Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

DAMPs

A

damage associated molecular patterns

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

PAMPs

A

pathogen associated molecular patterns
(eg flagellin & lipopeptides)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Toll-like receptors

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

complement/antibodies

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

anti-inflammatory mediators

A

IL-10, VEGF, TGFbeta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

adaptive immune response

A

defends against specific repeated threats

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IgM

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IgG

A

longer-lasting specific antibodies, common drug target

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

IgA

A

antibody specific to GI and respiratory illnesses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

IgE

A

allergic reactions

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

IgD/basophils

A

govern a different arm of allergic reaction that IgE

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

neutralisation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

complement fixation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

opsonisation

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

T cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

IFNy

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

IL4/13

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

IL-17/22

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Cytokines produced by Th Cells

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

CD8 T cell mechanism

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Immune disorders

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

immune co-morbidites

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Th stimulation of B cell

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Types of Th cell that can induce inflammation and tissue damage

A

Th1, Th7, Th17

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

serum

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions