Infection and immunity (Roger Booth lecture 5) Flashcards

1
Q

B cell ontogeny and immunoglobulin genes

A
  • Development in bone marrow (primary lymphoid organ)
  • Multiple V, D and J axons recombine = V region
    Recombination indépendant of antigen
    Variable region diversity arises from this
    B cells become committed to one Vh and one Vl
    Single constant region axons for each class
    Negative selection to remove strong self reactivity
    Class switching retains V-region, changing C region
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2
Q

T cell ontogeny

A

TCR genes re arrange from uncommitted thymocyte to a this T cell now begins to express both CD4 and CD8 (helper T cells use CD4 plus their TCR, and the cytotoxic lineage use CD8 and TCR)
need to make sure developing thymocytes can recognise HLA, so these cells are tested against some of the antigen presenting cells in the thymus to see whether they’re able to recognise HLA class I or II, using their TCR or CD4 or CD8. Then each cell down regulates the CD4 or CD8 that they don’t need.
Negative selection process: Before they head to the secondary lymphoid organs, this is to test whether they recognise HLA with self peptides very strongly, and if they do they’re gonna be strongly self reactive and potentially dangerous
Whats left: cells that recognise HLA but HLA that is associated with a foreign peptide, now these cells start expressing CD3
Export to secondary lymphoid organs

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3
Q

Thymus structure

A

T cell differentiation starts at the periphery / cortex and matures as they move inward towards the medulla

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4
Q

Important points: T cell ontogeny and T cell receptor genes

A

Development in the thymus (primary lymphoid organ)
Multiple V, D and J axons recombine = V region
Recombination indépendant of antigen
T cells become committed to one V alpha and one V beta
Positive selection for HLA class I or II recognition (requires CD8 or CD40
Negative selection against strong self reactivity
* even genetically identical twins won’t have the same B and T cell repitore

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5
Q

Hyper IgM syndrome

A

CD40 ligand mutation
High IgM but no antigen specific IgG
Inability to switch from the IgM class to the later classes
Class switch from IgM to IgG controlled by T cells, needs CD40-CD40ligand interaction

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6
Q

Microbial factors

A

type of organism induces different response (virus, bacteria, parasite)
Dose (degree of exposure)
Virulence
Route of entry

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7
Q

Host factors

A
Integrity of innate barriers (if broken a bit then expect to see an increase in infectious processes)  
Captive immune competence 
HLA, Ig and TCR genes 
Previous exposure 
Other infections
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8
Q

Antigens seen in viral infections

A
Lytic or integrated cycle 
Capsid antigens 
Internal structural components (HLA I) 
Metabolic products (HLA I)
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9
Q

antigens seen in bacterial infections

A

Extracellular (e.g. S aureus)
or intracellular (e.g. M tuberculosis)
Structural components
Metabolic products and toxins

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10
Q

parasites

A

Large (multicellular) (slower)
Life cycle changes
Radicle changes in antigenicity

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11
Q

Immune factors, what can the immune system do?

- soluble factor mediated effects

A

Direct neutralisation by antibodies
Opsonisation and phagocytosis
Complement mediated effects
Inflammatory and immnuregulatory cytokines esp antiviral cytokines (interferons)

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12
Q

Other non-soluble functions of the immune system?

A

HLA restricted T cell mediated cytotoxicity

NK cell mediated cytoxocitiy

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13
Q

Antibodies that are effective against antigens extraceullarly

A

Viruses (IgA, IgM and IgG)
Toxins (IgM IgG)
Extracellular bacteria (IgA, IgM, IgG)
Parasites (IgE, IgA)

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14
Q

Cytotoxic T cells: effective against intracellular protein antigens?

A

Virus infections
Timor cells
Transplanted organs

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15
Q

X linked agammaglobulinaemia

A

few detectable B cells and no tonsils

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16
Q

Local inflammation

A

Vascular permeability changes
Phagocyte recruitment
Acute phase protein (APP) induction
Local temp change

Leads to –> phagocytosis and complement activation

17
Q

NK cell recognition and killing

A
Ubiquitous molecules on the surface of all cells 
HLA class I recognised by the killer inhibitory receptor, this signal prevents killing by the NKC
18
Q

N/NK cell receptors

A

Killer activating receptor and killer inhibitory receptor, these allow the cell to recognise cells that might have changed HLA expression = natural killer activity

19
Q

NK cells

A

1-5% of blood mononuclear cells
CD16 (FcRgamma), CD56 and CD57 markers
Exhibit ADCC
Not classical B or T cells
Killer inhibitory receptor KIR binds HLA I
Activity enhanced by IL-2 and IFN- gamma
Early in viral infection and in cancer

20
Q

What does every body cell do when infected with a virus?

A

releases interferon molecules to tell the cells nearby to enter the transient state, to become less easily infected by viruses