lecture 8 Flashcards
bacteria disease example
salmonella
streptococci (tonsillitis)
viruses disease example
HIV
flu
cellular site of pathogen effects type of
immune response
vesicular (in vesicles) organism causing disease example
mycobacterium
innate defense mechanisms includes
physical barriers (e.g skin), complement system, phagocytes, NK cells and antimicrobial peptides
adaptive defense mechanisms
antibodies, cell mediated immunity
Th1 act against what type of pathogens
intracellular
what cells do Th1 cells activates
macrophages and cytotoxic t cells
Th2 act agsinst what type of pathogens
extracellular pathogens
what cells do Th2 cells activate
eosinophils, basophils and mast cells
support antibody production (particularly class switching to IgE)
what are the most prominent phagocyte
neutrophils
Th17 act against what
extracellular bacteria and fungi
does gram positive or negative bacteria have a thicker peptidoglycan cell wall
gram positive
gram negative bacteria have an outer membrane containing what
lipopolysaccharides (LPS)
toll-like receptors (TLR) on macrophage recognise what
distinct molecular patterns on pathogens that we dont have
NOD-like receptors (nucleotide binding oligomerization domain) are
intracellular sensors in cytoplasm
binding of PAMPs (pathogen associated molecular patterns) to TLR can
promote inflammation
promote dendritic cell maturation
influence differentiation of T cells
activate B cells by the TI-1 antigens
some bacteria have protective capsules
this doesnt allow what to occur
phagocytosis
role of antibodies in bacterial infection
neutralisation, opsonisation and complement activation
how do some bacteria survive in phagocytes
stop the fusion of the phagosome and the lysosome
what cytokines activate macrophages
TNFalpha and IFNgamma (from Th1)
tuberculoid leprosy
strong Th1 response
lepromatous leprosy
strong Th2 response and antibody responce
not effective as the mycobacterium leprae is intracellular
