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IMM2011 > B CELLS AND HUMORAL > Flashcards

B CELLS AND HUMORAL Flashcards

1
Q

Are B and T cells morphologically similar under a microscope?

A
  • YES! can’t tell them apart
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2
Q

What is the name of an effector B cell?

A
  • Plasma cells –> produces antibodies
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3
Q

When can the adaptive immune response be WELL detected?

A
  • Not until day 6
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4
Q

What is a feature of plasma cell under the microscope?

A
  • very HIGHLY developed ER
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5
Q

What is the lymphocyte clones with unique specificity INDEPENDENT of?

A
  • Foreign antigen

- i.e. there will already be an antigen specific clone floating in peripheral lymphoid organs–> just have to find it

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6
Q

Is the immune response dependent on a foreign antigen?

A
  • YES!

- Will actively find antigen specific clone

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7
Q

What types of antigens can a BCR recognsie?

A
  • ALL different types of antigens (3D conformation) –> e.g. lipids, metals, carbs, proteins ,DNA
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8
Q

Which part of the BCR is the binding site?

A
  • N terminus variable domains
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9
Q

What do the constant region of the heavy chains determine in B cells? -

A
  • The antibody isotype
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10
Q

Humoral immunity is important for which type of microbes?-

A
  • Exracellular microbes
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11
Q

What type of antibody is active against Helminths?

A
  • IgE
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12
Q

What occurs in B cell deficiency?

A
  • Person is susceptible to puss (pyogenic) forming bacteria (neutrophils)
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13
Q

Which type of response occurs in asthma?

A
  • IgE response (sm. muscle contraction)
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14
Q

What are the two types of ANTIBODY responses?

A
  • T cell dependent (high affinity Igs) and T cell independent (weak–> mainly IgM Igs and it is transient)
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15
Q

What is the function of T cell dependent antibodies ?

A
  • Can target polysaccharide capsule that bacteria use to evade phagocytosis (via IgM) thus will phagocytose
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16
Q

What feature is given to ANTIGENS that promote independent Ig repsonses?

A
  • They are polyvalent –> can cross link and BCR can give rise to strong signal e.g polysaccharides and nucleic acids
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17
Q

Do B or T cells express PRRs?

A
  • B cells express them! NOT T CELLS !!

- Because B cells can recognise the whole 3D conformation whereas T cells only recognise digested peptides

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18
Q

Can PAMPs costimulate B cells in T cell independent Ig respone?

A
  • YES!
  • In this case SINGAL 1= BCR
    and SIGNAL 2= PRR
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19
Q

Why don’t B cells illicit T cell help for polysaccharides and nucleic acids?

A
  • Because T cells recognise ANTIGEN (the peptide) and not the whole structure of the nucleic acids or polysaccharides (bc. no peptides in them)
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20
Q

What occurs in a T cell dependent response?

A
  • Isotype switching e.g. IgM –> IgG (on day 7)
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21
Q

Which day does the primary immune response peak?

A
  • Day 14 (approx.)
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22
Q

What is affinity maturation?

A
  • Quality of Ig (affinity to cognate antigen )

- Antibody affinity in second response generally higher than first response

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23
Q

What occurs in the first week and then after that of a T cell dependent Ig response ?

A
  • First week: IgM produced
  • After first week: Isotype switching IgM–> IgG, IgA
  • Memory forms to allow for faster and larger immune response
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24
Q

Is the affinity of Ig produced in secondary Ig response higher or lower than first?

A
  • HIGHER (via affinity maturation)

- Affinity of Ig produced and BCR increases with TIME and exposure to antigen (primary and secondary immune responses)

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25
Q

Why do TCRs not change affinity like BCR?

A
  • Because T cells aren’t as free to ‘mutate’–> has to bind to MHC + peptide
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26
Q

Is B cell signalling homologous to T cell signalling?

A
  • YES!

- Is homologous BUT identity of molecules is different

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27
Q

What does BOTH B and T cell signalling involve? -

A
  • RECEPTOR TYROSINE KINASES –> phosphorylating ITAMs (cytoplasmic regions) –> P’d Adaptor and scaffold proteins–> membrane proximal complex–> enzymes and second messengers–> TFs –> new proteins and genes
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28
Q

Is the BCR cytoplasmic domain short or long?

A
  • VERY SHORT

- so can’t transduce signals alone

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29
Q

Which two signalling chains help the BCR transduce the recognition signal?

A
  • Igalpha and Igbeta (ITAM motifs in cytoplasmic domain)
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30
Q

What is the equivalent molecule of Igalpha and Igbeta in T cells?

A

CD3

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31
Q

What happens to the Igalpha and Igbeta in the signalling pathway?

A
  • Get phosphorylated via tyrosine kinase (Fyn, Lyn, Blk)

- Create docking sites for signalling

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32
Q

Which 3 SRC family kinases can phosphorylate ITAMs of Igalpha and Igbeta? -

A
  • Fyn, Lyn , Blk
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33
Q

What is the T cell equivalent of Fyn, Lyn, and Blk?

A
  • Lck
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34
Q

What is the functional equivalent of Stk in T cells?

A
  • ZAP70
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35
Q

What is the B cell coreceptor complex comprised of?

A
  • CD21, CD19, CD81 (tetrospandin molecule)
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36
Q

How is complement involved in B cell signalling (signal 2) ?

A
  • If C3D (complement) on antigen –> CD21 sends signal (via CD19) –> to LOWER threshold of signalling needed for B cell activation
    (T cell equivalent is CD80/86-CD28)
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37
Q

What is upregulated in an activated B cell?

A
  • B7 and MHC II for interaction with helper T cells
  • Cytokine receptors
  • Expression of CCR7 (migrate out of B cell follicle into T cell zone)
  • Generation of plasma cells
  • Expression of survival proteins
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38
Q

What is the germinal center reaction?

A
  • B cells proliferate and differentiate (spleen and lymph node)
  • T cell dependent Ig responses occur
  • FDCs (Follicular Dendritic Cells) + TFH (T Follicular Helper cells) are involved
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39
Q

Do follicular dendritic cells present antigen ?

A
  • NO

- They are parenchymal cells

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40
Q

Do you find germinal centre reactions for T cell independent antibody responses? -

A
  • NO! Only for T cell dependent
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41
Q

What is the function of FDCs?

A
  • Antigen depot
  • Have intact antigen stuck to their surface (Fc and complement receptors) –> Intact antigen available for B cell to recognise and phagocytose
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42
Q

Where do antigen specific B cells acquire antigen from?

A
  • FDCs- displayed antigen via BCR
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43
Q

What do TFH cells do?

A
  • T helper cell
  • in B cell follicles
  • Driving isotype swtiching and affinity maturation
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44
Q

Which T cells do B cells present antigen to? -

A
  • TFH cells
    1. B cells get antigen from BCR (FDC source) –> endocytose digest and process antigen
    2. Peptide fragments presented on MHC II TO TFH cell
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45
Q

What response are TFH cells critical for?

A
  • T cell dependent Ig responses
46
Q

How does T cell help drive B cell proliferation and differentiation?

A
  • B cells have CD40 and T cells have CD40 L
  • Cytokines released by Th cell
  • These drive cell proliferation and isotype switching
47
Q

What are the 2 principal products of the germinal centre reaction ? ** (important)

A
  1. Plasma cells (secreting Ig)

2. Memory B cells

48
Q

What are the two zones of the germinal centre reaction and what do they represent?

A
  • DARK ZONE –> B cell proliferation

- LIGHT ZONE–> Interactions with Thelper and FDCs happens

49
Q

Which two processes occur in the germinal centres? -

A

Isotype switching –> light zone

Affinity maturation –> dark zone

50
Q

What occurs in somatic hypermutation (affinity maturation) and where does it occur?

A
  • occurs in germinal centre reaction (dark zone)
  • AICD (Activation Induced Cytidine Deaminase) enzyme causes somatic point mutations in IgV genes (random process)
  • Some will be HIGHER AFFINITY and SELECTED FOR in germline reaction
  • Some will be LOWER AFFINITY
51
Q

Where do high affinity B cells go after selection in the light zone?

A
  • Go to dark zone to proliferate and differentiate into plasma cells
52
Q

Do B cells or T cells drive isotype swithcing ?

A
  • T Cells!
  • CD40L is MANDATORY for this
  • Cytokines determine which Ig isotype is secreted
53
Q

Which Ig isotype is does the cytokine IFN-gamma drive?

A
  • IgG1 and IgG3 subclasses of IgG
54
Q

Which Ig type does Il-4 (made by Th2) drive?

55
Q

Which Ig type does TGF-Beta drive?

56
Q

What is the mechanism of isotype swithcing?

A
  • CD40L + cytokine signalling –> AICD changes nucleotides

- Switch regions cleaved then joined to other regions

57
Q

What occurs in Ig feedback?

A
  • B cells express FcgammaRIIB Tc receptor –> excess antibody (late immune response)
  • FCgammaRIIB recognises complexes –> transduces signals –> INHIBITION OF ACTIVATION
58
Q

What occurs in neutralisation?

A
  • High affinity Ig will neutralise important molecule on pathogen (e.g. glycoprotein that virus uses)
59
Q

What occurs in phagocytosis and opsonisation in terms of the effector functions of Ig ?

A
  • Occurs via complement and Fc recpetors
  • Opsonisation–> inflammation
  • Igs through interaction with complement can recruit phagocytes to site of infection
60
Q

What is lysis and cytotoxicity in terms of the effector functions of Ig?

A
  • Complement dependent mechanisms of lysis and Fc dependent
61
Q

Which 3 ways can Antibody fight infectious disease?

A
  1. neutralisation (only high affinity IgG and IgA)
  2. Opsonisation (IgG and IgA. IgM via complement)
  3. Lysis ( via complement -MAC- IgG, IgM)
    (ADCC–> IgG, IgA, IgE)
62
Q

What does ADCC stand for?

A
  • Antibody dependent cytotoxicity
63
Q

What are Fc receptors?

A
  • Receptors that bind to non-antigen binding region of Ig (constant domains of Ig heavy chains) –> Fc region
64
Q

Which two systems are involved in B cell effector mechanisms?

A
  • Fc receptors and complement

- Like giving the antibody teeth (‘deadly’ to pathogen)

65
Q

In general, when do Fc receptors and complement react with the constant region?

A
  • Once Ig has BOUND antigen
  • Ig changes conformation–> can now interact with Fc receptors and complement (exceptions to rule but don’t need to know)
66
Q

Where are most Fc receptors found ?

A
  • On immune cells
  • Some are inhibitory (on B cells) BUT most are ACTIVATING –> FcR binds Ig -antigen–> cell activated –> phagocytosis, degranulation, oxidative burst, cytokine production
67
Q

Why does the Ig need to be complexed with antigen before binding to Fc receptor to activate?

A
  • Bc. Fc receptor has low affinity for JUST antibody
68
Q

Which Fc receptor has extremely high affinity for its antibody?

A
  • FCER1 has HIGH AFFINITY FOR IgE (binds it monomerically)– without antigen -exception
69
Q

Is ADCC important for IgE?

A

YES!

- For Helminths

70
Q

Is there a lot of IgE in serum ?

A
  • NO!
  • because it is stuck on the cell surface of eosinophils, basophils, and mast cellsl–> very HIGH binding affinity
  • not soluble
71
Q

Which order do the complement proteins get activated in?

A
  • C1–> C4–> C2–> C3–> C5-C9
72
Q

What are complement proteins?

A
  • Soluble proteins in serum
73
Q

what are the 3 outcomes of triggering the complement pathway?

A
  • Inflammation
  • Opsonisation
  • Cell lysis
74
Q

Which complement pathway is the adaptive immune response?

A
  • Classical pathway (bc.Igs are involved)
75
Q

What ROUGHLY occurs in the classical complement activation?

A
  • Ig binds to antigen on cell surface
  • C1q RECOGNISES IgG or IgM bound to Ig
  • C1r + C15 CLEAVE C4–> C2–> C3 convertase –> C3convertase –C3b–> C5 convertase
  • then C 5 cleaved and later events occur
76
Q

What occurs in inflammation to trigger complement?

A
  • C3 + C5 proteolysis release soluble fragments C3a and C5a –> attract leukocytes to infection
  • Leukocytes have receptors for C3a and C5a (chemoattractant gradients)
77
Q

What occurs in opsonisation and phagocytosis to trigger complement?

A
  • C3b on surface of cell/microbe

- phagocytes have receptors for C3b–> microbe opsonised by C3b–> recognised by complement receptor and phagocytosed

78
Q

What occurs in lysis to trigger complement?

A
  • MAC–> pore in membrane –> osmotic lysis of microbe
79
Q

What does DAF do?

A
  • Binds to C3 convertases and dissociates them

- Used to regulate the complement pathway

80
Q

What are the 3 major regulatory molecules in complement activation?-

A
  • CD46
  • DAF (Decay Accelerating Factor)
  • CD59
81
Q

Which protein can inhibit complement in serum?

A
  • C1 INH prevents proteases from becoming proteolytically active
82
Q

5’ end of heavy Ig heavy chain is known as what?

A

VDJ segments

83
Q

What is the 3’ end of the heavy Ig chain gene known as?

A
  • Constant region- genes encoding different constant regions of heavy chain
84
Q

During germinal center reaction what occurs (roughly)?

A
  • Isotype swithcing occurs (AID cuts out switch regions and re-joins to change isotype)
85
Q

What determines whether an Ig isotype can interact with Fc receptors and/or complement?

A
  • Constant region on the Ig

- Fc and complement will ONLY react with constant region ONCE Ig has bound antigen

86
Q

Which Ig are there multiple subclasses for?

87
Q

What does IgD do?

A
  • Acts as a RECEPTOR for naive B cells
  • Not secreted
  • Function not sure
88
Q

What are IgM chacteristics?

A
  • Receptor of naive B cells
  • Needed for first adaptive immune response
  • pumped out by plasma cells BEFORE affinity maturation
  • LOW affinity so not good at neutralising
  • HIGH avidity (pentamer so good at activating complement)
89
Q

Does IgM activate complement well?

A
  • YES!
  • Better than IgG
  • C1q–> Binds to Fc region of IgM and IgG when bound to antigen
90
Q

What are some properties of IgG1?

A
  • 4 subclasses
  • MAJOR SERA Ig
  • ACTIVATES complement (but not as good as IgM)
  • GOOD OPSONISING Ig (because of Fc receptors)
  • Good at neutralising (bacterial toxins, viral receptors)
  • GOOD at ADCC (Antibody dependent Cellular cytotoxicity)–> via Fcgamma receptor of NK cells
  • CAN CROSS PLACENTA
91
Q

When is IgG formed in the immune response?

A
  • AFTER germinal centre reaction–> T cell help during GCR drives affinity maturation–> quality of Ig goes up later in immune response
92
Q

What are some properties of IgE and what is it found on?

A
  • Fights HELMINTHS
  • Allergy response
  • Found on surface of mast cells, eosinophils, basophils with FcER complexed on
93
Q

Why is there not much IgE in the sera?

A
  • Because it binds to FcER1 with HIGH AFFINTIY
94
Q

Can IgE activate complement?

95
Q

What are the effector functions of IgE dependent on?

96
Q

Is IgE a neutralising antibody?

A
  • NO bc. not found in sera
97
Q

How does IgE drive Mast cell activation?

A
  • covered with Fc receptors for IgE

- Must cell undergoes signal transduction –> degranulates –> produces histamine, pro-inflammatory cytokines

98
Q

What mediates the weep and sweep response and what responses do they cause?

A
  • Tries to physically expel the worms (IgE crosslinking mast cells via FcER1)
  • Pro inflamm cytokines
  • Vasoamines WITH IL-4 and IL-13 (Th2) involved
  • cause increase in smooth muscle contraciton
  • increase in intestinal permeabiliy
  • increase in mucous secretion by goblet cells in epithelium (wheezing in asthma attack), increased sensitivity of target cells to mast cell
99
Q

How does IgE mediate ADCC against helminths?

A
  • Eosinophils express FCER1 –> IgE with helminth crosslinking binds –> they become activated –> eosinophils degranulate –> toxic to larval stages of worms
100
Q

What are the two types of IgA?

A
  • Serum IgA (Proinflammatory)

- Secretory IgA (antiinflammatory)

101
Q

What are some properties of Serum IgA?

A
  • 15% in serum
  • Pro inflammatory
  • IgA binds to the IgA receptor (Fcalpha R1-CD89) found on Marophages, Eosinophils, DCs, Platelets, Kuffper cells
  • Activating phagocytosis, oxidative burst, ADCC, Proinflammatory cytokines (TNF, IL-1, IL-6)
102
Q

What are the proinflammatory cytokines?

A
  • TNF-alhpa
  • IL-1
  • IL-6
103
Q

What are some properties of secretory IgA?

A
  • IgA2 gene
  • forms dimers in mucosal secretions
  • Secretory IgA trransported across epithelia to intestinal lumen via TRANCYTOSIS
  • Then IgA is in lamina propria (connective tissue where there is lymphoid tissue)
  • IgA secreting plasma cell secretes dimeric IgA
  • Binds to poly-Ig-receptor on basolateral membrane of cell –> endocytosis–> trancytosis–> lumen of intestine (piece of poly-Ig receptor remains stuck to the IgA dimer–secretory component)
104
Q

When is IgA made in the immune response?

A
  • Made AFTER the germinal centre reaction

- Affinity maturation occured (high affintiy)

105
Q

What 3 things can IgA do if bacteria produce toxins?

A
  1. IgA can cross BACK into lamina propria and neutralise toxins (stop from damaging endothelial surface) -transported back into the lumen to neutralise
  2. On gut surface, can bind and nuetralise toxins and pathogens
  3. Internalised in endosomes
106
Q

Why is secretory IgA non inflammatory and which diseases can it go wrong in?

A
  • Bc. it must keep COMMENSAL bacteria alive!
  • Also make sure that they don’t go into another compartment
  • this goes wrong with ulcerative colitis, Chrons etc.
107
Q

What property must the Ig have for neutralisation to occur?

A
  • Ig must be high affinity –> can block by penetration of microbe by binding to it (only if microbe binds to a virus specific receptor)
  • e.g. diptheria, cholera, whooping cough
  • Ig blocks binding of toxin to cellular receptor (thus no necrosis)
108
Q

How important are Igs in cancer therapy?

A
  • Igs bind to CTLA-4 and PD-1 (which are normally inhibitory molecules of T cells)
  • igs binding turns OFF the inhibiotry signals
  • thus turns T cells on to make them a better killer of e.g Melanoma
109
Q

Why doesn’t IgE opsonise? -

A
  • IgE Fc receptor NOT expressed on phagocytes
  • Designed to kill larger helminths
  • phagocytes have receptors for C3b
110
Q

What are two effector subsets of Igs that come from Lysis and cytotoxicity?

A
  • Complement lysis

- Fc dependent ADCC

111
Q

What occurs in complement lysis?

A
  • MAC (C5b, C6,C7,C8,C9_ pokes holes in the pathogen membrane (osmotic shock)
112
Q

What occurs in Fc dependent ADCC?

A
  • Antibody Dependent Cellular Cytotoxicity
  • Ig–> Fc receptors and immune cells –> degranulation–> toxic to pathogen
    e. g. IgG antigen binding to low affintiy Fc receptor (CD16)
  • CD16 on NK cell causes killing of Ig coated cell

IMM2011 (7 decks)

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