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305 pharmacology > Immunology > Flashcards

Immunology Flashcards

1
Q

innate immune system

A

sentinel innate immune cells present in all externally exposed tissue detect DAMPs/PAMPs via TLRs to allow broadly-specific and consistent responses

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2
Q

DAMPs

A

damage associated molecular patterns

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3
Q

PAMPs

A

pathogen associated molecular patterns
(eg flagellin & lipopeptides)

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4
Q

Toll-like receptors

A

present in sentinel immune cells on surface and in vesicles/endosomes and bind PAMPs/DAMPs

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5
Q

Apoptosis (Immune)

A

triggered by NK/CTL (external) or DNA/mitochondrial (internal) signals
= cell shrinkage & chromatin condensation -> nuclear fragmentation & blebbing -> apoptotic body formation

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6
Q

Necrosis (Immune)

A

cell lysis caused by external (trauma, temp, ischaemia, NO, ROS, NK) or internal (viral) damage
= damage -> organelle/cell swelling, cell membrane ruptures, cell contents release (DAMPs)

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7
Q

innate immune response

A

sentinel cells produce inflammatory mediators in blood and surrounding tissue
- causes vasculature leakage, enabling immune cells to locate site of damage via inflammatory gradient
- complement proteins and antibodies bind microbes to neutralise and enable detection by neutrophils which phagocytose, and undergo apoptosis
- NK cells detect viruses/mutated cell surface structures, and release perforin and granzyme B to form pores causing apoptosis of infected cell

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8
Q

innate return to homeostasis

A

monocytes differentiate into macrophages which phagocytose complement/antibody-microbe complexes
- differentiate to produce IL-10, VEGG, TGFb to cease inflammatory actions and promote tissue repair

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9
Q

complement/antibodies

A

binds microbes to neutralise them and allows detection by neutrophils/macrophages

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10
Q

anti-inflammatory mediators

A

IL-10, VEGF, TGFbeta

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11
Q

adaptive immune response

A

defends against specific repeated threats

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12
Q

adaptive immune response activation

A

dendritic cells ingest proteins from pathogens and dying cells and process them into peptides, which are displayed on MHC complexes
DCs migrate to lymph node and present peptide-MHC complex to T helper and effector cells. T helper cells activate B cells.

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13
Q

B cells

A

exhibit specific antibodies, once antigen detected under go clonal expansion into
- antibody producing plasma B cells (amplification of response)
- memory B cells

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14
Q

antibodies

A

specialised proteins that recognise specific antigens
- contain a Fv region for specific recognition and Fc region for complement binding/Fc receptors on macrophages/NK cells

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15
Q

IgM

A

transient (allows detection of duration of infection)
governs initial recognition

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16
Q

IgG

A

longer-lasting specific antibodies, common drug target

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17
Q

IgA

A

antibody specific to GI and respiratory illnesses

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18
Q

IgE

A

allergic reactions

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19
Q

IgD/basophils

A

govern a different arm of allergic reaction that IgE

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20
Q

neutralisation

A

antibodies directly bind an antigen to block interactions
- IgM, IgG, IgA

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21
Q

complement fixation

A

antibodies bind complement to induce membrane attack complex, which forms pores in bacteria to cause death
- IgG, IgM

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22
Q

opsonisation

A

coating of pathogen with antibody and complement to increase recognition for phagocytosis
- IgG, IgM, + complement

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23
Q

antibody-dependent cellular toxicity

A

Recognition of IgG by NK cells causing perforin and granzyme B release to form pores and cause apoptosis

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24
Q

T cells

A

recognise peptide-MHC complexes to destroy pathogens (CD8/CTL) or help other immune cells (CD4)

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25
Q

activation of T cells

A

TCR binding to peptide-MHC complex
co-stimulation from CD80/86-CD28 and CD40-CD40L
co-stimulation from cytokines

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26
Q

activation of CD4 T cells

A

TCR binding to peptide-MHCII complex
co-stimulation from CD80/86-CD28 and CD40-CD40L
co-stimulation from cytokines (IFNa/b, IL-12)

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27
Q

action of CD4 T cells

A

differentiate into effector T helper (Th) cells which migrate to site of inflammation/MHC presentation through circulation

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28
Q

IFNy

A

cytokine produces by Th
promotes inflammatory response by activating macrophages and enhancing phagocytosis

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29
Q

IL4/13

A

cytokines produced by Th
activate eosinophils to kill parasites, and act of macrophages to promote tissue repair and fibrosis

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30
Q

IL-17/22

A

cytokines produced by Th cells
- promotes inflammatory response & recruits neutrophils to phagocytose bacteria & stimulates epithelial cell barrier responses

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31
Q

IL-10/TGFb

A

cytokines produced by Th cells
maintains and restores homeostasis by regulating other T cells, preventing self-reactive T cell action (autoimmunity)

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32
Q

Cytokines produced by Th Cells

A

IFNy, IL-4, IL-13, IL-17, IL-22, IL-10, TGFb

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33
Q

CD8 T cells/CTLs

A

TCR binding to peptide-MHCI complex
co-stimulation from CD80/86-CD28 and CD40-CD40L
co-stimulation from cytokines (IL-2)

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34
Q

CD8 T cell mechanism

A

detect infected cells, and release cytotoxic IFNy/TNFa/granzymeB/perforin to induce apoptosis

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35
Q

Immune disorders

A

hyper-stimulation of immune response by external (allergens/irritants) or internal (autoimmune) cues

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36
Q

immune co-morbidites

A

very high, as immune disorders result from an accumulation of genetic mutations/dysfunctional microflora

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37
Q

Th stimulation of B cell

A

TCR-MHCII
CD40L/CD40
IL-4, IL-6, IL-21

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38
Q

Types of Th cell that can induce inflammation and tissue damage

A

Th1, Th7, Th17

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39
Q

blood samples

A

used to isolate cells, proteins, and drugs circulating in blood. Centrifuge…
+ anticoagulant = erythrocytes, buffy coat, plasma
- anticoagulant = blood clot, serum

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40
Q

serum

A

contains water, hydrophilic drugs, nutrients, metabolic waste, and proteins (including cytokines and antibodies)

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41
Q

plasma

A

contains water, proteins (antibodies, cytokines), nutrients & metabolic waste, and electrolytes

42
Q

buffy coat

A

contains neutrophils, eosinophils, basophils, monocytes, lymphocytes, platelets, B Cells

43
Q

swabs

A

used to isolate live organisms, nucleic acids, proteins, and drugs in secretions
- live organisms (bacteria/viruses) can be cultured
- nucleic acids from dead cells, bacteria, and viruses can be detected by assay

44
Q

tissue biopsy

A

used to isolate whole disease tissue or live cells, proteins, or drugs from tissue
- tissue sections
- tissue homogenate

45
Q

tissue sectioning

A

tissue (from tissue biopsy) is obtained
- sliced by microtome
- fixed by freezing/paraffin fixation (cross-linking)
- contains fixed cells, nucleic acids, proteins to determine architecture

allows repeated analysis in cases of incorrect diagnosis
!! must reverse cross-linking before analysis!!

46
Q

tissue homogenate

A

tissue is homogenised by enzymatic reactions/sepharose beads/sonification
- contains live cells/proteins/chemicals + water
!! must apply protease inhibitor if looking at proteins to prevent protein degradation !!

47
Q

antibody testing

A

quick and accurate biochemical testing used to measure presence or concentration of a specific molecue

48
Q

analyte

A

specific molecule recognised by antibody

49
Q

polyclonal antibody generation

A
  • animals are immunised by injection of analyte into tissue over ~ 45 days
  • serum from blood is obtained
  • use of analyte-coated sepharose beads to obtain antibodies
  • obtain polyclonal antibodies (variety)
50
Q

monoclonal antibody generation

A
  • immunisation of animal over ~45 days by injection of analyte
  • collect buffy layer from blood
  • isolate antibody secreting plasma cells
  • breed plasma cells with myelomas = replicative immortality
  • screening and culturing to obtain specific antibodies
  • expansion of hybridomas
51
Q

advantages of monoclonal antibodies

A
  • production limited to mouse/rat/rabbit
  • continuous unlimited supply not dependent on animals
  • highly selective
  • reproducible
52
Q

disadvantages of monoclonal antibodies

A
  • takes months/years to validate
  • hybridoma can be lost/contaminated
  • limited use in assays due to specificity
  • expensive as hell
53
Q

advantages of polyclonal antibodies

A
  • rapid production in any species
  • quick and easy to purify
  • more sensitive; recognises antigens across species
  • inexpensive
54
Q

disadvantages of polyclonal antibodies

A
  • limited to life span of an animal
  • batch variation
  • greater false positives
  • less reliable
55
Q

ELISA

A

enzyme-linked immunosorbent assay, used to detect soluble targets in serum/plasma/secretions
- uses horseradish peroxide to convert H2O2 + OPC to a brown product
- performed in a 96 well format
- control with everything except analyte
- use standard curve to analyse absorbance-concentration relationship

56
Q

indirect ELISA

A

Analyte fixed on well surface
- primary binds analyte
- secondary binds primary
- secondary has conjugated enzyme that converts a substrate to a coloured product

good for isolating different polyclonal antibodies

57
Q

sandwich ELISA

A

antibody fixed in wells
- analyte added & binds
- washing of excess
- addition of secondary antibody
- washing of excess
- add substrates for enzymatic detection

58
Q

competitive ELISA

A

known concentration of competitive analyte fixed on plate
- addition of analyte of interest (unknown concentration)
- antibody binds either
- washing of excess
- quantification
- the less signal, the more competitive the analyte of interest, as the detector antibody was bound and washed away with it

59
Q

rapid antigen test

A
  • A diluted nasopharyngeal sample is dropped into the sample well (S)
  • Sample moves up test via capillary flow (wet-?dry)
  • Gold-labelled antibodies specific for virus antigen mix with the sample in the conjugate pad
  • SARS-CoV-2 antigens bound to gold antibodies are collected by antigen-binding immobilised antibodies in the testing (T) well
  • Residual gold-labelled antibodies (that do not bind SARS-CoV-2 antibody) are collected by Fc binding immobilised antibodies in the control (C) well
60
Q

Western blot

A

used to detect soluble/cell-surface targets in homogenised tissue/lysed cells
- proteins precipitated with antibody coated sepharose beads
- separation by size and charge via SDS-PAGE
- transferred onto PVDF or nitrocellulose
- immunohistochemistry
- quantification using chemiluminescent system

61
Q

Immunohistochemistry

A

used to detect location and abundance of soluble/cell surface target molecules in tissue sections
- cross sectional/longitudal sections of 4-20um
- fixation (cross linked), and frozen or embedded in paraffin wax
- reversal of cross linking
- antibody application (primary+secondary)
- detection via enzymatic or fluoresence
paraffin - polycloncal
frozen - monoclonal

62
Q

flow cytometry

A

used to detect cell-surface molecules in live cells from blood/tissue homogenate
- application of fluorescent antibodies
- cell-antibody passes through nozzle in single cells stream and passes through laser beam
FSC (forward scatter): cell size
SSC (size scatter): identified fluorescence/granularity
- # of positive cells/intensity of fluorescence detected

63
Q

cons of flow cytometry

A
  • limited use in diagnosis (expensive)
  • must use small cell count for diagnosis or analysis is complicated
  • only measures within/on cell content
64
Q

downstream adaptor molecules of TLR

A
  • MYD88, TRIF, TRAF
  • MAPK
  • IFR (interferon regulatory factors)
  • NF-kb
65
Q

drugs that target TLR

A
  • synthetic liposaccharides (CpG, dsDNA, ssRNA)
  • antibodes
  • antagonists
  • small molecule inhibitors of MYD88, TRIF, TRAF
    All kinda shit due to broad effect with broad toxicity, most drugs withdrawn
66
Q

imiquimod

A

targets endosomal TLR7
only used in skin conditions, topical action = reduced side effects

67
Q

Nk-kb mechanism

A

TLR activation initiates IKK complex
- (p) IkB inhibitory subunit of NF-kb complex
- IkB dissociates and is degraded by ubiquitination
- NF-kB enters nucleus
- transcription:
phospholipase A2 & COX2 (prostaglandin synthesis)
chemokines & adhesion molecules (immune recruitment)
cytokines (activate sentinel cells)

68
Q

Nk-Kb drug targeting

A

SHIT: damaging effects on immunity, repair and homeostasis = no approved drugs
- inhibits IKK complex, stabilise NF-kB complex, NF-kB translocation into nucleus, gene transcription

69
Q

glucocorticoid receptor agonists

A

SHIT: increased infection risk, healing impairments, complications with longterm use/withdrawal
- mimic cortisol action
- reduce NF-kB signalling

70
Q

Prostaglandin

A

a type of eicosanoid (lipid mediator of inflammation)

71
Q

prostaglandin synthesis

A
  • Phospholipase (A2) converts membrane lipids into arachidonic acid
  • COX converts into endoperoxidases, which form prostaglandins
72
Q

NSAIDS

A

pretty shit: target COX1 & COX2, leads to reduced prostaglandin synthesis
side effects: ulcers, bleeding, kidney issues

73
Q

COX2 inhibitors (Coxibs)

A

selectively target COX2, which is only present in inflamed tissue = more specific actions = reduced side effects
PRETTY OK

74
Q

TNF receptor ligands

A

TNFa/b, LT, CD40, FasL, BAFF, April, Ox40, GITR, nerve growth factor

75
Q

TNF action

A
  • downstream signalling via TRAF/TRADD
  • activates MAPK, NF-kB
  • overactivation = apoptosis
76
Q

targeting TNF

A

Target TNF present in blood via chimeric, humanised, truncated receptors.
= rejection and macrophage induced inflammation

= anaphylaxis, infection, bone marrow suppression, heart failure (SHIT)
(unless u conjugate receptor w/PEG)

77
Q

IL-1b inhibitors

A

Recombinant IL-1 receptors, receptor-Ig fusion proteins, and antibodies against IL-1b

Reduce T cell activation and inflammation = Risk of infection, bone marrow suppression and heart failure

78
Q

sIL-6R

A

antibodies against the soluble IL-6 receptor

Reduce T cell activation and inflammation = Risk of infection, bone marrow suppression and heart failure

79
Q

IFNa/R1 inhibitors

A

block cytokine receptor/signalling pathway
= block DC activation & autoimmune responses
= limits comms between adaptive and innate

risk of latent virus activation, and respiratory infection

80
Q

IL-12/23 inhibitors

A

target the p40 subunit of IL-12/23 cytokines
= Block T cell activation and inflammation & Risk of latent virus activation and respiratory infection

81
Q

IL-12/23 inhibitors

A

target the p40 subunit of IL-12/23 cytokines by modified human IgG
= Block T cell activation and inflammation & Risk of latent virus activation and respiratory infection

82
Q

Risk of latent virus activation and respiratory infection

A

best side effects possible for targeting immunity
(respiratory infection always requires a large response so any dampening will affect this)

83
Q

jakinibs

A

mimic SOCS
1st gen: non-selective (SHIT)
2nd gen: more selective, block specific cytokine signalling, thus side effects related to cytokine blocked
(topical reduce side effects)

84
Q

Treg cells

A

intervenes to stop inappropriate reactions to self-antigen by
- blocking DC binding to immune cells by binding CD80/86/MHCII via CTLA4/TCR
- produces immunosuppressant cytokines IL-10/TGF-b1 (act on effector T cells)

85
Q

CTLA4-Fc drug

A

mimics Treg activity by blocking site of co-stimulation on DCs
- risk of anaphylaxis and infection
- maintains basal T cell activation (allows return to homeostasis)
- mainly acts in lymph nodes & blood
- most effective at start of flare up
- lasts 4-8 weeks

86
Q

Co-stimulation downstream effects

A
  • calcineurin activation
  • NFAT activation
  • IL-2 transcription
  • IL2 acts on JAK-STAT receptor
  • mTOR activation
  • nucleotide synthesis for clonal expansion
87
Q

inhibiting nucleotide synthesis

A

small molecule inhibitors of purine/pyrimidine synthesis

FUCKING AWFUL SIDE EFFECTS: Off-target effects on gastrointestinal function, bone marrow (site of immune stem cells), liver enzymes, fetal development, general immune suppression due to suppression of both B/T cells

88
Q

inhibiting calcineurin

A

binding to cyclophilin/FK-binding protein 12
- inhibits IL-2 production; reduces T cell proliferation
- more specific to T cells
STILL SHIT: Off-target effects on kidneys, bone marrow, immune and healing responses (due to lack of T cells) & increased risk of skin cancer

89
Q

inhibiting mTOR

A

blocking binding of FK-binding protein 12 to mTORC1 complex
- inhibit IL-2 induced T cell proliferation
SHIT GENERAL SIDE EFFECTS: Off-target effects on gastrointestinal functions, endocrine system, kidneys, bone marrow, immune and healing responses

90
Q

IL-2R inhibition

A

binding to receptor with chimeric/humanised antibodies
- inhibit IL-2 induced proliferation
- maintains basal T cell signalling

PRETTY ALRIGHT: Off-target effects include respiratory and skin infections (due to immune suppression, skin and respiratory infection require big immune response)

91
Q

B cell receptor (BCR/CD20)

A

binds to antigen to induce proliferation and inflammation

92
Q

Other B Cell receptors

A

CD19: recruits signalling molecules triggered by the BCR
- CD21: binds complement, enhancing BCR signalling
- CD22: binds sugars modulating cell adhesion and BCR signalling

93
Q

BAFF, APRIL & IL-6

A

soluble factors that regulate B cell proliferation, activation and inflammation

94
Q

targeting BCR/CD20

A

by antibodies
= inducing cytotoxic killing of all bound B cells = cytokine storm = massive toxic inflammation and complete B cell depletion
= 15% chance of death by acute/pulmonary toxicity
AWFUL AWFUL DRUG DONT USE IT

95
Q

Targeting CD19/21/22

A

via antibody
- moderate B cell depletion
- lacking success
= NOT WORTH YOUR TIME

96
Q

Targeting IL-6

A

fusion with human(ised) antibodies with an albumin-fused nanobody
= confined to blood = good t1/2 and reduced toxicity
ITS OK?: Adverse effects include liver damage, gut perforation, bacterial or fungal infection

97
Q

targeting BAFF/APRIL

A

via receptor fusion, human antibodies and small molecule inhibitors for B cell -specific targeting
prevents B cell proliferation
=
SHIT: Side effects include gastrointestinal upset, kidney damage, lung and urinary infections, inflammatory reactions (related to essential action of B cells)

98
Q

cell adhesion/chemotaxis

A

Rolling adhesion/tight binding

T/B cells enter blood supply and navigate towards site of inflammation by chemotactic gradient (binds chemokines on cell surface receptors)
- Use cell adhesion molecules (selectins and integrins) to move (P/E selectins of endothelial cells bind L-selectins of T/B cells)
- These increase in number and selectivity closer to the site of inflammation

Diapedesis (enters cell) and Migration to infection

99
Q

targeting chemokines

A

FUCKING HORRENDOUS IDEA WHAT ARE YOU THINKING?!?!?
chemokines provide directions to ALL immune cells, interconnected effects = redundancy in targeting

100
Q

L-selectins

A

present on circulating immune cells, and bind P/E-selectins on endothelium & interact with sulphated polysaccharides
- facilitate rolling adhesion

101
Q

targeting selectins

A

EGG! NO! so many cells use this method to move through blood, massively broad side effects on normal and immune cells

305 pharmacology (4 decks)

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