Effector Responses of IS Flashcards
Effector responses
aim to eliminate pathogens and infected cells from the body + clear cells that are damaged or abnormal
Name the antibody isotopes.
IgM - produced 1st during infection
IgG - abundant in blood
IgA - in mucous membranes
IgE - against worm infection
What are the differences between the antibody isotopes?
~ differ in their Fc regions and hinge
~ diff. effector functions, depend on which Fc receptors they bind to
Name the functions of antibodies.
1) neutralisation
2) opsonisation
3) complement fixation
4) antibody-dependent cell-mediated cytotoxicity (ADCC)
5) Activation of granulocytes
Neutralisation
~ antibody binding to the surface of a virus can prevent cell entry
~ antibodies can bind toxins from bacteria, making them harmless
Opsonisation
~ 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
Complement fixation
~ 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)
Antibody-dependent cell-mediated cytotoxicity (ADCC)
~ 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
Activation of granulocytes
~ 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
Name the cytotoxic effector cells
~ 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
Generation of cytotoxic T-cells.
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
Action of cytotoxic T lymphocytes a.k.a. ‘kiss of death’
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
Perforins
~ monomers that assemble in the membrane of target cell to form a pore
Granzymes
~ serine proteases that cleave proteins in the target cell
~ enter through the pore created by perforins
Natural killer T-cells (5).
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