Immunology 1.2 Flashcards
how do innate and adaptive responses integrate?
macros recognize PAMPs, induce neutrophil infiltration, , dendritic cell takes it to lymph, interphase occurs in lymph node or spleen. gives long term response.
innate immunity
epithelial barriers
phagocytes
complement
NK cells
adaptive immunity
B cells»_space;» antibody
T cells»_space;» effector T cells (helper..)
usually the one that eradicates infection.
Defensin
small cysteine rich actinic proteins. host defense peptides. active agains bacteria, fungi and viruses.
made by leukocytes.
alpha defensins- paneth cells
beta defensins- epithelial cells
PMNs
phagocytes, from common myeloid progenitor.
average of 10^11 per day. live for days.
dont proliferate. kamikazee, death of neutrophils contributes to pus!!!
CGD
chronic granulomatous disease, due to defective NADPH oxidase in PMNS.
Macrophages
circulate as monocytes then differentiate to macros.
depending on where they are they have diff phenotypes.
kupffer, alveolar, osteoclasts, microglia
new research suggests resident macros actually come from yolk sac. so it’s embryonic!!!!!! intratissue proliferation.
PAMPs
host immune response uses it to recognize microbes.
NK cell
look up!
innate responses
interstitial spacesblood lymph,.> complement, macros, PMNS
epithelial surfaces > antimicrobial peptides ill gonorrhoea, worms, C albicans
cytoplasmic > NK cells kill viruses, listeria, protozoa vesicular > macros kill mycobacteria, trypanosomes, cryptococcus.
what is the first line of defense
EPITHELIUM. skin, GI, genital tract, eyes, respiratory.
mechanical defense
hard surface, fluid flow, perspiration, sloughing, mucus, saliva, urine, sperm, tears.
Chemical defense
sebum, acidity, enzymes, lysozyme, vaginal secretions, zinc in semen.
Microbiological defense
normal flora
pore formation model
defensin blocks pore
carpet model
defensin sits on top
specificity
innate- mannose receptors
adaptive- antigens
what does it mean to have clonal distribution?
clones of lymphocytes express different receptors. only in adaptive immunity.
discrimination-
look at table 2-1
PMN granules
primary- MPO, uses H2O2 that oxidizes amino acids.
**secondary- lactoferrin, sequester iron from bacteria. non specific. proteolytic enzymes most numerous.
tertiary- gelatinase, metalloproteinases hydrolyse proteins and carbs
how are PMNS activated
p-selectin, integrin, ICAM then it will diapedese. becomes active and will eat stuff. PMN will release nets, and die. macros will degrade them.
PMN bacterial recognition
Mannose receptror, glycan receptor, scavenger receptor, LPS receptor
how does a PMN kill something?
.
oxidative burst
generated by PMN which attacks and destroy bacteria.
defective in chronic granulomatous disease= defective NADPH oxidase, which begins oxidative burst.
NADPH oxidase complex
can be genetically defective, GP91 most common. X-linked. so it affects males more drastically.
granuloma
immune response can’t eradicate infection so it compounds around bacteria. because PMNs can’t form an oxidative burst
Chediak-Higashi syndrome
cannot form normal granules, can’t function well.
become deficient in immunity
blue minks
TLR-4
look up
TLR- 7, 8, 9.
look up