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YEAR 2 S2 IMMUNO > Theme 4 - 4c (GOD, B cells, antibodies) > Flashcards

Theme 4 - 4c (GOD, B cells, antibodies) Flashcards

1
Q

what does GOD stand for

A

generation of diversity

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2
Q

what are the 3 basic principles of the adaptive immune system

A
  • start with DIVERSE REPETOIRE of receptors so that there is more chance of finding a match to the pathogen
  • expand (and in some cases improve) the matched cell
  • maintain some of these matched cells for future “memory” against the pathogen
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3
Q

what is the primary response to an antigen in the adaptive immune response

A
  • IgM is detected in the serum first, but falls off rapidly
  • becomes switched antibody: IgG and IgA synthesis builds to maxiums over a LONGER PERIOD and becomes the predominant one
  • drop-off in serum IgG/IgA is later than for IgM
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4
Q

what is the secondary response to an antigen in the adaptive immune response

(ie the second time you are exposed to an antigen you’ve been exposed to before)

A
  • secondary response is a CONSEQUENT response to the same antigen
  • same IgM response as in primary repsonse
  • HOWEVER, SWITCHED ANTIBODY RESPONSE IS MUCH MORE RAPID AND REACHES A HIGHER TITRE
  • the drop off in serum IgG/IgA is later than for IgM
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5
Q

why is the adaptive immune system important

A

we can’t make enough pattern recognition receptors to deal with all pathogens, especially since many pathogens can evolve faster than us

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6
Q

how many different B and T cell receptors do we need?

A
  • there are ~500,000 different species of of pathogens

- total est no of HUMAN GENES is ONLY 20,000-25,000

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7
Q

describe the BCR (adaptive i.s)

A
  • heavy and light chain
  • membrane bound OR soluble as ANTIBODY
  • recognises antigens on whole molecules
  • can be different isotypes depending on the Fc
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8
Q

describe the TCR (adaptive i.s)

A
  • γδ or αβ T cells
  • membrane bound
  • recognises peptide antigen presented to it by MHC on other cells
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9
Q

what is a plasma cell derived from, what does it do

A
  • derived from B cells
  • produces ANTIBODIES
  • plasma cells has HIGH ER for synthesis of antibody
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10
Q

what does Fc region stand for on BCR

what does it do

A
  • Fragment constant region (the FUNCTIONAL REGION)
  • the other part is Fragment variable region (has diversity)
  • antibodies can have specificity for a certain antibody, but the Fc region CAN BE CHANGED O different FUNCTIONS
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11
Q

how does the B cell start off
what can BCR recognise
what can B cells differentiate into

A
  • start off as cells with receptor on surface of the cell
  • receptor recognises WHOLE ANTIGEN (without need for fragmentation or presentation)
  • differentiate into PLASMA CELLS that secrete the receptor as an ANTIBODY
  • ANTIBODY can bind to WHOLE PATHOGENS and faciliate a range of functions (depending on its Fc region)
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12
Q

what are the roles of antibody

A

1) NEUTRALISES toxins and viruses by blocking their interaction with cells (as antibodies are LARGE)
2) OPSONISES pathogens to promote PHAGOCYTOSIS and killing activity by other cells
3) ACTIVATES the COMPLEMENT CASCADE which helps kill pathogens
4) AGGLUTINATES particles (pathogen debris, viruses etc)
5) mediates ANTIBODY DEPENDENT CELL-MEDIATED CYTOTOXICITY (ADCC)

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13
Q

as well as synthesising antibodies what is another key role of B cells

A

they are APCs to T cells

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14
Q

what is the structure of an antibody

A
  • variable region with 2 BINDING SITES which determine the ANTIGEN SPECIFICITY
  • Fv region
  • Fc region - constant region which determines the CLASS of the antibody and O function
  • has 2x heavy and light chain
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15
Q

what is the role of the Fc region of an antibody

A

it is the functional region of the antibody, it determines which CLASS of antibody the antibody is in

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16
Q

how does a B cell change after it has seen antigen?

A

it undergoes CLASS SWITCHING

  • the Fc (which determines class) undergoes the switch (eg from IgM to IgG or IgA)
  • the Fv region is unchanged to keep the antigen specificity
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17
Q

what controls the class switching process

A
  • THE CYTOKINE ENVIRONMENT
  • O the change is FUNCTION specific
  • also CD40Ligand (found on helper T cells- which secrete cytokines)
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18
Q

what can cause class switching of a B cell from IgM to IgG

A
  • if there is a lot of IFNγ secreted by helper T cell
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19
Q

what can cause class switching of a B cell from IgM to IgA

A
  • if there is a lot of TGF-β, a mucosal tissue cytokine release
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20
Q

is antibody specificity changed during class switching

A

no , as the Fv region stays the same

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21
Q 
how do cells have specificity for different antibodies 
how does class switching affect this
A 
they may have receptors for a specific type eg IgA
- by class switching, you change the Fc region O you change the antibody, O you change the cells that it will bind to
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22
Q

what is IgA structure

where is it found/secreted

A

it is DIMERISED which PROTECTS it

  • it is secreted across mucosal epithelium into GUT
  • it could be DIGESTED in the gut but dimerisation PROTECTS it from that
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23
Q

what is the structure of IgM

A
  • can form pentamer
  • has many binding sites
  • latge molecule O it is not v good at diffusing through tissues
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24
Q

when is diversity initially generated

where for B and T cells

A
  • it is gene rearrangement and heterodimer formation
  • happens when cells are fist formed (before they see exogenous antigen)
  • in B cells this occurs in the BONE MARROW
  • in T cells it occurs in the THYMUS
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25
Q

what are the heterodimers in B and T cells

A

in B cells: heavy and light chains x2

in T cells: alpha with beta and gamma with delta

26
Q

do B cells have hypermutation

do T cells have hypermutation

A

B:yes
T: no

27
Q 
do B cells do class switching?
do T cells do class switching?
A

B: yes
T: no

28
Q

what is the role of IgD

A
  • it is a membrane bound form of Immunoglobulin on naive B cells (B cells early in development BEFORE they see an antigen)
29
Q

what is the role of IgM

A
  • The default immunoglobulin that B cells start with in development
  • the Fc region enables the molecules to form pentamers (useful in forming immune complexes, but which means that the molecules are too large to diffuse into tissues or cross the placenta)
  • Very efficient at activating complement through the classical activation pathway
30
Q

what is the role of IgG

A
  • IgG is the main antibody secreted into the blood after class switching
  • very good at opsonisation –coating pathogens so that phagocytic cells can recognise them
  • Pathogens coated in IgG also become targets for killing by Natural killer cells –ANTIBODY-DEPENDENT CELLULAR TOXICITY
  • there are 4 subclasses of IgG (IgG1,IgG2 etc)
31
Q

what is the role of IgA

A
  • the mucosal antibody –produced by B cells at mucosal surfaces and secreted into breast milk
  • actively secreted across mucosal surfaces
  • can form a dimer, which helps protect it from enzymatic breakdown (such as occurs in the gut), but generally exists in monomeric form in the plasma
  • there are two Subtypes (IgA1, IgA2)
32
Q

what is the role of IgE

A
  • IgE is important in parasitic infection
  • binds to the surface of Mast cells via it’s Fc receptor –even in the absence of antigen•Antigen cross-linking of IgE on Mast cells causes the mast cells to degranulate
  • Usually low in concentration, but higher in cases of allergy –especially immediate hypersensitivity
33
Q

what are the 3 types of antigen that can activate B cells

what is the importance of the 2nd and 3rd types

A

1) T-dependent (TD)
2) T-independent type I (TI-I)
3) T-independent type II (TI-II)

  • TI-I and TI-II are important because T cells can only recognise PEPTIDES and not all antigens are PEPTIDES O we need a T-independent way of activating B cells
34
Q

what are the different receptors involved in B cell activation

A
  • BCR (specificity)
  • innate immune receptors (that recognise PAMPs)
  • co-stimulatory molecules
  • cytokines
35
Q

describe T-dependent B cell activation

A
  • B cell binds to the peptide pathogen
  • B cell INTERNALISES and DEGRADES THE BCR and PATHOGEN
  • then it presents the peptide to MHC II (in the case of an exogenous antigen) which presents it to a CD4 T cell
  • this then activates the B cell
  • activated B cell produces antibody against pathogen
  • if it is an INTERNAL antigen (eg virus) then the viral particle binds the virus through viral COAT PROTEIN, then the viral particle is internalised and degraded
  • then peptides from internal viral proteins are presented to MHC I, which is presented to the CD8 T killer cells
36
Q

all APCs (including B cells) have to be able to what

A
  • take exogenous antigen, process and degrade (chop up) antigen and present to MHC class II which will present it to a CD4 T cell
37
Q

describe T-independent type I B cell activation

A
  • PAMP receptor (eg toll receptor) can be used
  • toll receptor can activate B cell regardless of what is on the BCR
  • this can cause POLYCLONAL B cell activation
  • this is a NONSPECIFIC ANTIBODY RESPONSE
38
Q

describe T-independent type II B cell activation

A
  • two receptors on a B cell that can recognise the same antigen can, due to the fluidity of the membrane end up next to each other
  • when a large molecule with a repeating determinant (eg S. pneumoniae) binds it causes CROSSLINKING
  • this causes ACTIVATION of the cell
  • if the molecule (eg S.pneumoniae) was bound to a dendritic cell in this manner it causes the B cell to come into contact with other cells that help the B cell find a B cell
  • also activated dendritic cells release BAFF cytokine, which INCREASES production of antibody against TI-II and induces class switching
39
Q

TD antigen does what as well as activating B cells

A

activates B cells AND primes T cells

40
Q

which type of T antigen is used in infants

A

TD and TI-1

41
Q

why are elderly and babies susceptible to pneumonia

A
  • requires TI-2 antigen
  • requires specialised B cells that are able to respond to pneumonia
  • we dont have them when we are very young
  • they deteriorate when we get old
42
Q

why are elderly and babies susceptible to pneumonia

A
  • requires TI-2 antigen
  • requires specialised B cells that are able to respond to pneumonia
  • we dont have them when we are very young
  • they deteriorate when we get old
43
Q

what is the effect of congenital athymia on T cells

A

you would have thought there would be no T cells BUT it has been shown that these indviduals have a small no of T cells (O could the T cells be produced in the gut?)
- if ALL T CELLS are removed then they can use TI-2

44
Q

what was the B in B cell actually named after

A

Bursa Fabricus in chickens (where B cells were originally found)

45
Q

what happens after B cell antigen specific clonal expansion
where does this happen
what is formed

A
  • go through HYPERMUTATION and CLASS SWITCHING in the GERMINAL CENTRE
  • plasma cells and memory B cells are formed
46
Q

is hypermutation of B cells before or after antigen exposure

A

AFTER

47
Q

is class switching of B cells before or after antigen exposure

A

AFTER

48
Q

what is VDJ gene rearrangement

what is VJ gene rearrangement

A
  • gene rearrangement in the heavy, beta and gamma genes of T cell
  • gene rearrangement in the light (kappa or lambda), alpha or gamma genes of T cell
49
Q

how does gene rearrangement work
what are the different regions
which enzymes are involved in this

A

one whole gene is made by combining different segments of the genes

  • there are V, D and J regions which are randomly put together
  • RAG1 and RAG2 (Recombination Activating Genes)
50
Q

why are the RAG enzymes important

A

if you have primary immunodeficiency you CANNOT MAKE B or T cells as the genes cannot be put together

51
Q

what is the purpose of gene rearrangement

A

you can get a lot more genes this way (there are a MUCH LARGER NUMBER of combinations) O more proteins

52
Q

what does the light chain consist of

A 
either kappa light chain or lambda light chain 
VJC
V being variable 
J being 'joining' joins V and C 
C being the constant region
53
Q

what does the heavy chain consist of

A 
VDJC 
V being variable 
D being 'diversity' 
J being 'joining' joins V and C 
C being the constant region
54
Q

how are the actual number of different Ig gene possibilities MORE THAN 5 MILLION

A
  • NTs can be accidently removed form V, D and J regions
  • NTs can be deliberately inserted between the V, D and J regions
  • the REGION WHERE THE DIFFERENT SEGMENTS JOIN together creates MORE diversity
  • also true for TCR
55
Q

which enyzme inserts random nucleotides (NTs) between V, D and J regions

A

by enzyme TdT

56
Q

wherew does affinity maturation and class switching of B cells take place

A
  • specialised microenvironment of GERMINAL CENTRE and require an enzyme called Activation Induced Cytidine Deaminase (AID)
  • both req help form outside the B cells in form of cytokines and contact with other cells (esp T helper cells)
57
Q

hwat occurs in the dark zone of the germinal centre

A

hypermutation

58
Q

what happens in the light zone of the germinal centre

A

SELECTION

  • they req T cells to survive
  • they die if they dont have T cells as they have lost Bcl2
  • T cell will only help those that BIND ANTIGEN VERY WELL
  • O only the B cells that have high affinity can survive
59
Q

how is class switching done

A

if the stop codon is moved (???) to the region you want to cut to
ie if you cut to an IgA, the Fc region will switch to IgA, if you cut to IgG, then the Fc region will be IgG

60
Q

summarise antibody affinity maturation

A

1) in the lymph node sinus, pathogen is ENGLUFED by B cell that has antigen specific antibodies
2) the B cell processes and presents the antigen to a T cell completes B cell activation
3) the B cell travels to the germinal centre of the secondary lymphoid organ (eg lymph nodes)
4) here, in the NUCLEUS of the activated B cell the genes for ANTIBODY ENCODING PROTEIN, the activation induced cytidine deaminase (AID) protein INDUCES POINT MUTATIONS
5) O the rate of mutation INCREASES BY 1MILLION
6) DNA is replicated
7) B cell divides O population of B cells expressing HYPERMUTATED GENES increases
8) O they produce antibodies with A RANGE OF AFFINITIES FOR TARGET ANTIGEN
9) germinal centre also contains DCs which present ANTIGEN
10) there is COMPETITION amongst the B cells for the antigen
11) the hypermutated antibodies of the B cells have VARYING AFFINITIES, those with low affinity don’t bind whereas highest affinity CAN BIND ANTIGEN and induce ‘spreading’ of the centrocyte/B cell O they can bind more ANTIGEN
12) the centrocyte/B cell strips the ANTIGEN
13) it is then presented to T cells
14) T cells then provide chemical survival signals for the B cell/centrocyte survival
15) O the centrocytes / B cells without hgih affinity do not receive the survival signals undergo APOPTOSIS
16) high affinity centrocytes/B cells cont to divide and mutate, thus giving further selction of B cells so each generation has increasing affinity
17) O there is an evolution as only the highest affinity centrocytes/B cells contribute genetic information to the next generation
18) the resulting cells can divide into IMMUNE EFFECTOR CELLS eg PLASMA CELLS which mass produce high affinity antibodies

YEAR 2 S2 IMMUNO (14 decks)

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