Immunology 5 Flashcards

Describe T cell activation and differentiation into cytotoxic T cells and T helper cells Describe B cell activation and differentiation into plasma cells Briefly describe the functions of different antibody classes Understand immunological memory Describe monoclonal and polyclonal antibodies, their production and applications

1
Q

What sort of tissue is included in Gut associated lymphoid tissue (GALT)?

(3 marks)

A
  • Tonsils
  • Peyer’s patchs
  • Lymphoglandular complexes
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2
Q

What is included in Bronchial associated lymphoid tissue (BALT)?

A

Bronchi of lung

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3
Q

What happens after a dendritic cell phagocytosed a pathogen and presents its antigen?

(5 marks)

A
  • Expresses receptors for chemokines made of lymph nodes
  • Lymph node will attract a licsenced dendritic cellwhich is attracted to lymph node by chemokine signalling
  • Dendritic cell with antigen meets naïve t cdell
  • T cell recognises pathogen and either becomes cytotoxic t cell
  • OR activates B cell which produces antibodies
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4
Q

What happens after a dendritic cell phagocytoses a pethogen and presents it on its cell surface?

(5 marks)

A
  • Expresses receptors for chemokines (made by lymph node)
  • Attracts liscened dendritic cell which is attracted to lymph node
  • Dendritic cell meets naive t cell which recognises pathogen
  • Activates t cell to either become cytotoxic
  • OR t cell will activate B cell which will produce antibodies
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5
Q

Summarise how a cytoxic t cell is activated.

(8 marks)

A
  • In paracrotex of lymph node naive CD8+ T cell recognises specific peptide antigen (via TCR) presented on antigen presenting cell MHC I molecule
  • CD8 assists binding of TCR and MHC I and increases signalling 100-fold.
  • B7 receptor on antigen presenting cell binds CD28 on naïve T cell and promotes survival of T cell.
  • IL-2 expression is induced in T cell and secreted IL-2 binds IL-2 receptors on T cell surface.
  • T cell proliferates and differentiates into a cytotoxic T cell.
  • Cytotoxic T cell travels to the site of infection.
  • Target cells infected with intracellular pathogen, present the same specific peptide antigen on MHC I molecules which is recognised by cytotoxic T cell.
  • Cytotoxic T cell secretes perforin and granzyme and apoptosis is induced in target cell.
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6
Q

Summarise the activation of a T helper cell

(6 marks)

A
  • In paracrotex of lymph node naive CD4+ t cell recognises specific peptide antigen presented on MHC II molecule
  • CD4 assists in binding TCR and MHC II increasing signalling
  • B7 receptor on MHC II binds to CD28 on naive T cell - promoting survival of T cell
  • Cytokine secretion by antigen presenting cell dictates differentiation of T cell
  • T cell differentiates into one of the following:

TH1, TH2, TH17, TFH or Itreg

  • TFH recognises specific peptide antigen on MHC II molecule of naive B cell and initiates B cell activation
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7
Q

What are the two types of B cell activation?

(2 marks)

A

T cell dependent

T cell INdependent

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8
Q

How does T cell independent activation happen?

(7 marks)

A
  • Naive b cell comes across antigen on pathogen and differentiates into plasma cell
  • Plasma cell can now secrete antibodies - kill pathogen, induce opsonisation
  • No T cell receptor needed as particular pathogen has repeats of same epitope
  • Lots of antibodies bind to surface of pathogen via epitope
  • Epitope brings antibodies in cluster, cluster activates them
  • Signals to cell to proliferate as recognised multiple copies of itself as real antigen
  • Together with TLR - bind more common pathogen and leads to activation of b cell
  • IgM made through this process
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9
Q

How does T cell dependent activation take place?

(5 marks)

A
  • B cells in naive state come into lymph node by cirulatory systems of bone marrow and sit in germinal centres
  • T cells come from thymus and sit in paracortex
  • Dendritic cell thats been at site of infection is phagocytosed and presenting an antigen
  • This cell comes to lymph node by lymphatic vessels and activates t cell
  • Pathogen that binds BCR and pathogen comes in from lymph node
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10
Q

What happens in the germinal centres of the lymph node to create a somatic mutation?

(4 marks)

A
  • In germinal centre of lymph node - naive B cell recognises pathogen with specific BCR and phagocytoses pathogen
  • Pathogen antigen presented on MHC II to T cell
  • B cell MHC II/ peptide complex is recognised by antigen-specific activated T cell - and so B cell survives
  • T cell signals to B cell to proliferate and B cell becomes centroblast
  • Centroblasts express AID (protein) and undergo somatic mutation of V region, which will either increase or decrease BCR (antibody) affinity for pathogen antigen
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11
Q

What happens in B cell activation after the somatic hypermutation?

(5 marks)

A
  • Proliferation will cease and the xentroblasts will enter the light zone
  • BCR affinity will be tested by follicular dendriteswhich trap and display intact pathogen
  • B cells with low affinity BCRs will no longer present MHC II/ peptides and will apoptose
  • B cells with high affinity BCR’s willl present many MHC II/peptides and antigen specific TFH cells promote survival
  • TFH cells induce cytokine specific heavy chain class switching
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12
Q

What is IgM and what does it do?

(5 marks)

A
  • Made in first T cell independent activation of B cells AND B cell activation
  • Activates complement proteins to cleave themselves when bound to surface of a pathogen
  • Found on surface of BCR
  • Secreted in t cell independent activation a large pentameter
  • Important for fighting blood infections
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13
Q

What does IgG do?

(3 marks)

A
  • Agglutination - neutralises toxins
  • Opsonisation
  • Released in tissues to fight infection

(most commonly found in serum)

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14
Q

What does IgA do?

(3 marks)

A
  • Secreted into mucus
  • Not in contact with complement proteins
  • In any secretions on surface of our tissue
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15
Q

What does IgE do?

A
  • Attactched to mast cells and activates them
  • Degranulates and releases all of its histamines and heparin and cytokines which is used for inflammation
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16
Q

What does IgD do?

A

Not known - all we know it is a BCR

17
Q

What is the first stage in the process of remembering infection?

(3 marks)

A
  • Naive B cell has just met antigen and expresses BCR in IgM class which has a low affinity for antigen
  • Binds to antigen and activated B cell undergoes somatic hypermutation whihc increases its affinity for the antibody
  • T cell induces a switch in B cell antibody and now has higher affinity as it has gone through hypermutation
18
Q

What happens in immunological memory after the class switch?

(3 marks)

A
  • Plasma cells secrete fast quantities of IgG antibody into fluid to fight infection
  • Mass production of antibody but also proliferation
  • Plasma cells reproduce cells and make clones so have loads of antibody
19
Q

What happens in the process of immunological memory after the plasma cells have mass produced antibodies?

(2 marks)

A
  • Get a memory cell which has the same class as the switched B cell but a higher affinity than BCR IgG
  • Memory cell however can’t secrete BCR - so BCR stays on surface of memory cell BCR with low porliferation
20
Q

What happens in the secondary immune response for immunological memory?

(5 marks)

A
  • Reinfection by same pathogen
  • Create many B cells with recognition of slihgtly different antigens on pathogen
  • Highest affinity BCR antibody recruited first - most efficient at pahgocytosing pathogen (expresses more MHC II)
  • Process much quicker - BCR IgG doesn’t need to class switch from IgM to IgG
  • Produce more antibody with higher affinity and memory cell with higher affinity than before
21
Q

What happens in the antibodies in doses of a vaccination?

(6 marks)

A
  • First immunisation cause T cell independent resopnse and b cells start to make IgM
  • Slower T cell dependent activation - T cell induces clonal expansion, somatic hypermutaion and class switch
  • Increasing IgG
  • Second vaccination goes round IgG memory cell
  • Get second round of somatic hypermutation and therefore increase in affintiy
  • With more vaccinations just increase IgG affinity
22
Q

What are the differnt forms of antibody technology?

(3 marks)

A
  • Polyclonal antiserum
  • Monoclonal antibodies
  • Antibody applications
23
Q

What does polyclonal antiserum production make?

(2 marks)

A
  • Mixture of antibodes produced that recognise different epitopes on surface of antigen
  • May be antibodies to any impurites injected with antigen
24
Q

What is the rationale for the production of monoclonal antibodies?

(2 marks)

A
  • Specifically recognise one epitope on antigen
  • Immortal source of antibodies
25
Q

What are some of the downsides to producing polyclonal antibodies?

(3 marks)

A
  • Each antiserum is differnt
  • Can only be produced in limited serums
  • Impossible to sue same antisera in multiple experiments
26
Q

How are monoclonal antibodies produced?

(7 marks)

A
  • Immunise mouse with antigen
  • Collect B cells
  • Fuse with myeloma cells creatign hybridoma cells
  • Isolate individual cells to get individual clones - MONOCLONAL
  • Test antibodies produced by cells for antigen binding
  • Grow hybridoma cells in large quantities
  • Freeze cells and get immortal source of antibody