abbas chapter 2 Flashcards
phagocytes
neutrophils are most abundant - production of them increases with infection
monocytes also
blood cells recruited to site of infection - ingest tiniest microbes for intracellular killing
healthy neutrophil count
4000-10000/mm^3
with infection can get up to 20000
production stimulated by cytokines
neutrophils
ingest macrophages etc in blood and enter tissue and ingest more microbes
die within a few hours
migrate by binding endothelial adhesion molecules and in response to chemoattractants that are produced on encounter with microbes
healthy monocyte count
500-1000 mm^3
monocytes
migrate by binding endothelial adhesion molecules and in response to chemoattractants that are produced on encounter with microbes - macrophages in tissue release cytokines
also ingest microbes in blood and tissues but differentiate into macrophages in tissue
TNF and IL1
act on endothelium of small vessels at site of infection
released by macrophages
E and P selectin and phagocytes binding to endo cells
adhesion molecules expressed by endo cells
neutrophils and macrophages have surface carbs that loosely bind to these
blood causes them to roll => repeated bindings
chemokines expressed on endo cells cause phagocytes to increase integrin expression => eventually in firm binding
chemokines
released by endo cells to increase phagocyte binding and by macrophages
stimulate motility - encourage phagocytes to migrate into extravascular space
inflammation
caused by accumulation of leukocytes, vascular dilation, and increased vascular permeability
toll-like receptors
specific for different composition of microbes
when engaged => activation of transcription factor NF-kappaB
actions of macrophages and neutrophils
phagocytose microbes
recruit more macrophages and lymphocytes => granulomas
granulomas
collections of cells around microbes
macrophages
can also release cytokines, GF and enzymes that remodel injured tissue and replace it with connective tissue
stimulate T-lymphocytes
natural killer cells
lymphocytes that repond to intracellular microbes by killing infected cella dn by producing the macrophage-activating cytokine IFN-8
recognize host cells that have been altered by microbial infection
when activated, release proteins from granules toward infected cells = molecules create holes in plasma membrane and other proteins that enter cells and induce apoptosis
also synthesize and secrete cytokines IFN-gamma
NK cell receptors
Killer cell Ig-like receptors (KIRs)
CD94 protein/lectin subunit NKG2
both have cytoplasmic domains with immunoreceptor tyrosine based inhibitory motifs (ITIMs)
phos on tyrosine residues when bind class I MHC
binding promotes activation of cytoplasmic protein tyrosine phosphatases - remove phos from secondary molecules => inhibits NK activity => keeps NK cells shut off when encounter self NK cells