Effector Mechanisms Of Adaptive Immunity Flashcards

1
Q

Antibody neutralisation

A

Blocks molecules important to pr neutralises the function of the pathogen by binding to the active part of the pathogenic cell

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2
Q

Complement activation

A

IgM and IgG can activate the classical complement pathway

-> which 1. Directly loses bacteria 2. Opsonises cells for uptake by phagocytes 3. Activates the immune response

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3
Q

Opsonisation

A

Phagocytes have receptors on their surface for antibodies (Fc receptors and complement)
If a pathogen has antibody and or complement deposited on its surface it is opsonised

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4
Q

Antibody dependent cell cytotoxicity

A

Infected cells have pathogen molecules on their surface -> Antibodies bind and mark them for killing -> NK cells ands neutrophils recognise antibodies and tell the cells to apoptosis via release of cytotoxic granules

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5
Q

Mobilisation of inflammatory mediators

A

Mast cells have high affinity Fc epsilon receptor 1 which binds free IgE -> When FCR1 receptors are criss linked, mast cells and basophils degranulate and rapidly release inflammatory compounds

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6
Q

B cell activation leads to class switching

A

Antibody function is determined by Fc region - termed isotopes

Naive B cells first express IgM

Activated B cells can switch (change constants region to ,ark IgG, IgA and IgE)

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7
Q

Antibody Fc receptors

A

Distinct Fc receptors for each isotope on immune cells for antibodies

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8
Q

IgG

A

Monomeric

Action depends on subclass, but can opsonise, neutralise, activate complement and antibody dependent cell cytotoxicity

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9
Q

IgM

A

Dimeric

First isotope to be produced
Great for trapping and neutralising lots of antigen, very good at activating complement, poor at opsonising and antibody dependent cell cytotoxicity

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10
Q

IgE

A

Monomeric
Best at activating basophils, mast cells an eosinophils
In allergy and parasite infections

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11
Q

IgA

A

Dimeric

Found in mucosa
Good at neutralising intestinal pathogens and ensuring they are flushed out
Poor at activating complement, opsonising and ADCC (as there is no neutrophils in the gut lumen)

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12
Q

Somatic hypermutation

A

Point mutations in variable regions of receptor/antibody

Activated B cells undergo this

Leads to antibodies with stronger or weaker binding to antigen

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13
Q

Affinity maturation

A

Generates antibodies that can bind strongly to monovalent antigens

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14
Q

CD4+ T helper cells

A

Act as a co-ordination for killing cells
T cells which when activated by dendritic cells carrying their specific antigen proliferate then go to B cell area to provide help by providing co-stimulation signal - they select B cells that make the strongest binding antibodies

CD4+ T cells select appropriate class of antibody during class switching

CD4+T cells stimulate innate cells

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15
Q

Linked recognition

A

CD4+ T cells only provide help to B cells which recognised the same antigen as them and present that peptide on MHC class two

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16
Q

Linked recognition prevents

A

CD4+ T cells helping B cells that recognise self/environmental conditions

17
Q

CD8+ cytotoxic T lymphocytes kills through

A

FAS litigation and perforin and grant me release

Fas litigation directly signals to induce apoptosis
Perforin forms pores allowing granzyme to enter
Granzyme activates caspases, DNAase activation and mitochondrial breakdown

18
Q

Cross presentation

A

Intial activation of MHC 1/ peptide on dendritic cell leads to activation in lymph node

19
Q

Natural Killer cells

A

Recognise down regulation of expression of MHC1 and kill cell