adaptive immunity (effector mechanisms) (W11) Flashcards

1
Q

antibody different name and 5 types?

A

immunoglobulin (Ig)
IgM, IgG, IgA, IgE, IgD

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2
Q

antibody neutralisation?

A

neutralises virulence factors - bind to components to stop them binding to the receptors on our cells

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3
Q

IgM structure?

A

5 antibodies linked together

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4
Q

which antibodies can activate the classical complement pathway

A

IgM and IgG

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5
Q

how do antibodies opsonise cells and drive phagocytosis

A

phagocytes have receptors on their surface for antibodies (Fc receptors). pathogens with antibodies on their surface have been opsonised, antibodies engage Fc receptors and drive phagocytosis

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6
Q

ADCC?

A

antibody-dependant cell cytotoxicity:
antibodies bind to pathogen molecules on infected cells surfaces
NK cells and neutrophils recognise antibodies and cause apoptosis vis cytotoxic granules

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7
Q

what receptors do mast cells and basophils have which bind to what

A

Fc receptors that bind to free IgE

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8
Q

what are mast cells and basophils particularly active in

A

anti-worm/allergy responses

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9
Q

what happens when IgE binds to mast cells

A

cross linking of IgE receptors triggering the mast cells to granulate releasing histamine

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10
Q

what happens when there is systemic mast cell degranulation

A

anaphylactic shock

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11
Q

what determines antibody function

A

Fc region (constant region) - isotypes

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12
Q

antibodies expressed by naïve B cells

A

IgM and IgD (not secreted, just on surface as a receptor)

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13
Q

what is class switching?

A

activated B cells can class switch to make IgG, IgA, IgE

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14
Q

different Fc receptors for each antibody isotype?

A

Fc-gamma for IgG
Fc-epsilon for IgE
Fc-alpha for IgA
Fc-mu for IgM

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15
Q

function of IgM

A

good at trapping and neutralising antigen
not good at opsonising and ADCC

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16
Q

function of IgA

A

good at neutralizing intestinal pathogens and ensuring they are flushed out
poor at activating complement, opsonising and ADCC

17
Q

function of IgG

A

action depends on subclass - can opsonise, neutralise, activate complement and ADCC depening

18
Q

function of IgE

A

best for activating basophils, mast cells and eosinophils (in allergy and infection)

19
Q

B cell activation and somatic hypermutation?

A

after B cell activation, point mutations in variable regions of receptor/antibody resulting in antigens with stronger/weaker binding to antigen. Stronger ones selected by affinity maturation.

20
Q

why is affinity maturation in IgG important

A

IgG is monomeric - only one attachment site so must be strong

21
Q

Th1 cytokine produced and function?

A

IFN-gamma
vs intracellular bacteria + viruses

22
Q

Th2 cytokine produced and function?

A

IL-4
vs parasitic worms

23
Q

Th17 cytokine produced and function?

A

IL-17
vs extracellular bacteria and fungi

24
Q

Treg cytokine produced and function?

A

IL-10
suppresses immune responses

25
Q

CD4+ helper cells functions?

A

provide co-stimulation to B cells
drive affinity maturation of B cells
drive class-switching of B cells
Activate innate immune cells

26
Q

how do CD4+ T cells help B cells

A

providing signal 2 (only when B cells present them with peptide/MCH2 that they recognise)

27
Q

what does linked recognition (following somatic hypermutation) by CD4+ T cells allow

A

selection of B cells expressing receptors/antibodies that bind antigen most strongly, therefore driving affinity maturation

28
Q

what does class-switching require from CD4+ T cells

A

co-stimulation

29
Q

CD4+ T cells stimulate innate cells (help brain doesn’t work)

A

AHHHHH

30
Q

2 mechanisms that CD8+ CTL use to kill

A

FAS ligation
perforin and granzyme release

31
Q

FAS ligation?

A

directly signals to induce apoptosis

32
Q

perforin and granzyme release?

A

perforin makes pore in cell allowing granzyme to enter. this activates caspases, DNAase activation and mitochondrial breakdown.