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Semester 4 > DEF > Flashcards

DEF Flashcards

1
Q

fates of self-reactive b-cells and t-cells in periphery and central

A

t-cells: central

  • 95% death by neglect
  • overly strong = negative selection via apoptosis
  • weakly bind = positive selection
  • slightly more stronger = regulatory CD4+ t cells

t-cells: peripheral

  • apoptosis
  • anergy
  • supression via regulatory t-cells

b-cell: central

  • apoptosis
  • anergy
  • ag receptor editing

b-cell: peripheral

  • apoptosis
  • supression via regulatory
  • anergy
  • blockage of activation by inhibitory receptors
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2
Q

what type of bond holds the chains of Ab together

A

disulphide

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3
Q

how many constant and variable domains of heavy and light chains of Ab

A

light chain (1 constant + 1 variable)

heavy chain (3 or 4 constant + 1 variable)

4 in IgM

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4
Q

what are hypervaribale regions

A

3 regions within variable domain that have high variations of AA –> 3 loops

consist of complementary-determining regions

  • CDR1
  • CDR2
  • CDR3 (highest variability due to junctional diversity)
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5
Q

why are natural immune responses “polyclonal”

A
  • more than 1 antigen on a pathogen
  • multiple epitopes per antigen
  • more than 1 Ab can recognise the same epitope

therefore more than one Ab will produced

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6
Q

generation of Ab

A

During b-cell development in bone marrow:
variable regions -

45 variability segments
23 diversity segments
6 junction segments

endonuclease –> D and J
then joined and only then will variable be cut and joined

VDJ = full functional recombined gene segment of VH

(testing occurs and then light VL is generated)

35V + 5J

VJ is tested

then junctional diversity via Terminal deoxynucleotidyl transferase adding random nucleotides

  • heavy chain = at D-J joining
  • light chain = at VJ joining

then transcribed
and splicing
joining of variable regions to constant regions

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7
Q

through what process does IgM–> the other 4 classes

A

IgD is co-expressed with IgM via differential splicing

isotope switching
IgM—> IgA, IgE, IgG
IgG—> IgA, IgE

Ag specificity does not change

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8
Q

what is required for isotope switching of B-cell to occur

A

t-cell tells it which class to switch to

TCR binds to processed-Ag (MHC+ peptide) of B-cell

b-cell will then express a molecule to recieve signals from helper t-cell

t-cell will also produce cytokines to help induce switching

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9
Q

cytokines released from t-helper cell for isotope switching

A

IFN-gamma—> IgG1 + IgG3

IL-4 —-> igE

TGF-beta—-> IgA

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10
Q

what occurs during isotope switching

A

only change in heavy chain

loop after IgM switch region to join with switch region of required constant domain

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11
Q

affinity maturation

A

requires signals from helper t-cells–> activate b-cells–> point mutations (somatic hypermutations of variable regions)

mutations will cause high or low affinity binding

positive selection for high

therefore the higher the exposure—> the more mutations–> better/more efficient the affinity

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12
Q

what do t-cells recognise

A

only processed antigens

CD4+ helper —> antigens expressed by MHC II (mainly APCs)

CD8+ cytotoxic—> expressed by MHC I (by ANY nucleated cell)

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13
Q

which APC can present to naive t-cells

A

dendritic cells

3 levels of signals

-TCR–> mhc/peptie
-co-stimulation
causing proliferation

-cytokines determining type of t-effector cell

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14
Q

which cytokines lead to Th1 and Th2

A

IL-12—> Th1 (macrophages)

IL-4—-> Th2 (mast cells/b-cells/eosinophils)

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15
Q

TCR structure

A

2 chains (alpha and beta)

1 variable and 1 constant/chain

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16
Q

MHC groove between what chains for MHC I and II

A

MHC I = a1 and a2

MHC II = a1 and b1

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17
Q

role of CD4/8 on t-cell in TCR-MHC/Ag recognition/binding

A

CD4/8 binds to MHC

so that threshold is lowered for t-cell activation (less complexes required to bind for activation)

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18
Q

which t-cell helps with macrophages / b-cells

A

CD4+

Th1–> macrophages
Th2–> B-cells

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19
Q

how are exogenous pathogens eliminated by t-cells

A

antigen taken in by macrophages/b-cells
phagolysosome
breakdown into peptides

MHC II produced in ER with invariant chain
travels to peptides via Golgi body/vesicle

removal of invariant
binding of peptide with MHC
expressed on surface for CD4+ t-cell to recognise

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20
Q

how are cytosolic (intrinsic) Ags eliminated by t-cells

A

antigen/virus taken in by any cell with a nucelus
production of viral proteins
proteasomes detect and break down into peptides +ibquinisation
peptides enter the ER via TAP
ER has produced MHC I
if a peptide binds to MHC I
Golgi body transports via vesicle to cell surface
expressed to CD8+ cytotoxic tcells

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21
Q

C3 and C5 convertases in the 3 complement pathways

A

alternative

  • C3 = C3bBb
  • C5 = C3bBbC3b

Classical +lectin

  • C3 = C4bC2a
  • C5 = C4bC2aC3b
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22
Q

which complements are responsible for inflammation

A

C3-5a

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23
Q

which complements are responsible for opsonisation of microbes

A

alternative = C3b

classical = C4b

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24
Q

which complements are responsible for lysis of microbe

A

C5-9 = MAC

C9 polymerises to make pore
H2O enters for lysis

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25
Q

how is the alternative, lectin and classical pathways activated

A

alternative = spontaneous cleavage of C3

classical = binding with a Ab-Ig
(C1q binding with a Fc region–> C1r cleaves C1s–> cleaves C4)

lectin = mannose binding lectin (MBL) to mannose / ficolins to n-acetyl glucosamine causing MASP1&2 to cleave C4 then C2

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26
Q

what stabilises C3 convertase

A

properdin

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27
Q

why is it important that the ig is bound to an Ag with the classical complement pathway

A

binding of ig for IgM exposes Fc region within pentamer so C1q can bind

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28
Q

how is complement activation regulated

A

C1INH (C3 convertase inhibitor) - classical pathway
-dissociates C1r, C1s from C1q

CD59 “protectin”(MAC inhibitor)

  • present on healthy cells
  • binds to C5-8
  • inhibits recruitment of C9
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29
Q

deficiency in complement proteins

A

SLE-like syndrome from C2,4,C1q deficiency

frequent serious infections with pyogenic bacteria e.g. Staphylococcus aureus with C3 deficiency

disseminated infections with Neisseria with MAC deficiency (C5-9)

C1INH deficiency–> hereditary angioedema

CD59 deficiency –> paroxysmal nocturnal haemoglobinuria

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30
Q

4 ABO groups

A

A
B
AB (A+B antigens, no Ab)
O (no antigens, have both anti-A + anti-B)

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31
Q

where in the blood are Ab

A

plasma

32
Q

inheritance pattern of ABO and RhD

A 
AB = codominatnt
OO = type O

D-antigen= autosomal dominant

33
Q

how do anti-d prophylaxis work

A

given to mother that is RhDneg

if RhDpositive foetal blood enters, it will bind to the D-antigens

stops mothers immune system seeing D-antigen = no anti-D produced by mother

34
Q

what kind of Ig is anti-d and anti-A/B

A

anti-D = igG

anti-A / B =igM

35
Q

zeta potential and what can be used to overcome this

A

the RBC = positive cloud

LISS (iat)

36
Q

2 parts of cross matching

A

immediate spin cross match (for ABO compatibility)

  • if patient Ab screen is neg for donor blood
  • no agglutination = ABO compatible (ISX neg)

full indirect Antiglobulin test cross match(using LISS)

  • if patient Ab screen is positive / known Ab history
  • agglutination = positive ISX
37
Q

4 type of toxins

A

1 - on cell membrane but not transported in (comprising metabolism)
- traveller’s diarrhoea (guanyl cyclase cGMP)

2 - on cell membrane - damaging cell membrane

3 - transported into host cell (intracellular damage)
-endopeptidases Zn (tetanus/botulism)

extracellular - damage cellular matrix + connective tissue

38
Q

diptheria

A

corynebacterium diphtheria (gram +)

upper resp tract infection

39
Q

tetanus and infantile botulism

A

tetanus–> spasptistic paralysis
Zn2+ endopeptidase for synaptobrevin blocks release of inhibitory NT at sensory motor neurones (continuous excitation)

botulism —> flaccid paralysis
Zn2+ endopeptidase for synaptobrevin at NMJ synapses preventing release of Ach

40
Q

what bacterial enzymes for streptococci and clostridium perfringes secrete

A

streptococci = hylaurondiase (breaks down hyaluronic acid important in extracellular matrix)

C.Perfringes = alpha-lecithinase (splits lecithin on surface of host cells causing death)

41
Q

how do bacterial endotoxins lead to leaky blood, clots everywhere, shock and unstoppable bleeding

A

increased cytokine release from stimulated macrophages
-increases endothelial permeability –> leaky

  • leaky —> loss of BV (into extravascular space) –> hypovolemic shock
  • complement system is activated –> clotting cascade–> uncontrolled clotting–> disseminated intravascular coagulation (DIC)
  • clotting factors used up–> more bleeding
42
Q

how can gram +ve bacteria eg. staph.aureus and strep. pyrogenes cause toxic shock syndrome

A

produce superantigens

  • TSST (S.A)
  • SPE (S.P)

they overstimulate t-cells–> massive inflammation–> hypovolemeic shock/gangrene/liver damage etc.)

43
Q

immunopathy hypersensitivity III and IV

A

III
-Ab produced for impetigo(strep.pyogenes) –>with Ag–> immune complexes–> deposited in kidney–> glomeronephritis

IV

  • toxic products of t-cells activation—> tissue damage
  • eg. mycobacterium tuberculosis—> granuloma formation + necrosis of granulomas

(other granulomas don’t have necrosis)

44
Q

hypersensitivity (I to IV)

A

I

  • sensitisation phase: allergens (Th2–> IL4–>IgE mediated)
  • effector phase: igE to mast cells so they can recognise when 2nd exposure to allergen–> histamine

II

  • IgM/G
  • Myasthenia Gravis(autoantibodies against Nic Ach receptors - weak contraction)
  • Rhesus isoimmunisation
  • graves disease (autoantibodies for TSH receptor high TH low TSR/TSH)

III

  • autoantibodies to circulating self antigens
  • SLE
  • fix complement response / deposit in glomerulus

IV

  • t-cell mediated
  • mantoux test
  • type 1 diabetes (beta cells = auto antigen)
  • coeliac disease (ILA anti-giladin/endomysium/reticulin
  • delayed hypersensitivity - takes a few days to develop
45
Q

immunodeficiency primary/secondary

A

primary - congenital/inherited

  • complement
  • phagocytes ( cheddar-higashi = failure of phagolysosomes)
  • bcells
  • tcells (digoerge syndrome = lack of thymus)

secondary - external factors

  • HIV
  • malnutrition
  • tumours
  • thearapy/ radiation/cytotoxic drugs
46
Q

why would you get increased ESR with inflammation

A

normally red blood cells fall slowly - leaving little plasma

when inflammation–> many proteins in blood so causes RBC to fall more rapidly increase ESR

ESR = measuring rate RBC sediment

47
Q

what is CRP

A

c-reactive protein

released by liver in inflammation
so high levels in blood= inflammation

48
Q

what enzyme is responsible for junctional diversity

A

terminal deoxynucleotidyl transferase

49
Q

what enzyme cleaves factor B in the alternative complement pathway

A

factor D

50
Q

at what degrees do you store plasma after centrifuging for short term vs long term

A

4 - short term

-20 long term

51
Q

what Ab would a patient who has resolved their infection present have in their blood

A

negative igM

positive igG

if massive no. of igG = has a recent re-exposure but little igM

52
Q

what are nucleic acid amplification (NAAT) tests good for

A

seeing progress with treatment

seeing how much Ag was present in blood

real time PCR - no need for gel electrophoresis
multiplex PCR - can see multiple Ag

53
Q

definition of vaccine

A

material from an organism that will actively enhance immunity

  • producing primed state (memory cells)
  • a rapid secondary response
  • prevents disease (but may not prevent infection eg. tetanus vaccine is against the toxin not bacteria)
54
Q

2 types of vaccines / 3 forms of vaccine

A

passive - short term

active - long term (own body produces Ab)

forms:

  • live attenuated
  • dead whole
  • subunits
55
Q

general principles of vaccine (5)

A

right type of response

right site

right duration of protection

age of vaccination

route of inoculation

56
Q

which vaccines are good/bad for mucosal immunity

A 
parenteral = bad 
oral = good bc processed by MALT
57
Q

which vaccines are live/dead/subunit

A

live - VZV/MMR/BCG(TB)/yellow fever/rotavirus

dead - pertussis/hepA/cholera

subunit - hep B/C

58
Q 
vaccine for:
HPV
diptheria
tetanus
influenza
whooping cough - pertussis
streptococcus pneumonia
n.meningitis
TB
A

DTaP = diphtheria + tetanus + pertussis

influenza = Hib

strep. pneumonia = PPV23(above 2yrs)/PCV-13(below 4yrs)
n. meningitis = menACWY / bexsero

HPV = Gardasil(6,11.16,18) / cervarix(16,18 only)

TB = BCG

59
Q

why do we give MMR at >12 months

A

because of maternal Ab in baby = neutralise the live vaccine = no immunity produced

we give a second dose even though it is live just to catch those who didn’t produce immune response first time round

60
Q

what does bexsero contain

A

we found capsule targeting vaccines for men B = ineffective

so this non-capsular vaccine
contains outer membrane vesicles + surface proteins:
-factor h protein
-n.heparin binding antigen
-n.adhesion A

but this vaccine does not cover all serotypes unlike MenC did

61
Q

who do we give BCG (TB) vaccine to

A

only children + those children living in high risk areas

62
Q

what part of the Ig changes during isotope switching

A

HEAVY CONSTANT domains

63
Q

what part of Ig is changed during affinity maturation

A

somatic hypermutation is localised in variable VDJ/VJ regions

64
Q

what cells express MHC I and II

A

all nucleated cells = MHC I

APC cells only MHC II

65
Q

which of the complements of MAC bind to the lipid membrane / cell membrane

A

C7 - lipid membrane

C8/9 - cell membrane

66
Q

c1q activation

A

igG: must bind to MORE THAN 1 Fc region of Abs (different) that are bound to Ags –> activates multiple heads of c1q(there are 6)

igM - only one can activate the globular heads of C1q

67
Q

lectin pathway: activation

A

via PRRs = MBL /Ficolin

they bind to PAMPs = Mannose / N-acteylglucosamine on microorganisms

activate MASP1&2 (MBL-associated-serine-proteases)

68
Q

2 ways body gets rid of RBCs with non-self Ags on them

A

Abs will coat them and then

directly –> cell cells break up in the blood stream (intravascular)

indirectly–> When the liver and spleen remove antibody coated cells (extravascular)

69
Q

immediate spin cross matching

Full Indirect Antiglobulin test cross-matching

A

Immediate

  • only testing igM antibody compatibility (ABO antigens)
  • patient sample + donors RBCs–> agglutination = incombatabile

full indirect

  • requires LISS
  • if patient has had + Ab screening /unknown
70
Q

what Ab do people with coeliac disease have

A

IgA anti-gliadin antiendomysium and anti-reticulin antibodies

71
Q

Substances that inhibit PCR

A

haem / bile salts

important to have a internal positive control

72
Q

2 ways herd immunity is boosted

A

vaccines

periodic outbreaks of disease in the community

73
Q

how long until Ab response after 1st exposure of an Ag

A

5-7days to start

2 weeks until FULL response

74
Q

which vaccines use the TOXINS the bacteria produces as their targets

A

diphtheria and tetanus

the vaccine = toxoids (subunit vaccine DTaP - requires boosters)

75
Q

clinical features of tetanus

A 
risus sardonic (spasm of face)
oposthotonus (backward arching)
76
Q

what is Hib vaccine made up of

A

vaccine for influenza

Capsule polysaccharide + conjugated toxoids of diphtheria + tentanus bacteria

77
Q

manoux test purpose

A

tells us if person has been infected with TB in past by measuring degree of hypersensitivity to tuberculin (TB toxin)

does NOT tell us the degree of immunity the person has against TB, it only shows us if they have been exposed

inject tuberculin into the skin and read a few days later.

Semester 4 (10 decks)

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