lecture 2 Flashcards
key functions of innate immunity
- prevent, control and eliminate infectious agents
- recognize and eliminate products of damaged/dead host cells -> initiate tissue repair
- stimulate and influence adaptive (special) immune repsonse
components of innate immunity
mechanical barriers chemical barriers physiological factors proteins cells initiates adaptive immune response disruption of innate immunity by microbes :(
mechanical barriers
intact skin
mucosal epithelia & mucus (sneezing, coughing, vomiting, diarrhea)
shedding of infected skins
flushing of bodily fluids (tears, saliva, sweat, pee)
chemical barriers
skin (sebum - sweat)
saliva (lysozyme and antibiotics
mucus (lysozyme and antibiotics)
tears (lysozyme)
DEFENSINS (alpha, beta and gamma - within skin, mucosal epithelial cells, neutrophils and NK cells)
CATHELICIDINS (neutrophils, skin epithelia, GI/respiratory mucosa - will poke hole in pathogen mwhaha)
LACTOFERRIN (bind to iron to create stabber for microbe… decreases RBC production, acute phase protein)
HCl (in stomach)
bile salts and acids
physiological factors
temperature (high fever reduces growth for microbes)
oxygen tension (high O2 makes anaerobic microbes die)
hormonal balance (corticosteroids lead to decreased inflammatory response which could lead to infection)
age (kids and gpas at higher risk to disease bc suboptimal immune systems)
effector proteins
complement mannose binding lectin c reactive protein cytokines (TNF, IL-1, chemokines, IFNalpha, IFNbeta, IFNg, IL12, IL15, IL10, TGFb, IL8) natural antibodies acute phase proteins (lactoferrins)
complement effector protein
kills microbes
opsonization of microbes (through initiating phagocytosis)
activation of leukocytes (WBC)
opsonization
extracellular protein that signals to phagocytizing cell to eat it and KILL, tag cells for phagocytosis
mannose binding lectin
collectin
binds carbohydrates
opsonization of microbes
activation of complement -> lectin pathway
C reactive protein
pentraxin
osponization of microbe
activation of complement
TNF, INL1, chemokines
inflammation
IFNa & b
resistance to viral infection
IFNg
macrophage activation (macrophage cant kill microbe unless activated!)
IL12
NK and Tcells make IFNg (macrophage activation!)
IL15
proliferation of NK cells
IL10, TGFb
control inflammation
IL8
CXCL8 - chemokine
chemoattractant of neutrophils
natural antibodies
made by B cell from fetal liver stem cells (hemopoetic)
acute phase proteins
lactoferrin
inflammation
alarmins
inflammatory molecule as result of damaged cell/tissue
heparan sulfate (repair ECM)
heat shock proteins (repair cytoplasm?)
vasoactive lipids
inflammatory molecule as result of damaged cell/tissue
prostaglandins
leukotrienes
generation of vasoactive lipids from cell membrane
damage to cell/tissue -> phospholipases activated -> cell membrane phospholipids broken -> arachidonic acid -> a. leukotriene -> b. prostaglandin
results in increased vascular permeability and smooth muscle contraction (swelling) or pain and vasodilation
5-lipoxygenase (enzyme for leukotriene)
cycloozygenase (enzyme for prostaglandin)
aspirin inhibits
cyclooxygenase -> so the pain and vasodilation response of prostaglandins is inhibited
steroids inhibit
phospholipase -> so the entire vasoactive lipid pathway is disrupted, no swelling or pain response