Lecture 7- Immune evasion Flashcards
different roles of adaptive and innate immunity
innate more for fast pathogens and early response, adaptive can become important for limiting growth and initiating clearance
examples of innate responses to salmonella
complement, enterocytes producing defensins, changes in mucus production
example of a parasite and a specific immune response related to it
nematodes- Th2 mediates explusion, mast cells, IgE important
also see changes in mucus and gut motility
6 evasion strategies
speed
inhibition
avoid detection
change rapidly
spoke-screen effects
‘wrong response’
speed- example
colds and flu, replicate quickly and spread before adaptive immunity can kick in
inhibition- example
cytomegalovirus- uses a ‘decoy receptor’ to prevent chemokine action
HIV can reduce levels of MHC I on the surface of cells, inhibiting responses from Th/NK cells etc
avoiding detection- example
plasmodium- using RBCs, which lack MHC
papilloma virus- replication only at outer skin layers, which have less strong immune detection mechanisms
rapid change- example
influenza- antigenic variation, has 8 RNA segments making up its antigen and these can change (recomb., point mutations etc)
covid- variants, idea of ‘escape variants’
can also happen in parasites within a host- trypanosome surface glycoproteins
what are smoke-screen effects
causing a response to a non-protective antigen/part of the pathogen
smoke-screen effects- example
N. meningitidis, can create a large volume of T cells against non-protective antigens
non-specific activation of the immune system can be induced
‘wrong response’ examples
virokine production- secreted from host cells to create a better environment for host infection
example of an impact on the complement system
pseudomonas- inactivation of C3b and C5a, prevents recruitment of innate immune cells
how can bacteria prevent phagocytosis
‘slippery’ capsules, and shedding the surface antibodies quickly- e.g. S. pneumonia
example of how cross-species events can lead to pathology
adaptation to oriignal host, e.g. covid-2- bats have high IFN but low PRR response, so covid interferes w IFN but less PRR- leads to greater inflammation