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DEF Flashcards

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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
how is the alternative, lectin and classical pathways activated
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
26
what stabilises C3 convertase
properdin
27
why is it important that the ig is bound to an Ag with the classical complement pathway
binding of ig for IgM exposes Fc region within pentamer so C1q can bind
28
how is complement activation regulated
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
29
deficiency in complement proteins
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
30
4 ABO groups
A B AB (A+B antigens, no Ab) O (no antigens, have both anti-A + anti-B)
31
where in the blood are Ab
plasma
32
inheritance pattern of ABO and RhD
``` AB = codominatnt OO = type O ``` D-antigen= autosomal dominant
33
how do anti-d prophylaxis work
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
what kind of Ig is anti-d and anti-A/B
anti-D = igG | anti-A / B =igM
35
zeta potential and what can be used to overcome this
the RBC = positive cloud LISS (iat)
36
2 parts of cross matching
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
4 type of toxins
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
diptheria
corynebacterium diphtheria (gram +) upper resp tract infection
39
tetanus and infantile botulism
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
what bacterial enzymes for streptococci and clostridium perfringes secrete
streptococci = hylaurondiase (breaks down hyaluronic acid important in extracellular matrix) C.Perfringes = alpha-lecithinase (splits lecithin on surface of host cells causing death)
41
how do bacterial endotoxins lead to leaky blood, clots everywhere, shock and unstoppable bleeding
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
how can gram +ve bacteria eg. staph.aureus and strep. pyrogenes cause toxic shock syndrome
produce superantigens - TSST (S.A) - SPE (S.P) they overstimulate t-cells--> massive inflammation--> hypovolemeic shock/gangrene/liver damage etc.)
43
immunopathy hypersensitivity III and IV
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
hypersensitivity (I to IV)
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
immunodeficiency primary/secondary
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
why would you get increased ESR with inflammation
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
what is CRP
c-reactive protein released by liver in inflammation so high levels in blood= inflammation
48
what enzyme is responsible for junctional diversity
terminal deoxynucleotidyl transferase
49
what enzyme cleaves factor B in the alternative complement pathway
factor D
50
at what degrees do you store plasma after centrifuging for short term vs long term
4 - short term -20 long term
51
what Ab would a patient who has resolved their infection present have in their blood
negative igM positive igG if massive no. of igG = has a recent re-exposure but little igM
52
what are nucleic acid amplification (NAAT) tests good for
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
definition of vaccine
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
2 types of vaccines / 3 forms of vaccine
passive - short term active - long term (own body produces Ab) forms: - live attenuated - dead whole - subunits
55
general principles of vaccine (5)
right type of response right site right duration of protection age of vaccination route of inoculation
56
which vaccines are good/bad for mucosal immunity
``` parenteral = bad oral = good bc processed by MALT ```
57
which vaccines are live/dead/subunit
live - VZV/MMR/BCG(TB)/yellow fever/rotavirus dead - pertussis/hepA/cholera subunit - hep B/C
58
``` vaccine for: HPV diptheria tetanus influenza whooping cough - pertussis streptococcus pneumonia n.meningitis TB ```
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
why do we give MMR at >12 months
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
what does bexsero contain
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
who do we give BCG (TB) vaccine to
only children + those children living in high risk areas
62
what part of the Ig changes during isotope switching
HEAVY CONSTANT domains
63
what part of Ig is changed during affinity maturation
somatic hypermutation is localised in variable VDJ/VJ regions
64
what cells express MHC I and II
all nucleated cells = MHC I APC cells only MHC II
65
which of the complements of MAC bind to the lipid membrane / cell membrane
C7 - lipid membrane | C8/9 - cell membrane
66
c1q activation
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
lectin pathway: activation
via PRRs = MBL /Ficolin they bind to PAMPs = Mannose / N-acteylglucosamine on microorganisms activate MASP1&2 (MBL-associated-serine-proteases)
68
2 ways body gets rid of RBCs with non-self Ags on them
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
immediate spin cross matching Full Indirect Antiglobulin test cross-matching
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
what Ab do people with coeliac disease have
IgA anti-gliadin antiendomysium and anti-reticulin antibodies
71
Substances that inhibit PCR
haem / bile salts important to have a internal positive control
72
2 ways herd immunity is boosted
vaccines periodic outbreaks of disease in the community
73
how long until Ab response after 1st exposure of an Ag
5-7days to start 2 weeks until FULL response
74
which vaccines use the TOXINS the bacteria produces as their targets
diphtheria and tetanus the vaccine = toxoids (subunit vaccine DTaP - requires boosters)
75
clinical features of tetanus
``` risus sardonic (spasm of face) oposthotonus (backward arching) ```
76
what is Hib vaccine made up of
vaccine for influenza Capsule polysaccharide + conjugated toxoids of diphtheria + tentanus bacteria
77
manoux test purpose
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.

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