intracellular infection Flashcards
how does the immune system recognise virus - viral patter recognition receptors as:
Viral capsid proteins: TLR2/6 & TLR4
Viral RNA (RNA virus) – TLR3
Endosomes – TLR3,7, 9
Cytoplasmic RNA receptors – RIG-I
( check slide 7)
innate immune response to viruses :
- after recognition , type —- are produced by infected cells which:
1- induction of an — state which — infected cells and cells nearby aka limits the — of infectious agents
2- increase — in all cells
3- activation of — cells nk cells macrophages dendritic cells
3- induction of —
- type I interferons ( IFNs)
- anti viral immune state
- shuts down
- limits the spread
- antigen presentation
- innate immune response
- adaptive immunity
effects of type I IFNs on immune cells :
1- —- up regulation
2- activates — and —
3- activates — which directly kill infected cells in —
4- activates — which directly kill infected cells in –
- MHC class I
- DC and macrophages
- cytotoxic T cells in adaptive immunity
- nk cells in innate immunity
nk cells are immune cells in – and have —– and are detached by —- which can be: – or —-
the nk cells have 2 types of receptors either — or —
1- — receptor binds to MHC class I
2- — receptor binds viral infected cells for example
- innate
- no specific antigen receptor
- altered self cells as kill virally infected cells and kill tumour cells
(They do not kill the pathogen, they kill
the cells infected by pathogens) - activatory and inhibitory
- inhibitory
- activator
- important info:
- uninfected cells:
when normal cells express mhc class I and +ve signal from inhibitory receptors so the nk won’t be activated - infected cells:
- Viruses can down-regulate MHC
class I to avoid attack by CTLs - No positive signal from
inhibitory receptor to balance a
positive signal from the
activatory receptor → NK cells activated
PLS CHECK SLIDE 14 13 )
antibody effector mechanism against viruses are:
- neutralisation ( prevetns antibody adherence , igG igA)
- opsonisation and complement activation which is insignificant for anti viral immunity
- opposinisation: aniotbody blocks the binding of microbe and infection of cells
- complment activation : antibody blocks infection of adjacent cells
—- Virally-infected cell will display viral antigens on MHC class I molecule
- Infected cell is now decorated with MHC class I bound to viral antigens
- packed full of — with —- for killing
- released once CTL is activated :
— forms pores in membrane
—- activates apoptosis
cytotoxic t lymphocyyte ( CTL) which are pre programmed to kill if they recognise an anitgen on MHC class I
vesicles w toxic enzymes
- perforin
- granzym
( check slide 20 )
innate immune response to virus:
viral — activated —> type — and — synthesised —> — innate immune response
so the viruses will stike back since hostile environment versus a
versatile opponent – THE IMMUNE SYSTEM
once of their strategies for survival is the inhibition of — and — production to resist immune response to infection
- PRR
- type I IFN and pro inflammatory
- mutlifaced
- viral detection and IFN production
mechanisms of how viruses can evade the immune response:
1—– mutate genes so aren’t recognised by MHC class I
2—- regulate MHC class I or prevent it from getting to the —
3- interferes w antigen processing as:
- epstein barr virus has a protein that inhibits —-
- HSV prevents —- and —-
( info: cells that downregualte MHC are now target for —- )
- viral genetic variation
- down regulate
- surface
- inhibits antigen processing
- peptide generation and transport
- nk cells
mechanisms of how infuelnza evade the immune response:
—- subtle changes in surface antigens on virus, generated by events like point mutations
the —- that neutralised the original virus will no longer work
it happens very —
other mehcnaims for immune evasion by infuenza:
—- major changes in viral
antigens, eg. caused by genetic
recombination between different viruses
this is when completely new – is created ad body has — immunity
it doesnt happen —-
- antigenic drift
anti viral antibodies
very frequently
antigenic shift ( not drift )
virus
historical
frequently
—– are important against mycobacterial infections
by which IL-12 — > — —> –
key functions:
- TH1
- TH1
- IFN -y
fucntions:
*Potent activation of macrophages
*Increases MHC class I and II and
antigen presentation
*activation of Nitric oxide synthase
and production of ROS
-Th1 cells produce — which activates — to kill —-
- — is a potent activator of macrophages
- up regulates stimulatory molecules — on macrophages
- upregulates co stimulatory ligand –
- increases —– and —–
- get activation of — and production of —
this leads to Collectively, get enhanced microbiocidal activity plus the activation of Th and cytotoxic T cells
- IFN-y
- macrophages
- MTb
- IFNy
- CD80/86 ( B7)
- CD40
- MHC class I and ii and antigen presentation
- nitric oxide sythesis and production of ROS
-Th1 induced macrophages maturation results in —-
- infection is sealed off by a —-
- the centre may become — and become —
- macrobacterum tubcelsosis MtB can persist for – or – in granuloma’s while host remains in good health
- MtB can be reactivated by —-
- ongoing Th1 response is critical for — control
- granuloma formation
- wall of immune cells
-hypoxic and undergo necrosis - years or decades
- reactivated by steroid treatment . malnutrions , immunosuppression as HIV
- lifelong
overall summary for both lectures :
1- extraceullar pathogens goal of the immune system is to kill —
the extracelullar bacteria has:
the helminth has:
2- intracellular pathigen goal of immune system is to kill —
- viruses as:
- intracellular bacteria has:
- pathogens
- neutrophils, macrophages, Th17, antibodies
- Th2, IgE antibodies, eosinophils and mast cells
- infected cells
- IFN response, NK cells and cytotoxic T cells, antibody neutralisation
- Th1, IFN-γ (here the immune system also tries to increase its microbiocidal weapons), macrophages
