Effector Responses of IS Flashcards

1
Q

Effector responses

A

aim to eliminate pathogens and infected cells from the body + clear cells that are damaged or abnormal

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2
Q

Name the antibody isotopes.

A

IgM - produced 1st during infection
IgG - abundant in blood
IgA - in mucous membranes
IgE - against worm infection

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3
Q

What are the differences between the antibody isotopes?

A

~ differ in their Fc regions and hinge

~ diff. effector functions, depend on which Fc receptors they bind to

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4
Q

Name the functions of antibodies.

A

1) neutralisation
2) opsonisation
3) complement fixation
4) antibody-dependent cell-mediated cytotoxicity (ADCC)
5) Activation of granulocytes

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5
Q

Neutralisation

A

~ antibody binding to the surface of a virus can prevent cell entry
~ antibodies can bind toxins from bacteria, making them harmless

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6
Q

Opsonisation

A

~ IgG and IgA surround pathogens can bind to Fc receptors (FcR) on macrophages
~ induces phagocytosis and the digestion of pathogens in lysosomes
~ can work together to make this happen

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7
Q

Complement fixation

A

~ IgG and IgM are recognised by the C1 complement complex –> activation of the classical complement pathway
~ this induces 1) optimisation by C3b and phagocytosis 2) lysis of the pathogen or the infected cell using the membrane attack complex (MAC)

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8
Q

Antibody-dependent cell-mediated cytotoxicity (ADCC)

A

~ IgG on the surface of infected cells binds to the FcgRIIIa receptor on Natural killer cells
~ this induces the degranulation of NK cells
~ NK cells granules contain performs and granzymes which induce apoptosis

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9
Q

Activation of granulocytes

A

~ IgE bound to parasites or allergens causes the degranulation of mast cells, eosinophils and basophils
~ this induces the release of histamine and other inflammatory mediators
~ this activates T(H)2 cells during

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10
Q

Name the cytotoxic effector cells

A
~ NK cells
~ CD8+ cytotoxic T lymphocytes (CTLs)
~ NK T-cells
~ all induce death by apoptosis
~ climate cells infected with intracellular pathogens, tumour or damaged cells
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11
Q

Generation of cytotoxic T-cells.

A

1) licensing of an antigen presenting cell (APC) - interaction w/ pathogen or activated T(H)1 cell
2) interaction of licensed APC w/ naïve CD8+ T-cell –> activation + differentiation into cytotoxic T-cell (CTL)
3) simultaneous interaction of APC with activated T(H)1 cell + CD8+ T-cell –> APC licensing + CD8+ T-cell activation
~ IL-2 (from T(H)1) promotes CTL differentiation = efficient

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12
Q

Action of cytotoxic T lymphocytes a.k.a. ‘kiss of death’

A

1) CTL forms immunological synapse w/ target cell
2) secretory granules move along microtubules
3) secretory granule fuse with the presynaptic men.
4) perforins assemble to make pores, granzyme causes apoptosis of target cell

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13
Q

Perforins

A

~ monomers that assemble in the membrane of target cell to form a pore

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14
Q

Granzymes

A

~ serine proteases that cleave proteins in the target cell

~ enter through the pore created by perforins

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15
Q

Natural killer T-cells (5).

A

a.k.a. NKT cells
~ type of T lymphocyte w/ similar properties to NK cells
~ develop in thymus
~ undergo TCR gene rearrangements BUT express invariant TCR = alpha-beta TCR –> recognises CD1d (non-classical MHC)
~ act as both helper + cytotoxic cells (inc. CD4- + CD4+)
~ lack some T-cell markers but have other

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