adaptive immunity (effector mechanisms) (W11) Flashcards
antibody different name and 5 types?
immunoglobulin (Ig)
IgM, IgG, IgA, IgE, IgD
antibody neutralisation?
neutralises virulence factors - bind to components to stop them binding to the receptors on our cells
IgM structure?
5 antibodies linked together
which antibodies can activate the classical complement pathway
IgM and IgG
how do antibodies opsonise cells and drive phagocytosis
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
ADCC?
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
what receptors do mast cells and basophils have which bind to what
Fc receptors that bind to free IgE
what are mast cells and basophils particularly active in
anti-worm/allergy responses
what happens when IgE binds to mast cells
cross linking of IgE receptors triggering the mast cells to granulate releasing histamine
what happens when there is systemic mast cell degranulation
anaphylactic shock
what determines antibody function
Fc region (constant region) - isotypes
antibodies expressed by naïve B cells
IgM and IgD (not secreted, just on surface as a receptor)
what is class switching?
activated B cells can class switch to make IgG, IgA, IgE
different Fc receptors for each antibody isotype?
Fc-gamma for IgG
Fc-epsilon for IgE
Fc-alpha for IgA
Fc-mu for IgM
function of IgM
good at trapping and neutralising antigen
not good at opsonising and ADCC
function of IgA
good at neutralizing intestinal pathogens and ensuring they are flushed out
poor at activating complement, opsonising and ADCC
function of IgG
action depends on subclass - can opsonise, neutralise, activate complement and ADCC depening
function of IgE
best for activating basophils, mast cells and eosinophils (in allergy and infection)
B cell activation and somatic hypermutation?
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.
why is affinity maturation in IgG important
IgG is monomeric - only one attachment site so must be strong
Th1 cytokine produced and function?
IFN-gamma
vs intracellular bacteria + viruses
Th2 cytokine produced and function?
IL-4
vs parasitic worms
Th17 cytokine produced and function?
IL-17
vs extracellular bacteria and fungi
Treg cytokine produced and function?
IL-10
suppresses immune responses
CD4+ helper cells functions?
provide co-stimulation to B cells
drive affinity maturation of B cells
drive class-switching of B cells
Activate innate immune cells
how do CD4+ T cells help B cells
providing signal 2 (only when B cells present them with peptide/MCH2 that they recognise)
what does linked recognition (following somatic hypermutation) by CD4+ T cells allow
selection of B cells expressing receptors/antibodies that bind antigen most strongly, therefore driving affinity maturation
what does class-switching require from CD4+ T cells
co-stimulation
CD4+ T cells stimulate innate cells (help brain doesn’t work)
AHHHHH
2 mechanisms that CD8+ CTL use to kill
FAS ligation
perforin and granzyme release
FAS ligation?
directly signals to induce apoptosis
perforin and granzyme release?
perforin makes pore in cell allowing granzyme to enter. this activates caspases, DNAase activation and mitochondrial breakdown.
