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MICR223 > MODULE 5 - Immunology II: Lymphocyte Biology > Flashcards

MODULE 5 - Immunology II: Lymphocyte Biology Flashcards

1
Q

what is the difference between the innate and adaptive immune systems?

A

innate system detect pathogens and tries to get rid of them and when it cannot it brings in the adaptive immune system which involves T and B cells because they can get rid of pathogens in a much more efficient and specific way

the main difference between innate and adaptive cells is the specificity of adaptive cells

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2
Q

what are antigens?

A

pathogens are made of macromolecules

these macromolecules are degraded inside cells and turned into antigens

antigens are recognised by T and B cell receptors

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3
Q

why is it important that each BCR or TCR needs to recognise only one type of antigen?

A

to avoid autoimmunity

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4
Q

what is recognition of antigen necessary to initiate?

A

an immune response

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5
Q

what is the theory of clonal selection?

A

that the cell which expresses the receptor with the correct specificity for the antigen present will proliferate

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6
Q

does the BCR recognise the same antigen as the cells antibody that it produces if it forms a plasma cell?

A

yep

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7
Q

what is the structure of the B cell receptor (BCR)?

A

light chain (two types) made up of two bits

heavy chain (five types) made up of four bits

constant region - structural component which helps it plug in and keep its shape

variable region - changes between every B cell so they can all recognise diff antigens

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8
Q

how can we get shit loads of combinations from a very small number of BCR genes?

A

there are small numbers of variable region genes (V), constant region genes (D) and joining genes (J) for both the heavy chain and light chain

these can be matched in many different ways however to ultimately result in millions of different receptors

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9
Q

what is the mechanism of recombination of B cell receptors?

A

each gene segment (V, D and J) has an adjacent recombination signal sequence (RSS)

RSS gets recognised by two proteins encoded by Recombination Activating Genes; RAG-1 and RAG-2

RAG-1 and RAG-2 proteins cut through both strands of DNA at the RSS forming ds breaks

usual machinery for repairing ds breaks (non-homologous end-joining) fixes these

ligated to form coding joint or signal joint

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10
Q

what are some other sources of variation for the BCR other than the mechanism of recombination?

A

the exact points of splicing between Vh and Dh and between Dh and Jh can vary over several nucleotides

extra nucleotides, called N regions, can also be inserted at these joints

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11
Q

how do antibodies get rid of pathogens?

A

through opsonisation, neutralisation and complement fixation

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12
Q

what are the main functions of B cells?

A

produce antibodies

act as antigen presenting cells

establish memory population

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13
Q

what are the two types of antibody production?

A

T cell dependent antibody production

T cell independent antibody production (not really relevant to us)

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14
Q

how does T cell dependent antibody production occur?

A
  1. BCR binds specific antigen
  2. B cell presents antigen on MHCII and up regulates CD40
  3. T cell gets activated by recognising specific antigen on MHCII on B cell acting as APC, upregulates CD40L which binds CD40 on B cell
  4. T cell releases cytokine signal to B cell
  5. B cell gets activated and develops into plasma cell which makes lots of antibody

So T cells help B cells become activated (with cytokines and CD40L) and B cells help T cells become activated (by presenting antigen on MHC) all at the same time

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15
Q

what are the roles of antibodies?

A

opsonisation - covering the bacteria to make it more tasty for macrophage e.g. putting chicken salt on my fries make jolly more likely to steal

agglutination - antibodies bind two microbes together making a big lump which again is more tasty to macrophage

neutralisation - neutralise virus by blocking its receptors so it can’t bind

precipitation - forming insoluble complexes of antigen and antibody

complement fixation - binds antigen and recruits complement to cause bacterial lysis

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16
Q

why are there different types of antibody and how are they different?

A

cause there are different types of pathogen, different sites of the body and replicating pathogens so we need different types of antibody

through recombination you get different isoforms of constant region of heavy chain or the antibody, while the variable region stays the same

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17
Q

what does Ig mean?

A

immunoglobulin

which just means antibody

you fucking slut

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18
Q

what are the main types of antibody?

A

IgM

IgG

IgA

IgE

IgD

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19
Q

what is IgM?

A

has a mew heavy chain making its shape pentameric

first antibody to appear (starts as BCR) and very good at activating complement but not super effective just like a nice start

found in the blood and lymph

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20
Q

what is IgG?

A

has a gamma heavy chain

is the major circulating antibody and is found in the extracellular fluid, blood and lymph

can cross the placenta which is why a babies first immune response is its mothers IgG

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21
Q

what is IgA?

A

has an alpha heavy chain

is the major secretory antibody which is why its generally found in secretory places such as mucosal surfaces and serum

is a monomer in blood and is a dimer in secretions (stable in dimer form as secretory component stabilising it)

22
Q

what is IgE?

A

epsilon heavy chain

involved in parasite killing by binding mast cells causing degranulation and histamine release - common side affect of this is allergy

found in the blood and lymph

23
Q

what is IgD?

A

has a delta heavy chain and is found in the blood and lymph

no one really knows what the fuck it does

24
Q

between all the different types of antibody, they will have different heavy chain structure, but what stays the same?

A

specificity to antigen

some fucking how

25
Q

how do we start with antibody being IgM and then get to antibodies such as IgA, IgE or IgG?

A

antibody class switching

26
Q

how does antibody class switching occur?

A

secreted antibody doesn’t change, antibody made by initial B cell changes

activated B cells start to divide and during this have to replicate DNA to make two daughter B cells. When this is happening they can switch up the heavy chain (leaving variable the same) so that now all the daughter cells will be getting signals to say actually make IgE cause there’s a big fuck of parasite we need to go scrap

so parent B cell makes IgM (default antibody), but as cells divide they change up the heavy chain based on cytokine signals from T cells creating subsequent populations of daughter B cells making antibody specific for parasite (IgE)

27
Q

outline the stages of antibody class switching?

A

antigen exposure occurs

B cells with BCR specific for that antigen start proliferating

B cells start to produce antibody (pretty much all making IgM)

as these B cells continue to divide they get signals from T cells to change antibody structure

as they fully develop into plasma cells (best antibody producing cell) they are all making the new antibody

however although the antibody is structured different it is still specific as it was when it recognised the antigen in context of a BCR

28
Q

why is the class switched antibody still specific?

A

cause it still has the same variable region

only constant region changed

29
Q

what is happening at a DNA level during antibody class switching?

A

constant region of heavy chain includes genes coding for M (which is at the start i.e. transcribed first hence why IgM is the first antibody made) and then D after that and then G and so on

as the cells proliferate and receive signals to change structure they can loop out certain genes so that they aren’t expressed e.g. if signal says to make IgG it will loop out the M gene and the D gene and so it will make an IgG heavy chain instead of IgM thus producing IgG antibody

30
Q

how does the B cell choose which antibody to make?

A

B cell gets signal from the pathogen (saying I’m a parasite or fungus or something) and signals from T cell in the form of cytokines

so depending on the cytokine being made (e.g. IL-4) it activates a programme in the B cell saying what antibody is best (e.g. IL-4 says its a parasite so B cell makes IgE)

31
Q

why was it a little bit of a lie saying that the variable region stayed the same during antibody class switching?

A

cause of somatic hypermutation

B cells proliferate fast as fuck meaning that there is a high rate of mutation (point mutations) in the variable region which results in more B cell diversity

32
Q

what is somatic hypermutation and how does it lead to affinity maturation?

A
  1. activation of B cells w antigen
  2. rapid proliferation of B cells
  3. high rate of point mutation during rapid proliferation
  4. daughter B cells a bit different to parent B cells, this results in more diversity among B cells

(that is somatic hypermutation, this is affinity maturation)

  1. diversity among B cells results in weak and strong binding antibodies
  2. high affinity receptors receive a strong survival signal with antigen and so these B cells are selected for and pass on their high affinity receptor genes to their daughter cells
  3. B cells expressing low affinity receptors don’t get strong survival signal and die off
33
Q

what does affinity maturation result in?

A

means that by the end of the immune response you have a bunch of B cells which very high antigen affinity (and also right structure cause best heavy chain was chosen)

these are the B cells which end up forming memory cells which is why when there’s a secondary immune response its v efficient (as they make antibody in best possible structure and antigen affinity)

34
Q

what are the key features of T cells?

A

inducibility - respond to infection/disease i.e. when pathogen introduced they become active

specificity - only respond to foreign and dangerous pathogens

memory - reservoir ready to fight reinfection

35
Q

what are effector T cells?

A

the ones that have been activated and are out to fuck up the pathogen

36
Q

what do the cytokines produced by CD4 helper cells do?

A

help out APCs, other CD4 cells, CD8 T cells, and also antibody production from B cells

37
Q

what are cytokines?

A

soluble signalling molecules which act non-enzymatically through specific receptors

found in low conc systematically and high conc locally

secreted locally and act locally

specific (production and reception) and regulate cell function

38
Q

what is clonal expansion?

A

there’s a diverse range of naive T cells with TCRs of different specificity to different antigen

when antigen present the T cell with TCR specific for that antigen will proliferate (IL-2 supports T cell expansion) until you get a big population of that T cell

so you go from large diverse population with differing specificities to a narrowly focused effector T cell population specific for the same antigen

a pathogen may generate clonal expansion of multiple T cell clones

39
Q

what does Th1 do?

A

APC activated by intracellular pathogen so produces IL-12 activating Th1 (via IL-12 receptor)

inflammatory T cell

secretes IFN-gamma (inflammatory cytokine)

40
Q

what does Th2 do?

A

APC activated by pathogen so produces IL-4 activating Th2 (via IL-4 receptor)

Th2 cell then secretes IL-5 which important for B cell proliferation

also IL-4 (extracellular pathogens e.g. parasites), IL-13

41
Q

what does Th17 do?

A

APC activated by pathogen so produces IL-23 activating Th17 (via IL-23 receptor)

Th17 then secrete IL-17

42
Q

what does IFN-gamma cytokine (prod by Th1) do?

A

activate macrophages so we get more phagocytosis

activate CD8 T cells making them cytotoxic

enhance antibody production from B cells to enhance phagocytosis

note how these all important for intracellular infections

43
Q

what do the Th2 cytokines (IL-4, IL-5, IL-13) do?

A

tell mast cells to kill parasites (extracellular pathogens)

activate CD4 T cells to make more IL-4, 5 and 13

B cell activation and antibody production (to go bind pathogens)

44
Q

what does IL-17 produced by Th17 do?

A

causes inflammation by acting on neutrophils

tells CD4 T cells to make IL-22

this is important immune response for extracellular pathogens but also autoimmunity (as often inccorectly activated e.g. MS and IBD)

45
Q

what happens in the T cell between reception of the cytokines from APC and production of cytokines (same for all)?

A

APC secreted cytokine which binds to receptor on T cell

this leads to downstream signalling and transcription of genes for whatever cytokine T cell then secretes

46
Q

what are T follicular helper cells (Tfh)?

A

found in follicles of secondary lymphoid tissues (named after where they are found)

live in close proximity to B cells in germinal centres in a lymph node when activated by pathogen encounter

produce cytokines which determine which class and antibody should switch to

47
Q

what cell determines antibody class switching?

A

T follicular helper cells

via specific cytokines for each class of antibody

48
Q

when CTLs are killing cunts, what does granzyme activate to trigger cell death?

A

caspase pathway

49
Q

what are the three mechanisms CTLs can use to kill an infected cell?

A

perforin/granzyme mediated cytotoxicity

FasL/Fas mediated cytotoxicity

TNF/IFN-gamma mediated cytotoxicity

50
Q

outline the CTL FasL/Fas mechanism of cell killing?

A

FasL on CTL will bind Fas receptor on infected cell

this triggers caspase pathway leading to cell death

51
Q

outline the TNF/IFN-gamma mechanism of cell killing?

A

CTL secretes TNF or IFN-gamma cytokine which bind specific receptors on infected cell triggering caspase pathway leading to cell death

52
Q

what do Tregs do?

A

regulate immune responses through production of anti-inflammatory cytokines such as IL-10

MICR223 (7 decks)

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