamines)

133
Q

What is the effect of Mast cell degranulation on resp. tract?

A
  • Vasodilate blood vessels and make them more permeable (can cause restriction of airway)
  • SM contraction also restricting airway
    This effect is called type 1 hypersensitivity reaction aka anaphylaxis
134
Q

What antibody would be used to fight a parasite in the GI tract and how would the mechanism work?

A

IgE

- Attracts/activates eosinophils which then attack parasite

135
Q

What is the structure of IgD?

136
Q

Where are IgD antibodies found?

A

On the surface of plasma cells (B cell receptor)

137
Q

What antibodies can act as B cell receptors?

138
Q

How long is the ‘lag period’ during the primary immune response?

139
Q

What antibody is produced first after the ‘lag period’ during the primary immune response?

140
Q

What antibody is produced after the IgM in the primary immune response?

A

IgG when there is a shift from IgM to IgG it is called somatic hypermutation

141
Q

What antibdies are produced in the secondary immune response?

A

No lag period - small amount of IgM and large amount of IgG produced

142
Q

What are the 2 types of immunity called?

A
  • Passive immunity

- Active immunity

143
Q

What is an example of naturally acquired passive immunity?

A
  • IgG from placenta

- IgA from milk

144
Q

What is an example of artificially acquired passive immunity?

A
  • Immunoglobulins (antibodies) against pathogen (e.g anti-venom)
145
Q

What is an example of naturally acquired active immunity?

A
  • Actually being infected by the pathogen
146
Q

What is an example of artificially acquired active immunity?

A

Vaccines / booster shots

147
Q

Structure of antibody

148
Q

What bonds keep the structure of the antibody?

A

Disulfide bonds

149
Q

Where are T cells produced?

A

Within the red bone marrow

150
Q

Where is the thymus located?

A

Within the mediastinum anterior to the heart

151
Q

What is a primary lymphoid organ?

A
  • Bone marrow

- Thymus

152
Q

When does the thymus activity start to decline?

A

Early adolesence

153
Q

What chemotactic agents does the thymus produce?

A
  • Thymosin
  • Thymotaxin
  • Thymopoetin
  • Thymic factors
154
Q

How does the thymus attract the T cells?

A

Through chemotactic agents

155
Q

What do T cells produce in response to Thymic chemotacic agents?

A

RAG1 and RAG2
- Recombinases which produce different types of TCRs

Activate CD4&8 proteins

156
Q

What do RAG1 and 2 cause the production of?

A

TCR

- T cell receptor

157
Q

What happens if a T cells CD8s and CD4s are not recognised by the thymic cells MHCI and II?

A
  • Thymic cells secrete FAS which binds to a receptor on the T cell triggering apoptosis
  • This process is called positive selection
158
Q

What happens if the TCR on the T cell recognises the self peptides on the thymic cell?

A

Triggered to undergo apoptosis through FAS

  • Process is called negative selection
159
Q

What happens if the T cells CD4s recognise the MHC-II but they CD8s do not interact with the MHC-I?

A

T helper cell created

- The CD4 molecules are upregulated and CD8s are downregulated

160
Q

What happens if the T cells CD8s are recognised by the MHC-I but the CD4s are not recognised by the MHC-II?

A

Cytotoxic T cell created

- CD8s upregulated and CD4s are downregulated

161
Q

How are T regulatory (suppressor) cells created?

A
  • Created from T helper and cytotoxic T cells
  • Differentiation caused by CD25 and IL-2
  • They contain TCRs as well as either CD4s or CD8s
162
Q

What is the function of T regulatory cells?

A

They prevent autoimmune diseases by regulating CD4 and 8 cells

163
Q

Where are mature T cells located?

A

Deep part of cortex of lymph node

White pulp of spleen
- Form around sinusoidal capillaries creating periarteriolar lymphoid sheaths

164
Q

Where are the T regulatory cells located?

A

Concentrated in Hassal’s (thymic) corpuscles

165
Q

Stem cells of blood cells or whatever

166
Q

What interleukins activate NK cells?

A

IL-2 and IL-12

Barts - Foundations for Clinical Practice (2 decks)

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